U.S. cancer scientists say they've demonstrated a gene involved in regulating aging also blocks prostate cancer cell growth.
Dr. Richard Pestell and colleagues at the Kimmel Cancer Center at Thomas Jefferson University say they hope the newly found connection will aid in better understanding the development of prostate cancer and lead to new drugs against the disease.
The gene, SIRT1, is a member of a family of enzymes called sirtuins that have far-reaching influence in all organisms, including roles in metabolism, gene expression and aging.
"We know that sirtuins play a role in aging, and that the risk for prostate cancer increases with aging, but no one has ever linked the two until now," said Pestell, professor and chairman of cancer biology at Jefferson Medical College. "We've shown that by making a prostate cancer with cells overexpressing a mutation for the androgen receptor, which is resistant to current forms of therapy, we can almost completely block the growth of these cells with SIRT1."
The study is reported in the journal Molecular and Cellular Biology.
Tuesday, November 28, 2006
Prostate cancer screenings in men 70 and older
THE QUESTION: Are doctors doing unnecessary screening for prostate cancer in men 70 and older?
THE CONTEXT: For men with a life expectancy of less than 10 years, the risks associated with screening for prostate cancer outweigh the benefits. But some reports have suggested that many sick, elderly men are being screened.
THE STUDY: Researchers studied the records of nearly 600,000 men age 70 and older who were treated by the Department of Veterans Affairs (VA) in 2002 and 2003. They analyzed their health status and whether or not they were given prostate-specific antigen screening, also known as PSA screening.
THE RESULTS: In all, 56 percent of the men received PSA screening. The percentage of men who were screened declined with age. But within each age group, men who had lower life-expectancy - and therefore stood to benefit less from screening - were screened roughly as often as healthier men with a higher life expectancy.
Among men 85 and older, fewer than 10 percent have a life expectancy of 10 years or more. Nevertheless, roughly one-third were screened -- a figure that held constant for the healthiest and sickest subgroups.
The authors concluded that screening rates among men with low life expectancies should be "much lower than the current practice.''
The abstract of the study, which was published in the Journal of the American Medical Association, is available online at jama.ama-assn.org.
THE CONTEXT: For men with a life expectancy of less than 10 years, the risks associated with screening for prostate cancer outweigh the benefits. But some reports have suggested that many sick, elderly men are being screened.
THE STUDY: Researchers studied the records of nearly 600,000 men age 70 and older who were treated by the Department of Veterans Affairs (VA) in 2002 and 2003. They analyzed their health status and whether or not they were given prostate-specific antigen screening, also known as PSA screening.
THE RESULTS: In all, 56 percent of the men received PSA screening. The percentage of men who were screened declined with age. But within each age group, men who had lower life-expectancy - and therefore stood to benefit less from screening - were screened roughly as often as healthier men with a higher life expectancy.
Among men 85 and older, fewer than 10 percent have a life expectancy of 10 years or more. Nevertheless, roughly one-third were screened -- a figure that held constant for the healthiest and sickest subgroups.
The authors concluded that screening rates among men with low life expectancies should be "much lower than the current practice.''
The abstract of the study, which was published in the Journal of the American Medical Association, is available online at jama.ama-assn.org.
Monday, November 20, 2006
Prostate Cancer and Association With Plasma Cholesterol
Prostate cancer patients who had lower levels of cholesterol in their blood had a significantly reduced chance of developing more aggressive forms of the disease, compared to patients with higher cholesterol readings.
These findings may help explain the earlier discovery, reported by the same team of researchers at the AACR annual meeting in 2005, that men who used statin drugs experienced half the risk of developing advanced prostate cancer.
"Statin drugs reduce cholesterol in the blood, but they also influence a number of different pathways," said the study's lead researcher, Elizabeth Platz, ScD, MPH, an associate professor in the Department of Epidemiology at Johns Hopkins Bloomberg School of Public Health. "This study suggests that the ability of statins to lower cholesterol may be important to prostate carcinogenesis, but we are continuing to examine other pathways with which statin drugs interact, such as reduction of inflammation."
The researchers looked at cholesterol levels first because cholesterol affects cell signaling and survival. Some scientists theorize that a large quantity of cholesterol in the blood could stimulate the survival of abnormal prostate cells.
They studied blood drawn from 698 men before they were diagnosed with prostate cancer and matched it to blood taken from 698 men who had not been diagnosed with the disease. All of the men participated in Harvard University's Health Professionals Follow-up Study, a group of 18,018 participants who provided a blood sample between 1993 and 1995.
They found that mean cholesterol levels did not differ between the men with prostate cancer and the control participants, suggesting that cholesterol was not involved in the initial development of prostate cancer, Platz said.
But when comparing men who had the lowest quartile of serum cholesterol to men who had the highest, they found that prostate cancer patients with lower cholesterol had the lowest risk of developing a more worrisome form of the disease. They specifically found that the risk of being diagnosed with high-grade or advanced cancer was reduced by 40 percent and 50 percent, respectively.
Platz says it is not clear at what levels serum cholesterol may stimulate the abnormal growth seen in cancer development. "The findings suggest either that high cholesterol may push existing prostate cancer to become aggressive, or, alternatively, very low levels of cholesterol may provide protection against development of an aggressive cancer," she said. "We just don't know which it is at this point."
She also said that because the findings come from an observational study, not a trial, it is impossible to conclude that men can lower their risk of developing an aggressive form of prostate cancer by reducing their intake of saturated fat, the type of fat that increases serum cholesterol, which some studies have linked to an increased risk of advanced prostate cancer.
"It is too soon to say that such measures would be specifically beneficial to lowering such a risk, but for good health in general, it is prudent to consume a diet that contains healthful fats that do not increase serum cholesterol," she said.
These findings may help explain the earlier discovery, reported by the same team of researchers at the AACR annual meeting in 2005, that men who used statin drugs experienced half the risk of developing advanced prostate cancer.
"Statin drugs reduce cholesterol in the blood, but they also influence a number of different pathways," said the study's lead researcher, Elizabeth Platz, ScD, MPH, an associate professor in the Department of Epidemiology at Johns Hopkins Bloomberg School of Public Health. "This study suggests that the ability of statins to lower cholesterol may be important to prostate carcinogenesis, but we are continuing to examine other pathways with which statin drugs interact, such as reduction of inflammation."
The researchers looked at cholesterol levels first because cholesterol affects cell signaling and survival. Some scientists theorize that a large quantity of cholesterol in the blood could stimulate the survival of abnormal prostate cells.
They studied blood drawn from 698 men before they were diagnosed with prostate cancer and matched it to blood taken from 698 men who had not been diagnosed with the disease. All of the men participated in Harvard University's Health Professionals Follow-up Study, a group of 18,018 participants who provided a blood sample between 1993 and 1995.
They found that mean cholesterol levels did not differ between the men with prostate cancer and the control participants, suggesting that cholesterol was not involved in the initial development of prostate cancer, Platz said.
But when comparing men who had the lowest quartile of serum cholesterol to men who had the highest, they found that prostate cancer patients with lower cholesterol had the lowest risk of developing a more worrisome form of the disease. They specifically found that the risk of being diagnosed with high-grade or advanced cancer was reduced by 40 percent and 50 percent, respectively.
Platz says it is not clear at what levels serum cholesterol may stimulate the abnormal growth seen in cancer development. "The findings suggest either that high cholesterol may push existing prostate cancer to become aggressive, or, alternatively, very low levels of cholesterol may provide protection against development of an aggressive cancer," she said. "We just don't know which it is at this point."
She also said that because the findings come from an observational study, not a trial, it is impossible to conclude that men can lower their risk of developing an aggressive form of prostate cancer by reducing their intake of saturated fat, the type of fat that increases serum cholesterol, which some studies have linked to an increased risk of advanced prostate cancer.
"It is too soon to say that such measures would be specifically beneficial to lowering such a risk, but for good health in general, it is prudent to consume a diet that contains healthful fats that do not increase serum cholesterol," she said.
Monday, November 13, 2006
Proteins to Treat Prostate Cancer!
Here is good news for the patients with prostate cancer. According to a new study, researchers have come out with a new type of therapy that would be very effective in treating prostate cancer.
Earlier tests conducted on mice have proved that this new therapy called, PRX302 is capable of killing the cancerous prostate cells without destroying or harming the healthy cells. Therapy PRX302 uses a protein for treating prostate cancer and the interesting thing about this protein is that it is produced by the cancerous cells themselves.
So, it would not be wrong saying that now doctors will use protein made of cancer cells to treat the deadly cancer.
Earlier tests conducted on mice have proved that this new therapy called, PRX302 is capable of killing the cancerous prostate cells without destroying or harming the healthy cells. Therapy PRX302 uses a protein for treating prostate cancer and the interesting thing about this protein is that it is produced by the cancerous cells themselves.
So, it would not be wrong saying that now doctors will use protein made of cancer cells to treat the deadly cancer.
Tuesday, November 07, 2006
Prostate Cancer Risk Factors
A risk factor is anything that may increase a person’s chance of developing a disease. It may be an activity, such as smoking, diet, family history, or many other things. Different diseases, including cancers, have different risk factors. In general, all men are at risk for prostate cancer. However, there are specific risk factors that increase the likelihood that certain men will develop the disease, including the following:
Age is a risk factor for prostate cancer, especially men age 50 and older. More than 80 percent of all prostate cancers are diagnosed in men over the age of 65. Race: Prostate cancer is nearly twice as common among African-American men than it is among Caucasian-American men. Japanese and Chinese men native to their country have the lowest rates of prostate cancer.
Diet: Data suggests that the diet consumed in Western industrialized countries may be one of the most important contributory factors for developing prostate cancer. The following information regarding diet and its effect on the risk for prostate cancer include men who eat a high-fat diet may have a greater chance of developing prostate cancer. Dietary fiber intake may decrease the progression of prostate cancer. Soy protein lowers fat intake, and the isoflavones in soy have been found to inhibit the growth of prostate cancer. Vitamin E and selenium Vitamin E, an antioxidant, combined with selenium, has been shown to inhibit tumor growth in laboratory animals. Carotenoids Carotenoids containing lycopenes have been shown to inhibit the growth of human prostate cancer cells in tissue cultures. The primary source of lycopenes is processed tomatoes in tomato juice and tomato paste. Obesity Obesity not only contributes to diabetes and high cholesterol, but has also been associated with some common cancers including prostate cancer.
Vasectomy, BPH (benign prostatic hyperplasia), or STD (sexually transmitted disease) Researchers have looked at whether men who have had a vasectomy, BPH, or those who have had exposure to STD’s are at increased risk for prostate cancer. Some studies suggest a link, while others don’t. Family history of prostate cancer. A father or brother with prostate cancer doubles a man’s risk of developing prostate cancer. The risk is even higher for men with several affected relatives. Geneticists divide families into three groups, depending upon the number of men with prostate cancer and their ages of onset, including the following: Sporadic - a family with prostate cancer present in one man, at a typical age of onset. Familial - a family with prostate cancer present in more than one person, but with no definitive pattern of inheritance and usually an older age of onset. Hereditary - Five to 10 percent of prostate cancer cases are considered hereditary. Genetic Approximately 9 percent of all prostate cancers and 45 percent of cases in men younger than age 55 can be attributed to a cancer susceptibility gene that is inherited as a dominant trait (from parent to child).
Age is a risk factor for prostate cancer, especially men age 50 and older. More than 80 percent of all prostate cancers are diagnosed in men over the age of 65. Race: Prostate cancer is nearly twice as common among African-American men than it is among Caucasian-American men. Japanese and Chinese men native to their country have the lowest rates of prostate cancer.
Diet: Data suggests that the diet consumed in Western industrialized countries may be one of the most important contributory factors for developing prostate cancer. The following information regarding diet and its effect on the risk for prostate cancer include men who eat a high-fat diet may have a greater chance of developing prostate cancer. Dietary fiber intake may decrease the progression of prostate cancer. Soy protein lowers fat intake, and the isoflavones in soy have been found to inhibit the growth of prostate cancer. Vitamin E and selenium Vitamin E, an antioxidant, combined with selenium, has been shown to inhibit tumor growth in laboratory animals. Carotenoids Carotenoids containing lycopenes have been shown to inhibit the growth of human prostate cancer cells in tissue cultures. The primary source of lycopenes is processed tomatoes in tomato juice and tomato paste. Obesity Obesity not only contributes to diabetes and high cholesterol, but has also been associated with some common cancers including prostate cancer.
Vasectomy, BPH (benign prostatic hyperplasia), or STD (sexually transmitted disease) Researchers have looked at whether men who have had a vasectomy, BPH, or those who have had exposure to STD’s are at increased risk for prostate cancer. Some studies suggest a link, while others don’t. Family history of prostate cancer. A father or brother with prostate cancer doubles a man’s risk of developing prostate cancer. The risk is even higher for men with several affected relatives. Geneticists divide families into three groups, depending upon the number of men with prostate cancer and their ages of onset, including the following: Sporadic - a family with prostate cancer present in one man, at a typical age of onset. Familial - a family with prostate cancer present in more than one person, but with no definitive pattern of inheritance and usually an older age of onset. Hereditary - Five to 10 percent of prostate cancer cases are considered hereditary. Genetic Approximately 9 percent of all prostate cancers and 45 percent of cases in men younger than age 55 can be attributed to a cancer susceptibility gene that is inherited as a dominant trait (from parent to child).
Monday, November 06, 2006
Study urges earlier prostate exams
The dubious rite of passage when a man turns 50 might arrive even earlier, based on a study that suggests screening for prostate cancer should begin at 40.
Men are advised to get a yearly screening based on the amount of the prostate hormone PSA found in their blood. A high level is a warning sign of prostate cancer.
Now, a team of Johns Hopkins researchers says screening should begin about age 40 but be done less frequently. The team also recommends basing a diagnosis on multiple readings over time that would show how a man's PSA level changes.
Those changes, the researchers say, would reduce the number of men treated unnecessarily and would better identify potentially deadly tumors that require aggressive treatment.
Their findings, published Wednesday in the Journal of the National Cancer Institute, were based on their study of nearly 1,000 men who volunteered for a long-term study of aging that began in 1958.
Using frozen blood samples, the Hopkins researchers explored whether the speed at which a man's PSA levels changed was a good predictor of his chances of dying of prostate cancer.
Current PSA tests, the researchers said, look at the concentration of the hormone in a man's blood at one point. If the man has a high PSA level, the next step is a biopsy to determine whether he has a cancerous prostate tumor.
Researchers found that the faster a man's PSA level increased, the more likely he was to die of prostate cancer, said Dr. H. Ballentine Carter, a professor of urology and oncology at the Johns Hopkins University School of Medicine and the study's lead author.
''We don't need to diagnose more prostate cancer,'' he said. ''We need to find the prostate cancers that are fatal.''
The current method of looking at a single reading of a man's PSA level proved less effective.
In many cases, Carter said, a man's PSA level increased rapidly before it reached a concentration so high that it would prompt a doctor to order a biopsy. The PSA rise in men who eventually died of prostate cancer sometimes began before age 50. Using the rate of increase -- a measure called PSA velocity -- would have provided an earlier alert, he said.
Carter said that method also would reduce the number of men who undergo treatment for tumors that diminish neither their quality of life nor length of life.
Dr. Mark S. Litwin, who had not seen the Hopkins study, questioned the wisdom of PSA testing for men younger than 50.
Prostate cancer cases are rare in men in their 40s, said Litwin, a professor of urology and oncology at the University of California-Los Angeles. He argued that earlier testing should be reserved for high-risk patients, such as blacks and people with family histories of prostate cancer.
He did agree that looking at the speed at which a man's PSA level changed is a good tool.
''It sounds like it's certainly consistent with prior research,'' he said of the Hopkins study.
This year, the American Cancer Society estimates, more than 234,000 American men will be diagnosed with prostate cancer and 27,000 will die from it.
Men are advised to get a yearly screening based on the amount of the prostate hormone PSA found in their blood. A high level is a warning sign of prostate cancer.
Now, a team of Johns Hopkins researchers says screening should begin about age 40 but be done less frequently. The team also recommends basing a diagnosis on multiple readings over time that would show how a man's PSA level changes.
Those changes, the researchers say, would reduce the number of men treated unnecessarily and would better identify potentially deadly tumors that require aggressive treatment.
Their findings, published Wednesday in the Journal of the National Cancer Institute, were based on their study of nearly 1,000 men who volunteered for a long-term study of aging that began in 1958.
Using frozen blood samples, the Hopkins researchers explored whether the speed at which a man's PSA levels changed was a good predictor of his chances of dying of prostate cancer.
Current PSA tests, the researchers said, look at the concentration of the hormone in a man's blood at one point. If the man has a high PSA level, the next step is a biopsy to determine whether he has a cancerous prostate tumor.
Researchers found that the faster a man's PSA level increased, the more likely he was to die of prostate cancer, said Dr. H. Ballentine Carter, a professor of urology and oncology at the Johns Hopkins University School of Medicine and the study's lead author.
''We don't need to diagnose more prostate cancer,'' he said. ''We need to find the prostate cancers that are fatal.''
The current method of looking at a single reading of a man's PSA level proved less effective.
In many cases, Carter said, a man's PSA level increased rapidly before it reached a concentration so high that it would prompt a doctor to order a biopsy. The PSA rise in men who eventually died of prostate cancer sometimes began before age 50. Using the rate of increase -- a measure called PSA velocity -- would have provided an earlier alert, he said.
Carter said that method also would reduce the number of men who undergo treatment for tumors that diminish neither their quality of life nor length of life.
Dr. Mark S. Litwin, who had not seen the Hopkins study, questioned the wisdom of PSA testing for men younger than 50.
Prostate cancer cases are rare in men in their 40s, said Litwin, a professor of urology and oncology at the University of California-Los Angeles. He argued that earlier testing should be reserved for high-risk patients, such as blacks and people with family histories of prostate cancer.
He did agree that looking at the speed at which a man's PSA level changed is a good tool.
''It sounds like it's certainly consistent with prior research,'' he said of the Hopkins study.
This year, the American Cancer Society estimates, more than 234,000 American men will be diagnosed with prostate cancer and 27,000 will die from it.
Sunday, November 05, 2006
Newer Approach Urged In Screening For Aggressive Prostate Cancer
Researchers at the Johns Hopkins University School of Medicine say that how fast the amount of PSA (prostate-specific antigen) in a man's blood increases, or PSA velocity (PSAV), is an accurate gauge of tumor aggression and danger, even when PSA levels are so low as to not warrant a biopsy.
Findings of a Hopkins study of PSAV, in this month's Journal of the National Cancer Institute, may add a new level of predictive accuracy to prostate cancer testing, the value of which has remained controversial under currently accepted guidelines, the investigators say.
"Our data provide a further argument for PSA testing that begins relatively early in life, when PSA levels are usually lower and prostate enlargement is not a confounding factor in diagnosis," says H. Ballentine Carter, M.D., the director of the Johns Hopkins Division of Adult Urology at the Brady Urological Institute and lead author of the study. "We would recommend that men at around age 40, not 50, have their PSA checked to develop a baseline against which to compare future changes (velocity), since even a slight rise in PSA may indicate a potential for cancer down the road."
An estimated 234,460 men in the United States will be diagnosed with prostate cancer this year, according to the American Cancer Society.
"The main debate over how to use PSA has centered on the choice of the level that is used to trigger a biopsy," says Carter, a professor at the Johns Hopkins University School of Medicine. "Lowering the level that triggers a biopsy leads to detection of more harmless cancers, and higher levels could miss the opportunity to detect an important cancer early. We have found that the rate at which a man's PSA rises may be more important than any absolute level for identifying men who will develop life-threatening cancer while their disease is still curable. In addition, PSA velocity could be a useful method for identifying those men with a prostate cancer that could be safely monitored - an approach termed 'active surveillance'."
PSA is a protein found in the bloodstream of men, produced by the prostate gland and found at increased levels in those with prostate cancer. In previous research, PSA velocity in the year before prostate cancer diagnosis has been shown to identify men who are likely not to be cured by surgery. However, Carter's latest findings show that PSA velocity can also identify men with life-threatening disease at a time when it is still curable.
Using serum samples dating as far back as 1958, frozen as part of an ongoing randomized health study of men, Carter and his team determined PSA velocity in 980 of those study participants (856 without prostate cancer, 104 with the disease and 20 who died from it) up until May of 2005. They found that the PSA velocity determined at a time when PSA levels would not have triggered a biopsy were predictive of death from prostate cancer 20 to 30 years later.
Those men whose PSA velocity was lower had a 92 percent chance of not dying of prostate cancer 25 years later; whereas those with a higher PSA velocity had a 54 percent chance of not dying of prostate cancer. The rates of prostate cancer death were 1,240 in 100,000 for subjects with a higher velocity compared to 140 in 100,000 for those with lower velocities.
Carter emphasizes that an important difference between the current research and previous studies is that the subjects in the current study were not selected, but rather taken at random from a large, ongoing study, thus more accurately representing the U.S. population.
Findings of a Hopkins study of PSAV, in this month's Journal of the National Cancer Institute, may add a new level of predictive accuracy to prostate cancer testing, the value of which has remained controversial under currently accepted guidelines, the investigators say.
"Our data provide a further argument for PSA testing that begins relatively early in life, when PSA levels are usually lower and prostate enlargement is not a confounding factor in diagnosis," says H. Ballentine Carter, M.D., the director of the Johns Hopkins Division of Adult Urology at the Brady Urological Institute and lead author of the study. "We would recommend that men at around age 40, not 50, have their PSA checked to develop a baseline against which to compare future changes (velocity), since even a slight rise in PSA may indicate a potential for cancer down the road."
An estimated 234,460 men in the United States will be diagnosed with prostate cancer this year, according to the American Cancer Society.
"The main debate over how to use PSA has centered on the choice of the level that is used to trigger a biopsy," says Carter, a professor at the Johns Hopkins University School of Medicine. "Lowering the level that triggers a biopsy leads to detection of more harmless cancers, and higher levels could miss the opportunity to detect an important cancer early. We have found that the rate at which a man's PSA rises may be more important than any absolute level for identifying men who will develop life-threatening cancer while their disease is still curable. In addition, PSA velocity could be a useful method for identifying those men with a prostate cancer that could be safely monitored - an approach termed 'active surveillance'."
PSA is a protein found in the bloodstream of men, produced by the prostate gland and found at increased levels in those with prostate cancer. In previous research, PSA velocity in the year before prostate cancer diagnosis has been shown to identify men who are likely not to be cured by surgery. However, Carter's latest findings show that PSA velocity can also identify men with life-threatening disease at a time when it is still curable.
Using serum samples dating as far back as 1958, frozen as part of an ongoing randomized health study of men, Carter and his team determined PSA velocity in 980 of those study participants (856 without prostate cancer, 104 with the disease and 20 who died from it) up until May of 2005. They found that the PSA velocity determined at a time when PSA levels would not have triggered a biopsy were predictive of death from prostate cancer 20 to 30 years later.
Those men whose PSA velocity was lower had a 92 percent chance of not dying of prostate cancer 25 years later; whereas those with a higher PSA velocity had a 54 percent chance of not dying of prostate cancer. The rates of prostate cancer death were 1,240 in 100,000 for subjects with a higher velocity compared to 140 in 100,000 for those with lower velocities.
Carter emphasizes that an important difference between the current research and previous studies is that the subjects in the current study were not selected, but rather taken at random from a large, ongoing study, thus more accurately representing the U.S. population.
Monday, May 08, 2006
Prostate cancer gene discovered
A genetic variant that puts around one man in every 10 at higher risk of prostate cancer has been discovered, marking a milestone in understanding and diagnosing the most common cancer among men.
This is the first identification of a major genetic risk factor for prostate cancer in the general population: one fifth of men of European ancestry with prostate cancer carry at least one copy of the newly discovered variant, which confers an approximately 60 per cent increase in risk of the disease and accounts for approximately eight per cent of all cases.
The milestone in understanding, diagnosing and treating the cancer, which is rising in incidence with over 30,100 new cases a year in Britain, was announced yesterday in the journal Nature Genetics by a team at Decode genetics, a biopharmaceutical company, with academic colleagues in Iceland, the United States and Sweden.
"This is one of the first genetic variants ever found to confer significant risk of a major cancer among the population in general," said Dr Kari Stefansson, chief executive of Decode genetics and senior author on the study.
This variant also appears to be associated with the development of more aggressive prostate tumours, suggesting that it specifically increases the risk of malignant disease.
A diagnostic test for the variant may enable doctors to make more informed decisions as to how closely they should monitor those who are at high risk, and how aggressively they should treat the disease once it presents.
"We plan to use this discovery as the basis for the development of such a diagnostic test," said Dr Stefansson.
This is the first identification of a major genetic risk factor for prostate cancer in the general population: one fifth of men of European ancestry with prostate cancer carry at least one copy of the newly discovered variant, which confers an approximately 60 per cent increase in risk of the disease and accounts for approximately eight per cent of all cases.
The milestone in understanding, diagnosing and treating the cancer, which is rising in incidence with over 30,100 new cases a year in Britain, was announced yesterday in the journal Nature Genetics by a team at Decode genetics, a biopharmaceutical company, with academic colleagues in Iceland, the United States and Sweden.
"This is one of the first genetic variants ever found to confer significant risk of a major cancer among the population in general," said Dr Kari Stefansson, chief executive of Decode genetics and senior author on the study.
This variant also appears to be associated with the development of more aggressive prostate tumours, suggesting that it specifically increases the risk of malignant disease.
A diagnostic test for the variant may enable doctors to make more informed decisions as to how closely they should monitor those who are at high risk, and how aggressively they should treat the disease once it presents.
"We plan to use this discovery as the basis for the development of such a diagnostic test," said Dr Stefansson.
Wednesday, April 26, 2006
Colon and prostate cancer abstracts accepted by American Society of Clinical Oncology
ChondroGene Limited (TSX Venture: CDG - News) announced today that two abstracts have been accepted for presentation at the American Society of Clinical Oncology (ASCO) Annual Meeting being held in Atlanta from June 2 to 6. The two abstracts detail results of the Company's work in identifying blood-based biomarkers for colon cancer and for prostate cancer. Both abstracts demonstrate the power and flexibility of the Sentinel Principle(TM), ChondroGene's proprietary approach to identify molecular signatures of disease in blood.
The first abstract entitled, "Novel blood biomarker panel detects human colorectal cancer" was authored by M. Han, C. T. Liew, H. W. Zhang, K. T. Yip, Z. Y. Song, H. M. Li, X. P. Geng, L. X. Zhu, K. W. Marshall, C. C. Liew. ChondroGene scientists worked with researchers at the Chinese University of Hong Kong, Hong Kong, China, Lam Wah Ee Hospital, Penang, Malaysia, The 2nd Affiliated Hospital of Zhejiang University, Hangzhou, China and Anhui Medical University, Hefei, China. The abstract reports results from a study that identified gene signatures from blood cells which were then used to identify and characterize a set of biomarkers able to differentiate patients with colorectal cancer from controls.
The second abstract entitled "Blood-based biomarkers for detecting aggressive prostate cancer at time of biopsy" was authored by R. K. Nam, K. W. Marshall, R. Zheng, H. W. Zhang, S. A. Narod, C. C. Liew. This study, conducted with research collaborators at the University of Toronto, identified a set of blood biomarkers that were able to distinguish patients with aggressive forms of prostate cancer from controls.
"We are pleased that our two abstracts were accepted for presentation at this conference. The annual ASCO meeting is an important international conference where many new cancer diagnostic and therapeutic innovations and discoveries are first disclosed," stated K. Wayne Marshall, MD, PhD, President and CEO of ChondroGene. "We, along with our collaborators, are very encouraged by our initial results in colon and prostate cancer detection using blood samples. We continue to collect additional patient samples and conduct further studies in order to refine our tests in these two areas as we prepare to commercialize our first products."
The first abstract entitled, "Novel blood biomarker panel detects human colorectal cancer" was authored by M. Han, C. T. Liew, H. W. Zhang, K. T. Yip, Z. Y. Song, H. M. Li, X. P. Geng, L. X. Zhu, K. W. Marshall, C. C. Liew. ChondroGene scientists worked with researchers at the Chinese University of Hong Kong, Hong Kong, China, Lam Wah Ee Hospital, Penang, Malaysia, The 2nd Affiliated Hospital of Zhejiang University, Hangzhou, China and Anhui Medical University, Hefei, China. The abstract reports results from a study that identified gene signatures from blood cells which were then used to identify and characterize a set of biomarkers able to differentiate patients with colorectal cancer from controls.
The second abstract entitled "Blood-based biomarkers for detecting aggressive prostate cancer at time of biopsy" was authored by R. K. Nam, K. W. Marshall, R. Zheng, H. W. Zhang, S. A. Narod, C. C. Liew. This study, conducted with research collaborators at the University of Toronto, identified a set of blood biomarkers that were able to distinguish patients with aggressive forms of prostate cancer from controls.
"We are pleased that our two abstracts were accepted for presentation at this conference. The annual ASCO meeting is an important international conference where many new cancer diagnostic and therapeutic innovations and discoveries are first disclosed," stated K. Wayne Marshall, MD, PhD, President and CEO of ChondroGene. "We, along with our collaborators, are very encouraged by our initial results in colon and prostate cancer detection using blood samples. We continue to collect additional patient samples and conduct further studies in order to refine our tests in these two areas as we prepare to commercialize our first products."
Tuesday, April 25, 2006
A Better Way To Gauge Prostate Cancer Risk?
A team of American researchers has developed a "risk calculator" that they say is a better tool for predicting a man's odds of developing prostate cancer than prostate-specific antigen blood testing alone.
The calculator - posted online for use by both patients and physicians - adds age, race, family history of prostate cancer, prior biopsy findings and digital rectal exam results into the mix alongside PSA levels to assess a man's risk before having a new biopsy.
"PSA is a very important predictor of cancer, but is only one part of the picture of a man's risk of cancer," explains study author Dr. Ian M. Thompson, professor and chairman of the department of urology at the University of Texas Health Science Center in San Antonio.
His team describes the new screen in the April issue of the Journal of the National Cancer Institute.
According to the American Cancer Society, prostate cancer is the second leading cancer killer for men. An estimated one in six men will receive a prostate cancer diagnosis in their lifetime, and more than 30,000 Americans currently die of the disease each year.
For healthy men over the age of 50, the ACS now recommends an annual PSA blood test, as well as a digital rectal exam. The organization advises that men at higher risk -- such as blacks and patients with a history of prostate cancer in their family -- begin such testing at age 45.
While 50 percent of older men now undergo routine PSA screenings, Thompson says his prior work suggests that PSA results are more useful when taken in context with other factors. Too often, he says, PSA levels are interpreted as black-and-white indicators of either "normal" or "elevated" risk status. The truth is that rising PSA levels reflect a more graduated increase in cancer risk.
Looking for a more accurate method, Thompson and his colleagues collected data from more than 5,500 healthy men over the age of 55 who had participated in a large-scale prostate cancer prevention trial.
For a period of seven years, all the men underwent annual PSA and digital rectal exam testing, and well as having at least one prostate biopsy conducted over the study period. By the study's end, nearly 22 percent of the men went on to develop prostate cancer, and 5 percent developed high-grade disease.
At the seven-year mark, the researchers fed a combination of accumulated data -- biopsy findings, patient age, race, family history of prostate cancer, previous biopsy history, along with PSA levels and DRE results - into their "statistical risk models."
Thompson's team found that a family history of prostate cancer, or an abnormal result from the PSA or DRE test, were all strongly associated with an increased risk for prostate cancer.
Race and age also figured in the equation, with blacks and older men at relatively high risk for prostate cancer.
Having had a prior negative biopsy result was found to be associated with a decreased risk for the disease.
By compiling such patient variables together, the Texas group say they were able to develop a prostate risk calculator that provides better predictive accuracy than an analysis of PSA levels alone.
"This study provides a way to integrate other important risk factors to allow men and their doctors to better understand their risk and make a more intelligent decision whether to proceed with further testing," Thompson says.
But in an accompanying editorial, Dr. H. Ballentine Carter, of the Johns Hopkins School of Medicine, cautioned that the calculator's current design fails to distinguish between slow-growing cancers and more life-threatening varieties.
This, he says, could lead to a rash of unnecessary biopsies.
Robert Smith, director of cancer screening at the American Cancer Society, says the new model has its pros and cons.
"It does not distinguish between significant and not-significant disease, so the calculator provides some help, but not enough help," he says. "But it also allows an individual to take their PSA level and actually interpret it in the context of some other information based on the experience of a large number of men, to understand what is the likelihood that they have prostate cancer. So I think it could actually be useful."
A second study, also published in the April of the same journal, suggests that new prostate cancer treatments currently undergoing clinical trials could be better and more quickly assessed by tracking ongoing changes in patients' PSA levels, rather than by waiting to tally long-term patient survival.
The team of Columbia University researchers working at New York-Presbyterian Hospital/Columbia in New York City based their conclusions on an analysis of the progress of 551 men undergoing a new treatment for prostate cancer.
They found that a 30 percent drop in PSA levels in the first three months of treatment correlated with a 50 percent drop in their risk of death -- a "surrogate" marker that could be used in place of the usual endpoint, survival. Use of this marker might mean a treatment's effectiveness could be evaluated much earlier.
The researchers noted that the U.S. Food and Drug Administration currently bases its "endpoint" assessment of a given treatment's success solely on long-term patient survival.
The calculator - posted online for use by both patients and physicians - adds age, race, family history of prostate cancer, prior biopsy findings and digital rectal exam results into the mix alongside PSA levels to assess a man's risk before having a new biopsy.
"PSA is a very important predictor of cancer, but is only one part of the picture of a man's risk of cancer," explains study author Dr. Ian M. Thompson, professor and chairman of the department of urology at the University of Texas Health Science Center in San Antonio.
His team describes the new screen in the April issue of the Journal of the National Cancer Institute.
According to the American Cancer Society, prostate cancer is the second leading cancer killer for men. An estimated one in six men will receive a prostate cancer diagnosis in their lifetime, and more than 30,000 Americans currently die of the disease each year.
For healthy men over the age of 50, the ACS now recommends an annual PSA blood test, as well as a digital rectal exam. The organization advises that men at higher risk -- such as blacks and patients with a history of prostate cancer in their family -- begin such testing at age 45.
While 50 percent of older men now undergo routine PSA screenings, Thompson says his prior work suggests that PSA results are more useful when taken in context with other factors. Too often, he says, PSA levels are interpreted as black-and-white indicators of either "normal" or "elevated" risk status. The truth is that rising PSA levels reflect a more graduated increase in cancer risk.
Looking for a more accurate method, Thompson and his colleagues collected data from more than 5,500 healthy men over the age of 55 who had participated in a large-scale prostate cancer prevention trial.
For a period of seven years, all the men underwent annual PSA and digital rectal exam testing, and well as having at least one prostate biopsy conducted over the study period. By the study's end, nearly 22 percent of the men went on to develop prostate cancer, and 5 percent developed high-grade disease.
At the seven-year mark, the researchers fed a combination of accumulated data -- biopsy findings, patient age, race, family history of prostate cancer, previous biopsy history, along with PSA levels and DRE results - into their "statistical risk models."
Thompson's team found that a family history of prostate cancer, or an abnormal result from the PSA or DRE test, were all strongly associated with an increased risk for prostate cancer.
Race and age also figured in the equation, with blacks and older men at relatively high risk for prostate cancer.
Having had a prior negative biopsy result was found to be associated with a decreased risk for the disease.
By compiling such patient variables together, the Texas group say they were able to develop a prostate risk calculator that provides better predictive accuracy than an analysis of PSA levels alone.
"This study provides a way to integrate other important risk factors to allow men and their doctors to better understand their risk and make a more intelligent decision whether to proceed with further testing," Thompson says.
But in an accompanying editorial, Dr. H. Ballentine Carter, of the Johns Hopkins School of Medicine, cautioned that the calculator's current design fails to distinguish between slow-growing cancers and more life-threatening varieties.
This, he says, could lead to a rash of unnecessary biopsies.
Robert Smith, director of cancer screening at the American Cancer Society, says the new model has its pros and cons.
"It does not distinguish between significant and not-significant disease, so the calculator provides some help, but not enough help," he says. "But it also allows an individual to take their PSA level and actually interpret it in the context of some other information based on the experience of a large number of men, to understand what is the likelihood that they have prostate cancer. So I think it could actually be useful."
A second study, also published in the April of the same journal, suggests that new prostate cancer treatments currently undergoing clinical trials could be better and more quickly assessed by tracking ongoing changes in patients' PSA levels, rather than by waiting to tally long-term patient survival.
The team of Columbia University researchers working at New York-Presbyterian Hospital/Columbia in New York City based their conclusions on an analysis of the progress of 551 men undergoing a new treatment for prostate cancer.
They found that a 30 percent drop in PSA levels in the first three months of treatment correlated with a 50 percent drop in their risk of death -- a "surrogate" marker that could be used in place of the usual endpoint, survival. Use of this marker might mean a treatment's effectiveness could be evaluated much earlier.
The researchers noted that the U.S. Food and Drug Administration currently bases its "endpoint" assessment of a given treatment's success solely on long-term patient survival.
Friday, April 14, 2006
High cholesterol levels could boost prostate cancer risk
Men with high cholesterol levels have a 50 per cent higher risk of prostate cancer, says Italian research.
High cholesterol levels, hypercholesterolaemia, have a long association with many diseases, particularly cardiovascular disease. The link with prostate cancer is backed up by only limited evidence.
Over half a million men worldwide are diagnosed with prostate cancer every year, with over 200,000 deaths from the disease. The lowest incidence of the cancer is in Asia and the Far East, in particular India, Japan and China.
The new study, published on-line in the Annals of Oncology (doi: 10.1093/annonc/mdl080), reported: "The present study found a direct association between hypercholesterolaemia and prostate cancer, which has been only sporadically reported previously."
The case-control study, led by Francesca Bravi from the Istituto di Ricerche Farmacologiche Mario Negri in Milan, investigated cholesterol levels of 1294 men with clinically diagnosed prostate cancer, and 1451 controls with no prostate cancer.
Medical histories were obtained by self-reporting methods, not verified by using medical records, using a questionnaire. Despite the cases and controls being interviewed in hospital by trained interviewers, the self-reporting is a weakness in the study.
Results were adjusted to allow for possible confounding factors, such as body mass index, smoking habits, alcohol consumption, and family history of the disease.
After taking into account these possible complicating factors, the researchers found that hypercholesterolaemia was associated with a 50 per cent increase in the risk of prostate cancer.
The risk is even higher for hypercholesterolaemic men over 65, who increase their risk of the cancer by 80 per cent, whereas younger men had a 32 per cent increased risk.
The researchers suggest that the increased risk is linked to higher levels of prostate specific antigen (PSA), a protein that is used as a marker for the disease, in men with high cholesterol levels. Raised levels of PSA are indicative of prostate cancer risk, although two-thirds of men with high PSA levels will not have prostate cancer.
Some experts argue against the cholesterol-PSA link, saying that the metabolic products of cholesterol are carcinogenic and that this may be the mechanism responsible.
Chris Hiley, head of policy for the UK's Prostate Cancer Charity said that the study was very interesting, and may help explain why Western, developed countries with had such high incidences of the disease.
"It also suggests that if men make lifestyle changes and adopt a healthy, low cholesterol diet it might reduce their risk of prostate cancer.
"Further research is needed to confirm this, but in the meantime the health benefits of a varied diet are indisputable. We encourage men to cut down their intake of fatty foods and red and processed meat, but continue to eat oily fish and a high fibre diet with porridge oats, as well as plenty of fresh fruit and vegetables daily," she added.
Food industry executives polled by Reuters Business Insight last year predicted that by 2009, cholesterol-lowering foods would be the most profitable health food, far ahead of recently trendy products such as low-carb foods.
High cholesterol levels, hypercholesterolaemia, have a long association with many diseases, particularly cardiovascular disease. The link with prostate cancer is backed up by only limited evidence.
Over half a million men worldwide are diagnosed with prostate cancer every year, with over 200,000 deaths from the disease. The lowest incidence of the cancer is in Asia and the Far East, in particular India, Japan and China.
The new study, published on-line in the Annals of Oncology (doi: 10.1093/annonc/mdl080), reported: "The present study found a direct association between hypercholesterolaemia and prostate cancer, which has been only sporadically reported previously."
The case-control study, led by Francesca Bravi from the Istituto di Ricerche Farmacologiche Mario Negri in Milan, investigated cholesterol levels of 1294 men with clinically diagnosed prostate cancer, and 1451 controls with no prostate cancer.
Medical histories were obtained by self-reporting methods, not verified by using medical records, using a questionnaire. Despite the cases and controls being interviewed in hospital by trained interviewers, the self-reporting is a weakness in the study.
Results were adjusted to allow for possible confounding factors, such as body mass index, smoking habits, alcohol consumption, and family history of the disease.
After taking into account these possible complicating factors, the researchers found that hypercholesterolaemia was associated with a 50 per cent increase in the risk of prostate cancer.
The risk is even higher for hypercholesterolaemic men over 65, who increase their risk of the cancer by 80 per cent, whereas younger men had a 32 per cent increased risk.
The researchers suggest that the increased risk is linked to higher levels of prostate specific antigen (PSA), a protein that is used as a marker for the disease, in men with high cholesterol levels. Raised levels of PSA are indicative of prostate cancer risk, although two-thirds of men with high PSA levels will not have prostate cancer.
Some experts argue against the cholesterol-PSA link, saying that the metabolic products of cholesterol are carcinogenic and that this may be the mechanism responsible.
Chris Hiley, head of policy for the UK's Prostate Cancer Charity said that the study was very interesting, and may help explain why Western, developed countries with had such high incidences of the disease.
"It also suggests that if men make lifestyle changes and adopt a healthy, low cholesterol diet it might reduce their risk of prostate cancer.
"Further research is needed to confirm this, but in the meantime the health benefits of a varied diet are indisputable. We encourage men to cut down their intake of fatty foods and red and processed meat, but continue to eat oily fish and a high fibre diet with porridge oats, as well as plenty of fresh fruit and vegetables daily," she added.
Food industry executives polled by Reuters Business Insight last year predicted that by 2009, cholesterol-lowering foods would be the most profitable health food, far ahead of recently trendy products such as low-carb foods.
Tuesday, April 11, 2006
Tesco claims tomato will help fight prostate cancer
A TOMATO containing high levels of an antioxidant that may cut prostate cancer risk is to be launched in the UK.
Tesco says its new "healthy living" tomato contains roughly a third more lycopene than other vine varieties.
Its launch is part of the chain's move into "functional foods", which are developed to have added health benefits. The new variety was naturally bred in Holland using different tomato types with high lycopene levels.
It was then grown near Chichester, West Sussex.
A Tesco spokesman said lycopene had been linked with a potential reduction in the risk of prostate cancer.
Tesco says its new "healthy living" tomato contains roughly a third more lycopene than other vine varieties.
Its launch is part of the chain's move into "functional foods", which are developed to have added health benefits. The new variety was naturally bred in Holland using different tomato types with high lycopene levels.
It was then grown near Chichester, West Sussex.
A Tesco spokesman said lycopene had been linked with a potential reduction in the risk of prostate cancer.
Monday, April 10, 2006
16-Gene Signature Predicts Prostate Cancer Relapse: Presented at AACR
A new gene expression assay appears to be a better predictor of relapse and disease-free survival than the Gleason score in patients who have undergone prostatectomy for prostate cancer, researchers report.
Tracy M. Downs, MD, assistant clinical professor of surgery, Department of Urology, University of California, San Diego, United States, presented the findings at a press conference here on April 3rd in a poster session at the 97th Annual Meeting of the American Association for Cancer Research (AACR).
"It's a real problem to stratify prostate cancer patients who have a Gleason score of 6 or 7 after surgery," Dr. Downs said during a press conference held to announce the findings. "Half of patients with these scores do well, and the other half don't, but we cannot now predict who will fall into those groups."
In an attempt to move beyond Gleason scores, Dr. Downs and colleagues profiled formalin-fixed, paraffin-embedded samples of prostate carcinoma using an oligo-probe set for 512 prioritized genes with read-out on universal fiber optic bead arrays.
Tissue samples were obtained from 74 patients, retrieved from the VA San Diego Healthcare System a median of 44 months after surgery. Samples were excluded if patients received adjuvant therapy or if there was residual cancer in the prostate after resection.
From this the researchers identified 16 genes that are predictive of relapse, said Jian-Bing Fan, PhD, director of scientific research, Illumina, Inc, San Diego, California, United States. Illumina, Inc. is developing the assay and funded the research.
The gene expression signature is based on 11 genes that correlated positively and 5 genes that correlated negatively with Gleason scores obtained from histological examination (R =.63).
"This gene expression score seems to work much better than the Gleason score," Dr. Fan said. "Using it, we were able to stratify patients into 2 very distinct groups, 1 that has a 75% chance of relapse and 1 that only has a 20% chance of relapse."
Further study to validate the assay is planned.
Tracy M. Downs, MD, assistant clinical professor of surgery, Department of Urology, University of California, San Diego, United States, presented the findings at a press conference here on April 3rd in a poster session at the 97th Annual Meeting of the American Association for Cancer Research (AACR).
"It's a real problem to stratify prostate cancer patients who have a Gleason score of 6 or 7 after surgery," Dr. Downs said during a press conference held to announce the findings. "Half of patients with these scores do well, and the other half don't, but we cannot now predict who will fall into those groups."
In an attempt to move beyond Gleason scores, Dr. Downs and colleagues profiled formalin-fixed, paraffin-embedded samples of prostate carcinoma using an oligo-probe set for 512 prioritized genes with read-out on universal fiber optic bead arrays.
Tissue samples were obtained from 74 patients, retrieved from the VA San Diego Healthcare System a median of 44 months after surgery. Samples were excluded if patients received adjuvant therapy or if there was residual cancer in the prostate after resection.
From this the researchers identified 16 genes that are predictive of relapse, said Jian-Bing Fan, PhD, director of scientific research, Illumina, Inc, San Diego, California, United States. Illumina, Inc. is developing the assay and funded the research.
The gene expression signature is based on 11 genes that correlated positively and 5 genes that correlated negatively with Gleason scores obtained from histological examination (R =.63).
"This gene expression score seems to work much better than the Gleason score," Dr. Fan said. "Using it, we were able to stratify patients into 2 very distinct groups, 1 that has a 75% chance of relapse and 1 that only has a 20% chance of relapse."
Further study to validate the assay is planned.
Thursday, April 06, 2006
Scientists see progress in prostate cancer tests
Two companies have developed genetic tests that eventually could help doctors better predict which prostate cancer patients have serious cases that need aggressive treatment, U.S. researchers reported on Wednesday.
One test, developed by San Diego-based Illumina Inc., was designed to help physicians tell which patients considered at medium risk will have their cancer recur after the prostate is removed. Those patients typically have a score of six or seven on the 10-point Gleason scale that is among the standard tests for prostate cancer.
Researchers used the Illumina test to analyze prostate cancer tissue samples for 16 genes and studied how patients fared. They said they could use the information to give patients a score indicating whether they were likely to experience a recurrence of cancer within the next five years.
If confirmed in future studies, "this information could be used to make the next leap as to what (treatment) a patient should or should not have," said Dr. Tracy Downs, a urologic oncologist at the University of California at San Diego.
Another test developed by Berlin-based Epigenomics AG detected a gene called PITX2 and its "methylation," a chemical alteration that controls how active a gene is. The PITX2 gene is thought to play a role in regulating hormones, which can fuel cancer growth.
Men whose tissue samples tested positive on the Epigenomics test were three times more likely to experience cancer recurrence after having their prostate removed, researchers said.
"Those are the people that are really possibly good candidates for early (post-surgical) therapy," said Susan Cottrell, a senior scientist at Epigenomics's Seattle-based U.S. unit.
The company plans to seek Food and Drug Administration approval of the test if its effectiveness is confirmed in a larger study, Cottrell said. The test could be available for use in patients "in another couple years," she added.
Findings on both tests were released at a meeting of the American Association for Cancer Research.
Neither test was designed to replace the Gleason score or the PSA test that doctors typically use to determine the severity of prostate cancer, the researchers said.
Prostate cancer is the most common cancer in U.S. men. It is diagnosed in 232,000 men every year and kills up to 30,000 of them. Worldwide, 221,000 men die from prostate cancer each year.
One test, developed by San Diego-based Illumina Inc., was designed to help physicians tell which patients considered at medium risk will have their cancer recur after the prostate is removed. Those patients typically have a score of six or seven on the 10-point Gleason scale that is among the standard tests for prostate cancer.
Researchers used the Illumina test to analyze prostate cancer tissue samples for 16 genes and studied how patients fared. They said they could use the information to give patients a score indicating whether they were likely to experience a recurrence of cancer within the next five years.
If confirmed in future studies, "this information could be used to make the next leap as to what (treatment) a patient should or should not have," said Dr. Tracy Downs, a urologic oncologist at the University of California at San Diego.
Another test developed by Berlin-based Epigenomics AG detected a gene called PITX2 and its "methylation," a chemical alteration that controls how active a gene is. The PITX2 gene is thought to play a role in regulating hormones, which can fuel cancer growth.
Men whose tissue samples tested positive on the Epigenomics test were three times more likely to experience cancer recurrence after having their prostate removed, researchers said.
"Those are the people that are really possibly good candidates for early (post-surgical) therapy," said Susan Cottrell, a senior scientist at Epigenomics's Seattle-based U.S. unit.
The company plans to seek Food and Drug Administration approval of the test if its effectiveness is confirmed in a larger study, Cottrell said. The test could be available for use in patients "in another couple years," she added.
Findings on both tests were released at a meeting of the American Association for Cancer Research.
Neither test was designed to replace the Gleason score or the PSA test that doctors typically use to determine the severity of prostate cancer, the researchers said.
Prostate cancer is the most common cancer in U.S. men. It is diagnosed in 232,000 men every year and kills up to 30,000 of them. Worldwide, 221,000 men die from prostate cancer each year.
Wednesday, April 05, 2006
Another Gene Rearrangement Involved In Prostate Cancer Identified
Researchers at the University of Michigan Medical School have identified a third gene involved in prostate cancer, expanding their groundbreaking announcement, published last October in Science, that the majority of prostate cancers carry a malignancy-inducing fusion of genes never before seen in solid tumors. The new findings appear in the April 1 issue of Cancer Research. Since prostate cancer is a cancer of the epithelial cells lining organs, lead researcher Arul Chinnaiyan and his colleagues believe it likely that other gene re-arrangements may be responsible for other cancers of epithelial tissue, including breast, colon and lung.
Scott Tomlins, a MD/PhD graduate student in Dr. Chinnaiyan's laboratory and the lead author of the Science paper, presented the study Tuesday, April 4, at Experimental Biology 2006 in San Francisco. The presentation was part of the scientific program of the American Society for Investigative Pathology (ASIP) held at Experimental Biology, and Mr. Tomlins is the winner of the 2006 ASIP Experimental Pathologist-in-Training Award.
The ETV4 gene is a member of the same family as the two other genes, ETV1 and ERG, reported earlier. All three are ETS genes, a group of approximately 30 genes that encode related transcription factors. Like other family members, ETV4 has a role in normal cell division but is unusually active, or overly expressive, only when it becomes fused with other genes on different chromosomes. Using the same technology as the earlier study, the scientists were able to demonstrate that the ETV4 gene had become fused with another prostate cancer gene on another chromosome.
But the new ETV4 gene has two important differences from the ETV1 and ERG genes. First, while not overexpressed in individuals without prostate cancer, ETV4 is overexpressed in a much smaller fraction of patients with prostate cancer than the malignancy-causing genes described earlier. Second, the over-expressed ETV4 gene appeared in two prostate cancer patients in whom the ETV1 and ERG genes were not overexpressed, suggesting that fusions involving any of the three family members may lead to prostate cancer.
This finding confirms the importance of the ETS gene pathway in causing prostate cancer, say Chinnaiyan and Tomlins. The scientists believe fusions involving these three genes probably account for the majority of prostate cancers.
Citing the power of modern technology, including large gene databases (this study mined the Oncomine database, created by the Chinnaiyan laboratory, for ETS expression in two studies, one from the Chinnaiyan laboratory and the other from Stanford University), bioinformatics approaches that allow the rapid processing of previously unimaginable amounts of information, and an algorithm also created in the Chinnaiyan laboratory, the scientists will continue to look at other components of the ETS pathway, including genes that may get turned on inappropriately but may not be able to be detected through over-expression. Dr. Chinnaiyan also has plans to look for similar gene rearrangements in other solid tumors such as breast cancer.
Scott Tomlins, a MD/PhD graduate student in Dr. Chinnaiyan's laboratory and the lead author of the Science paper, presented the study Tuesday, April 4, at Experimental Biology 2006 in San Francisco. The presentation was part of the scientific program of the American Society for Investigative Pathology (ASIP) held at Experimental Biology, and Mr. Tomlins is the winner of the 2006 ASIP Experimental Pathologist-in-Training Award.
The ETV4 gene is a member of the same family as the two other genes, ETV1 and ERG, reported earlier. All three are ETS genes, a group of approximately 30 genes that encode related transcription factors. Like other family members, ETV4 has a role in normal cell division but is unusually active, or overly expressive, only when it becomes fused with other genes on different chromosomes. Using the same technology as the earlier study, the scientists were able to demonstrate that the ETV4 gene had become fused with another prostate cancer gene on another chromosome.
But the new ETV4 gene has two important differences from the ETV1 and ERG genes. First, while not overexpressed in individuals without prostate cancer, ETV4 is overexpressed in a much smaller fraction of patients with prostate cancer than the malignancy-causing genes described earlier. Second, the over-expressed ETV4 gene appeared in two prostate cancer patients in whom the ETV1 and ERG genes were not overexpressed, suggesting that fusions involving any of the three family members may lead to prostate cancer.
This finding confirms the importance of the ETS gene pathway in causing prostate cancer, say Chinnaiyan and Tomlins. The scientists believe fusions involving these three genes probably account for the majority of prostate cancers.
Citing the power of modern technology, including large gene databases (this study mined the Oncomine database, created by the Chinnaiyan laboratory, for ETS expression in two studies, one from the Chinnaiyan laboratory and the other from Stanford University), bioinformatics approaches that allow the rapid processing of previously unimaginable amounts of information, and an algorithm also created in the Chinnaiyan laboratory, the scientists will continue to look at other components of the ETS pathway, including genes that may get turned on inappropriately but may not be able to be detected through over-expression. Dr. Chinnaiyan also has plans to look for similar gene rearrangements in other solid tumors such as breast cancer.
Tuesday, March 28, 2006
Researchers find better prostate cancer indicators
Identifying alterations in DNA methylation may also be useful in determining cancer progression
Researchers at Mayo Clinic have narrowed the search for effective prostate cancer biomarkers (genetic variations that point to a specific disease or condition), identifying changes in the expression of genes of the whole genome closely correlated to prostate cancer development and progression. They also showed that DNA hypermethylation (DNA modification without changing sequence) plays a significant role in these processes. Results of their study were published in the Feb. 15 issue of Clinical Cancer Research.
"This is good news in an area where our ability to diagnose and predict has previously been less than stellar," said Krishna Donkena, Ph.D., Mayo Clinic urologic researcher. "Our only tool is the PSA test, which has little predictive value. These findings move us much closer to a more accurate test."
The search to identify biomarkers that can be translated into affordable and effective medical tests can be complicated. Prostate cancer causes differential expression of hundreds of different genes, each potentially an indicator of whether a man may get the disease, or already has it. They also may be used to provide information on the development of the cancer, without the need for a painful tumor biopsy.
When seeking to narrow their search to a manageable level, the researchers analyzed 32 cancerous and eight benign patient-tissue samples using genome microarrays representing 33,000 human genes. The information they gleaned from this analysis allowed them to identify 624 differentially-expressed genes between cancerous and benign tissue. They validated these findings in the original 40 tissue samples as well as in 32 additional samples (20 cancerous, 12 benign). The results showed eight genes with significant under-expression and three with significant over-expression, strongly implicating them in prostate cancer development and progression.
Over the years, research has shown that DNA methylation is commonly linked to the development and progression of cancers. This epi-genetic alteration results in silencing or seriously inhibiting gene expression, which in turn lessens the body's ability to defend against cancer. Current research has not done enough to discover ways to convert this information into a useful medical test, in large part due to the limited number of genes that have been thoroughly studied, and their insufficient sensitivity and specificity (probability of getting a true positive or true negative) for prostate cancer detection.
Dr. Donkena's team looked at 62 cancerous and 36 benign tissue samples to assess the degree of methylation in the three previously identified under-expressed genes, comparing two known methylated genes. They determined that one gene, PDLIM4, had hypermethylation that could serve as an effective sensitivity marker, accurately detecting prostate cancer 95 percent of the time. The researchers further determined that the combined measurement of a previously known gene, GSTP1, and PDLIM4 improved the detection rate to 98 percent.
Prostate cancer is the second leading cause of cancer death for men in the United States, exceeded only by lung cancer. The sooner a cancer can be diagnosed, the better treatment outcomes will be, so Dr. Donkena and her colleagues are constantly looking for ways to predict who will get prostate cancer, as well as to find better ways to diagnose early or even prevent this disabling and often fatal disease. "We hope that in addition to being a valuable diagnostic and prognostic tool, our discoveries about these genes will help us develop new treatments for prostate cancer," she said.
Other Mayo researchers involved in this study include Karla Ballman, Ph.D.; Bruce Morlan; John Cheville, M.D.; Roxann Neumann; Michael Lieber, M.D.; Donald Tindall, Ph.D.; and Charles Young, Ph.D.
This research was funded by grants from the National Institutes of Health and is the result of ongoing studies conducted under the auspices of a National Cancer Institute (NCI) SPORE grant -- Specialized Programs of Research Excellence. Mayo Clinic currently is working on projects under six SPORE grants: breast, brain, lymphoma, myeloma, pancreas and prostate cancer.
Researchers at Mayo Clinic have narrowed the search for effective prostate cancer biomarkers (genetic variations that point to a specific disease or condition), identifying changes in the expression of genes of the whole genome closely correlated to prostate cancer development and progression. They also showed that DNA hypermethylation (DNA modification without changing sequence) plays a significant role in these processes. Results of their study were published in the Feb. 15 issue of Clinical Cancer Research.
"This is good news in an area where our ability to diagnose and predict has previously been less than stellar," said Krishna Donkena, Ph.D., Mayo Clinic urologic researcher. "Our only tool is the PSA test, which has little predictive value. These findings move us much closer to a more accurate test."
The search to identify biomarkers that can be translated into affordable and effective medical tests can be complicated. Prostate cancer causes differential expression of hundreds of different genes, each potentially an indicator of whether a man may get the disease, or already has it. They also may be used to provide information on the development of the cancer, without the need for a painful tumor biopsy.
When seeking to narrow their search to a manageable level, the researchers analyzed 32 cancerous and eight benign patient-tissue samples using genome microarrays representing 33,000 human genes. The information they gleaned from this analysis allowed them to identify 624 differentially-expressed genes between cancerous and benign tissue. They validated these findings in the original 40 tissue samples as well as in 32 additional samples (20 cancerous, 12 benign). The results showed eight genes with significant under-expression and three with significant over-expression, strongly implicating them in prostate cancer development and progression.
Over the years, research has shown that DNA methylation is commonly linked to the development and progression of cancers. This epi-genetic alteration results in silencing or seriously inhibiting gene expression, which in turn lessens the body's ability to defend against cancer. Current research has not done enough to discover ways to convert this information into a useful medical test, in large part due to the limited number of genes that have been thoroughly studied, and their insufficient sensitivity and specificity (probability of getting a true positive or true negative) for prostate cancer detection.
Dr. Donkena's team looked at 62 cancerous and 36 benign tissue samples to assess the degree of methylation in the three previously identified under-expressed genes, comparing two known methylated genes. They determined that one gene, PDLIM4, had hypermethylation that could serve as an effective sensitivity marker, accurately detecting prostate cancer 95 percent of the time. The researchers further determined that the combined measurement of a previously known gene, GSTP1, and PDLIM4 improved the detection rate to 98 percent.
Prostate cancer is the second leading cause of cancer death for men in the United States, exceeded only by lung cancer. The sooner a cancer can be diagnosed, the better treatment outcomes will be, so Dr. Donkena and her colleagues are constantly looking for ways to predict who will get prostate cancer, as well as to find better ways to diagnose early or even prevent this disabling and often fatal disease. "We hope that in addition to being a valuable diagnostic and prognostic tool, our discoveries about these genes will help us develop new treatments for prostate cancer," she said.
Other Mayo researchers involved in this study include Karla Ballman, Ph.D.; Bruce Morlan; John Cheville, M.D.; Roxann Neumann; Michael Lieber, M.D.; Donald Tindall, Ph.D.; and Charles Young, Ph.D.
This research was funded by grants from the National Institutes of Health and is the result of ongoing studies conducted under the auspices of a National Cancer Institute (NCI) SPORE grant -- Specialized Programs of Research Excellence. Mayo Clinic currently is working on projects under six SPORE grants: breast, brain, lymphoma, myeloma, pancreas and prostate cancer.
Monday, March 27, 2006
Gene-Diet Link May Shield Some Men From Prostate Cancer
Men with a common gene variation may be able to reduce their prostate cancer risk simply by altering their diet to include more antioxidants, a new study suggests.
The study of more than 1,000 men found that about 25 percent of them carried the AA gene variant of a specific gene called MnSOD.
"Specifically, we found that men carrying the AA genotype are more susceptible to prostate cancer if their antioxidant levels are low," study leader Dr. Haojie Li, of Brigham and Women`s Hospital in Boston, said in a prepared statement.
"The good news is that if these men get adequate antioxidants from food and possibly from supplements, they seem to be even more likely to benefit from the nutrients` cancer fighting properties than other men," Li said.
In men with the AA gene variant, increased levels of selenium, vitamin E and the tomato pigment lycopene greatly reduced prostate cancer risk, the researchers report in the current issue of Cancer Research.
The effect was weak in men who carried other variants (VV or VA) of the MnSOD gene, however.
Previous research in breast cancer has linked similar interactions between variations in the MnSOD gene and dietary antioxidant.
"Our findings suggest that certain individuals are more sensitive to antioxidant status," Li said.
The study of more than 1,000 men found that about 25 percent of them carried the AA gene variant of a specific gene called MnSOD.
"Specifically, we found that men carrying the AA genotype are more susceptible to prostate cancer if their antioxidant levels are low," study leader Dr. Haojie Li, of Brigham and Women`s Hospital in Boston, said in a prepared statement.
"The good news is that if these men get adequate antioxidants from food and possibly from supplements, they seem to be even more likely to benefit from the nutrients` cancer fighting properties than other men," Li said.
In men with the AA gene variant, increased levels of selenium, vitamin E and the tomato pigment lycopene greatly reduced prostate cancer risk, the researchers report in the current issue of Cancer Research.
The effect was weak in men who carried other variants (VV or VA) of the MnSOD gene, however.
Previous research in breast cancer has linked similar interactions between variations in the MnSOD gene and dietary antioxidant.
"Our findings suggest that certain individuals are more sensitive to antioxidant status," Li said.
Thursday, March 23, 2006
Going with the flow
Prostate vaporization is:
A. the subject of a lost "Star Trek" episode featuring an ill-fated Scotty
B. in some countries, the punishment for leaving the toilet seat up
C. a legitimate medical procedure - you hope
Yes, despite the sinister-sounding name, prostate vaporization is an actual procedure. In fact, if you're a man who's having a little trouble "going with the flow," it might be right up your alley.
Used by urologists to treat enlarged prostates, the vaporization technique is accomplished with a system known as GreenLight PVP, which uses a laser to zap prostate tissue that is blocking urine flow. This clears a path for a normal stream and provides fast relief of symptoms and little postoperative bleeding.
Enlargement of the prostate - a condition known in the medical community as benign prostatic hyperplasia, or BPH - is pretty common and occurs naturally with the aging process. The result of all this growth in some men is a constriction of the urethra - a tube that transports urine out of the body and passes through the prostate and into the bladder.
According to the Mayo Clinic, half of men in their 60s have BPH symptoms; in those over the age of 80, it's about 90 percent. Symptoms of the condition include dribbling after urination, frequent urination (especially at night), a hesitant or weak urine stream, a sudden or urgent need to urinate and the feeling of having a not-quite-empty bladder.
If BPH is left untreated, it could lead to frequent urinary tract infections, a weakened bladder or chronic kidney infections.
Not exactly a pleasant list.
So it's no surprise that Mid-Hudson Urological Associates in Newburgh sees a fair share of enlarged prostates come through the door.
Out of the multitude of surgical treatment options out there for BPH, the minimally invasive GreenLight has become one of the favorites, says Dr. Conrado Tojino Jr. of Mid-Hudson Urological. He's been using the device since last year, and so far, patients have been very pleased with the results. "They have a strong stream, and it's like they're 20-year-olds again," he says.
The gold standard for treating enlarged prostates has been to carve out meddlesome enlarged prostate tissue with a special cutting instrument (during a procedure known as TURP, or transurethral resection of the prostate). Patients can expect to spend a few recovery days in the hospital with a catheter. Despite the improved urine flow and long-lasting results, the invasive surgery can be bloody and involve a six- to eight-week healing period, Tojino says. There is also the risk of side effects such as impotence and incontinence.
The GreenLight, which has been on the market for five years, has proven to be just as effective, delivering high-powered green laser light to literally vaporize prostate tissue. Depending on the size of the prostate - normally the size of a walnut but in many cases enlarged to the size of a plum - the procedure can take from as little as 30 minutes to an hour and a half. The device also cauterizes as it goes along, so there is little to no blood loss during surgery.
The patient has an overnight hospital stay with a catheter and then is on his way, "peeing up a storm," Tojino says.
Besides the benefit of a shorter hospital stay, the procedure doesn't carry the same risk for impotence or incontinence because the laser's energy is more targeted - meaning no risk of injuring the nearby nerve that aids erections or the muscle that helps prevent urine leakage.
Possible side effects following the procedure include burning urination for a couple of weeks and a condition known as retrograde ejaculation - when semen pushes back into the bladder instead of going out through the urethra.
There is also the possibility that in 10-15 years the prostate tissue may grow back. The area can always be retreated, Tojino says.
Unlike the hush-hush world of women's urinary problems, Tojino says most of his patients are pretty open with their issues. "Men at this age are OK with saying, 'Doc, I can't pee. I need some help,'" he says.
Monday, March 20, 2006
Hot chilli peppers a remedy for prostate cancer a study claims
The ingredient in jalapeno peppers, which makes them hot also destroys prostate cancer cells, according to a study.
Tests showed that capsaicin in the peppers triggered 80% of the cells to start to die.
The US research in the journal Cancer Research also found tumours treated with capsaicin diminished and capsaicin was also found to reduce the amount of prostate-specific antigen (PSA), a protein produced by cancer cells.
UK prostate experts agreed that capsaicin could be the basis for a future drug but they cautioned against eating too many hot peppers because of a link with stomach cancer.
In the study at Cedars-Sinai Medical Centre mice genetically modified to have human prostate cancer cells were investigated.
The animals were given a dose of pepper extract that would be equal a man of 200 pounds (90.7kg) taking 400 milligrams of capsaicin three times weekly.
This would be the equivalent of having between three and eight fresh habanera peppers, which are the highest rated peppers for capsicum content.
Dr Soren Lehmann, who led the research, said: "Capsaicin had a profound anti-proliferative effect on human prostate cancer cells in culture.
"It also dramatically slowed the development of prostate tumours."
Chris Hiley, head of policy and research at The Prostate Cancer Charity, said: "This is interesting laboratory-based work on cells but we don't yet know how, if at all, it might help men with prostate cancer.
"Eventually, it may be possible to extract the capsaicin and make it available as a drug treatment," he added.
Tests showed that capsaicin in the peppers triggered 80% of the cells to start to die.
The US research in the journal Cancer Research also found tumours treated with capsaicin diminished and capsaicin was also found to reduce the amount of prostate-specific antigen (PSA), a protein produced by cancer cells.
UK prostate experts agreed that capsaicin could be the basis for a future drug but they cautioned against eating too many hot peppers because of a link with stomach cancer.
In the study at Cedars-Sinai Medical Centre mice genetically modified to have human prostate cancer cells were investigated.
The animals were given a dose of pepper extract that would be equal a man of 200 pounds (90.7kg) taking 400 milligrams of capsaicin three times weekly.
This would be the equivalent of having between three and eight fresh habanera peppers, which are the highest rated peppers for capsicum content.
Dr Soren Lehmann, who led the research, said: "Capsaicin had a profound anti-proliferative effect on human prostate cancer cells in culture.
"It also dramatically slowed the development of prostate tumours."
Chris Hiley, head of policy and research at The Prostate Cancer Charity, said: "This is interesting laboratory-based work on cells but we don't yet know how, if at all, it might help men with prostate cancer.
"Eventually, it may be possible to extract the capsaicin and make it available as a drug treatment," he added.
Friday, March 17, 2006
PSA Velocity and Prostate Cancer Detection: The Absence of Evidence is not the Evidence of Absence
Paul Perrin
Centre Hospitalier Lyon Sud, France
The article by Schröder et al. [1] touches on an important topic and shows evidence that adds to the current confusion about the role of prostatespecific antigen velocity (PSAV) in prostate cancer early detection and screening: in a prescreened population for prostate cancer (second round) once the serum (total) PSA has reached the cut-off value of 4 ng/ml, the PSAV adds no new information about the presence of a cancer. This is disappointing, considering the urgent need to improve the discriminative power of serum total PSA to separate subjects with prostate cancer from those without.
When evaluating this study, its design needs to be kept in mind, since it deals with men who went from a PSA below 4 to a PSA above 4 during the four-year interval between screens in the programme. The conclusion of this article relates ‘‘only’’ to the use of PSAV as an addition to serum total PSA retrospectively once the PSA is above 4 and cannot be generalized to an a priori utilisation of PSAV in a second-round screening.
This article complements a previous report by the same group that highlights the lack of value of PSAV on prescreened men with a PSA below 4 ng/ml [2]. Again the design of the study suffers the same limitations described earlier: selection of the men who had a serum PSA below 4 and remained below 4 during the time of the study and excluding those where PSA rose above 4. A global analysis of the entire population (including men with PSA below and above 4 ng/ml) may give a better view of the place of PSAV in a prescreened population.
There is an increasing body of evidence in favour of the use of PSAV to predict prostate cancer either in symptomatic patients or in the context of screening programmes. Carter et al. [3] were the first to advocate the use of PSAV to distinguish prostate cancer from benign lesions. The use of a PSAV cut-off of 0.1 ng/ml/yr is associated with an OR of 6.53 for men with a PSA between 2 and 4 ng/ml [4]. Berger et al. [5] in a screened population clearly demonstrated that the PSAV differs between cancer and no cancer (0.409 ng/ml versus 0.03 ng/ml). Nadler et al. [6] in men with PSA of 2.6–4 ng/ml noted a significantly greater PSAV in men with cancer (as opposed to those without (0.47 ng/ml versus 0.05 ng/l). Eggener et al. [7], in a study of men with a previous negative biopsy, showed that PSAV is a significant risk factors among others, albeit weak. In a nomogram for predicting a positive repeat biopsy in prostate with previous negative biopsy, Lopez-Corona et al. [8] stressed the impact of PSA slope as a significant risk predictor.
Only the series from Lynn et al. [9] showed that the short-term PSAV alone had the same diagnostic accuracy as the serum PSA level. The absence of evidence is not the evidence of absence [10].
None of these studies prove the diagnostic value of PSAV, but a significant difference of PSAV between prostate cancer and no cancer is a sufficient indication to deserve a study on a population that is representative of the question: Is PSAV better at predicting prostate cancer than a fixed serum total PSA cut-off in early detection or primary or secondary screening?
The amount of benign prostatic hyperplasia in the prostate gland may account for the lack of specificity of total PSA. It is one important reason why the evaluation of PSAV carries so much hope [6]. Even the Schro ¨der group, when analyzing the secondround screening population with the whole range of PSA values included, was able to demonstrate a clear difference in PSAV between prostate cancer and prostate without cancer (0.62 ng/ml/yr versus 0.42 ng/ml/yr) and a modest diagnostic benefit over a PSA cut-off of 3 ng/ml (at a cut-off of 0.02 ng/ml/yr, PSAV will save 12.5% of unnecessary biopsies with a sensitivity of 95%) [11]. Noteworthy is the PSAV of the noncancer population that is among the highest reported in the literature.
To explain the lack of diagnostic value of PSAV in their prescreened population, the authors have postulated that the interval between the two rounds may not allow a difference in PSAV to appear in a screened population that has already been cleared from some prostate cancer with PSA above 4 ng/ml in round one. The graph from Berger [5] shows that the slopes take four years to diverge between population with cancer versus the population without cancer. This fact is already mentioned by Carter et al. [3] and Fang et al. [4].
The relationship between the aggressiveness of prostate cancer and PSAV is an important working track at present, especially since D’Amico et al. pointed out an increase risk of death for patients, treated by surgery [12] or radiation [13], with a PSA greater than 2 ng/ml/yr. In addition to its potential better specificity, PSAV may allow earlier detection of men at risk of prostate cancer [14].
In conclusion, the clinical utility of PSAV has not yet been demonstrated. But there is an accumulation of good data that indicates its usefulness. Given the importance of the stakes: improved specificity of the diagnostic test, earlier detection of cancer, definition of aggressive cancer, we can only encourage the pursuit of the quest for evidence.
References
[1] Schröder FH, et al. Does PSA velocity predict prostate cancer in pre-screened populations? Eur Urol 2006;49: 460–5.
[2] Roobol MJ, et al. Prostate-specific antigen velocity at low prostate-specific antigen levels as screening tool for prostate cancer: results of second screening round of ERSPC (ROTTERDAM). Urology 2004;63(2):309–13, discussion 313–5.
[3] Carter HB, et al. Recommended prostate-specific antigen testing intervals for the detection of curable prostate cancer. JAMA 1997;277(18):1456–60.
[4] Fang J, et al. PSA velocity for assessing prostate cancer risk in men with PSA levels between 2.0 and 4.0 ng/ml. Urology 2002;59(6):889–93, discussion 893–4.
[5] Berger AP, et al. Longitudinal PSA changes in men with and without prostate cancer: assessment of prostate cancer risk. Prostate 2005;64(3):240–5.
[6] Nadler RB, et al. Use of 2.6 ng/ml prostate specific antigen prompt for biopsy in men older than 60 years. J Urol 2005;174(6):2154–7, discussion 2157.
[7] Eggener SE, Roehl KA, Catalona WJ. Predictors of subsequent prostate cancer in men with a prostate specific antigen of 2.6 to 4.0 ng/ml and an initially negative biopsy. J Urol 2005;174(2):500–4.
[8] Lopez-Corona E, et al. A nomogram for predicting a positive repeat prostate biopsy in patients with a previous negative biopsy session. J Urol 2003;170(4 Pt 1):1184–8, discussion 1188.
[9] Lynn NN, Collins GN, O’Reilly PH. The short-term prostate-specific antigen velocity before biopsy can be used to predict prostatic histology. BJU Int 2000;85(7): 847–50.
[10] Altman DG, Bland JM. Absence of evidence is not evidence of absence. BMJ 1995;311(7003):485.
[11] Raaijmakers R, et al. Prostate-specific antigen change in the European Randomized Study of Screening for Prostate Cancer, section Rotterdam. Urology 2004;63(2): 316–20.
[12] D’Amico AV, et al. Preoperative PSA velocity and the risk of death from prostate cancer after radical prostatectomy. N Engl J Med 2004;351(2):125–35.
[13] D’Amico AV, et al. Pretreatment PSA velocity and risk of death from prostate cancer following external beam radiation therapy. JAMA 2005;294(4):440–7.
[14] Riffenburgh RH, Amling CL. Use of early PSA velocity to predict eventual abnormal PSA values in men at risk for prostate cancer. Prostate Cancer Prostatic Dis 2003;6(1): 39–44.
Source: European Urology March 2006
Friday, March 10, 2006
Awards for Cardiff prostate cancer team
Cancer researchers at Cardiff University have been recognised for their ground-breaking work into the spread of prostate cancer by the American Society of Clinical Oncology (ASCO) the world's largest oncology society.
The Metastasis and Angiogenesis Research Group, concerned with how and why cancer spreads, in the School of Medicine has received four Investigators Merit Awards at the ASCO Foundation conference on prostate cancer in San Francisco, a unique situation where all four awards came to members of the same research group.
Although this is world class recognition, the awards are tinged by sadness due to the unexpected death of one of the winners, Dr Gaynor Davies, who had developed a hugely respected reputation in the field of prostate cancer research.
The other winners included Mr Azad Howizy, Mr Jo Lewis-Russel and Dr Lin Ye.
Professor Wen G Jiang, of the School's Department of Surgery, who oversaw the research said, "We are delighted with this well deserved success for some very eminent young researchers but the loss of Gaynor has taken some of the sheen off the awards. Our thoughts are very much with Gaynor's family at this time."
Cancer Research Wales, which has a keen interest in prostate cancer, provided the funding for this work.
The Metastasis and Angiogenesis Research Group, concerned with how and why cancer spreads, in the School of Medicine has received four Investigators Merit Awards at the ASCO Foundation conference on prostate cancer in San Francisco, a unique situation where all four awards came to members of the same research group.
Although this is world class recognition, the awards are tinged by sadness due to the unexpected death of one of the winners, Dr Gaynor Davies, who had developed a hugely respected reputation in the field of prostate cancer research.
The other winners included Mr Azad Howizy, Mr Jo Lewis-Russel and Dr Lin Ye.
Professor Wen G Jiang, of the School's Department of Surgery, who oversaw the research said, "We are delighted with this well deserved success for some very eminent young researchers but the loss of Gaynor has taken some of the sheen off the awards. Our thoughts are very much with Gaynor's family at this time."
Cancer Research Wales, which has a keen interest in prostate cancer, provided the funding for this work.
Monday, February 27, 2006
UCSF team uncovers possible link between virus and prostate cancer
Researchers in San Francisco have discovered a new virus inside the tumors of some men with prostate cancer, raising the possibility that a viral infection may play a role in that disease as it does in a handful of other cancers.
The virus, a close relative of a microbe known to cause cancer in mice, was spotted by UCSF researchers using the same molecular screening equipment that helped find the SARS virus in 2003.
UCSF researcher Joseph DeRisi, who won a 2004 MacArthur Foundation "genius grant" after his work on the SARS investigation, said he did not expect to see a virus in any of the prostate tumors. "To my amazement, we found it," he said. "And it was a new virus, which was more amazing.''
Although the discovery may be an important break in the long effort to implicate a virus in prostate cancer, this new virus was found only in a small percentage of prostate tumors -- almost exclusively among men who are missing genes that normally help cells fight off viruses.
It will take more studies to determine whether the new virus, dubbed XMRV, plays any role at all in causing prostate cancer, or is merely a microbial bystander found at the tumor site.
As a result of the findings, researchers are developing a blood test to detect antibodies to the XMRV. The test would be used at first only in the laboratory so scientist can learn more about it.
The work was reported on Friday by Dr. Eric Klein, a prostate cancer specialist at the Glickman Urologic Institute of the Cleveland Clinic, during an American Society of Clinical Oncology symposium in San Francisco.
Klein has been hunting a prostate cancer-causing virus for nearly a decade, and 18 months ago began collaborating with DeRisi and his UCSF colleague, Dr. Don Ganem.
"Ten years ago, research suggested that certain genes predispose some men to prostate cancer,'' Klein said.
These men were missing a gene that produced a natural virus-fighting chemical. That suggested to Klein that prostate cancer might be caused by a virus that could exploit this weakness, and the hunt for a culprit was on.
Samples of prostate tumors were run in DeRisi's screening test, which can detect up to 2,000 known plant and animal viruses. After the test found evidence of a virus similar to one that infects mice, the UCSF researchers used additional lab work to fish out a copy of XMRV.
Some viruses have been clearly implicated in cancer. Hepatitis B increases the risk of liver cancer 100 fold. Cervical cancer is caused by infection with the human papilloma virus, which also causes genital warts.
Klein concedes that the evidence for a viral role in prostate cancer is not nearly as strong.
The XMRV virus was found in half of a small group of men with prostate cancer who also inherited from both parents the trait that disables the virus fighting enzyme. Only about 13 percent of males have such a genetic vulnerability.
Still, Klein would like to find out whether the virus infects a much larger portion of the population, and only lingers in those who lack the virus-fighting enzyme. Blood tests for exposure to the virus among prostate cancer sufferers may eventually show whether XMRV could have infected them long ago, possibly causing enough damage to start a slow-growing prostate tumor that shows up years after the virus has been cleared from their systems.
The virus, a close relative of a microbe known to cause cancer in mice, was spotted by UCSF researchers using the same molecular screening equipment that helped find the SARS virus in 2003.
UCSF researcher Joseph DeRisi, who won a 2004 MacArthur Foundation "genius grant" after his work on the SARS investigation, said he did not expect to see a virus in any of the prostate tumors. "To my amazement, we found it," he said. "And it was a new virus, which was more amazing.''
Although the discovery may be an important break in the long effort to implicate a virus in prostate cancer, this new virus was found only in a small percentage of prostate tumors -- almost exclusively among men who are missing genes that normally help cells fight off viruses.
It will take more studies to determine whether the new virus, dubbed XMRV, plays any role at all in causing prostate cancer, or is merely a microbial bystander found at the tumor site.
As a result of the findings, researchers are developing a blood test to detect antibodies to the XMRV. The test would be used at first only in the laboratory so scientist can learn more about it.
The work was reported on Friday by Dr. Eric Klein, a prostate cancer specialist at the Glickman Urologic Institute of the Cleveland Clinic, during an American Society of Clinical Oncology symposium in San Francisco.
Klein has been hunting a prostate cancer-causing virus for nearly a decade, and 18 months ago began collaborating with DeRisi and his UCSF colleague, Dr. Don Ganem.
"Ten years ago, research suggested that certain genes predispose some men to prostate cancer,'' Klein said.
These men were missing a gene that produced a natural virus-fighting chemical. That suggested to Klein that prostate cancer might be caused by a virus that could exploit this weakness, and the hunt for a culprit was on.
Samples of prostate tumors were run in DeRisi's screening test, which can detect up to 2,000 known plant and animal viruses. After the test found evidence of a virus similar to one that infects mice, the UCSF researchers used additional lab work to fish out a copy of XMRV.
Some viruses have been clearly implicated in cancer. Hepatitis B increases the risk of liver cancer 100 fold. Cervical cancer is caused by infection with the human papilloma virus, which also causes genital warts.
Klein concedes that the evidence for a viral role in prostate cancer is not nearly as strong.
The XMRV virus was found in half of a small group of men with prostate cancer who also inherited from both parents the trait that disables the virus fighting enzyme. Only about 13 percent of males have such a genetic vulnerability.
Still, Klein would like to find out whether the virus infects a much larger portion of the population, and only lingers in those who lack the virus-fighting enzyme. Blood tests for exposure to the virus among prostate cancer sufferers may eventually show whether XMRV could have infected them long ago, possibly causing enough damage to start a slow-growing prostate tumor that shows up years after the virus has been cleared from their systems.
Prostate Cancer Treatment And Bone Loss - Common Osteoporosis Treatment May Help
Men with prostate cancer who experience bone loss from cancer treatment could benefit from a weekly oral therapy commonly given to women with osteoporosis, according to a study presented by the University of Pittsburgh Medical Center (UPMC) at the American Society of Clinical Oncology Prostate Cancer Symposium, Feb. 24 to 26 at the San Francisco Marriott. The study, abstract number 139, will be featured in a press program at the meeting, 7:30 a.m., Sunday, Feb. 26.
"In previous studies, we have determined that men who receive androgen deprivation therapy, a frequently used treatment for prostate cancer, suffer from severe drops in bone mass and are at an increased risk for fracture," said study principal investigator Susan Greenspan, M.D., professor of medicine, University of Pittsburgh and director, Osteoporosis Prevention and Treatment Center, UPMC. "In an attempt to mitigate these effects, we gave men using this therapy a once-weekly oral agent called alendronate that is commonly used to treat osteoporosis. We found that men who received it had significantly increased bone mass compared to those who did not receive the therapy."
The study included 112 men with prostate cancer with an average age of 71. After an average of two years androgen deprivation therapy for prostate cancer, only 9 percent of the men had normal bone mass, while 52 percent had low bone mass and 39 percent developed osteoporosis. To study the effect of alendronate on these men, they were randomized into two groups to receive either alendronate once a week through an orally administered pill or a placebo. At one year follow-up, bone mass in the spine and hip increased significantly in the men treated with alendronate, 4.9 percent and 2.1 percent respectively. By comparison, men in the placebo group had significant losses of bone mass in the spine and hip, 1.3 percent and .7 percent respectively. In addition, the therapy was well-tolerated and easily administered.
"Since most men with prostate cancer remain on androgen deprivation therapy for an indefinite amount of time, bone loss can be a serious and long-term side effect from therapy," said Joel Nelson, M.D., co-author of the study and professor and chairman of the department of urology at the University of Pittsburgh School of Medicine. "With more than 230,000 men being diagnosed with prostate cancer each year, the addition of alendronate therapy could help to prevent the incidence of debilitating bone fractures."
Androgen deprivation therapy works by depriving the body of testosterone, an androgen hormone that increases the growth of prostate tumors. However, testosterone also is essential to maintaining bone mass in men. While doctors have been using this type of therapy for more than a decade to treat men with late-stage metastatic prostate cancer, they have begun using it more recently in men with earlier-stage disease and for longer periods of time; this increased exposure increases the risk for developing osteoporosis.
"These results suggest to us that men who are under treatment for prostate cancer should be encouraged to get a bone density test and that those at risk could benefit greatly from bone-preserving therapy," said Dr. Greenspan.
"In previous studies, we have determined that men who receive androgen deprivation therapy, a frequently used treatment for prostate cancer, suffer from severe drops in bone mass and are at an increased risk for fracture," said study principal investigator Susan Greenspan, M.D., professor of medicine, University of Pittsburgh and director, Osteoporosis Prevention and Treatment Center, UPMC. "In an attempt to mitigate these effects, we gave men using this therapy a once-weekly oral agent called alendronate that is commonly used to treat osteoporosis. We found that men who received it had significantly increased bone mass compared to those who did not receive the therapy."
The study included 112 men with prostate cancer with an average age of 71. After an average of two years androgen deprivation therapy for prostate cancer, only 9 percent of the men had normal bone mass, while 52 percent had low bone mass and 39 percent developed osteoporosis. To study the effect of alendronate on these men, they were randomized into two groups to receive either alendronate once a week through an orally administered pill or a placebo. At one year follow-up, bone mass in the spine and hip increased significantly in the men treated with alendronate, 4.9 percent and 2.1 percent respectively. By comparison, men in the placebo group had significant losses of bone mass in the spine and hip, 1.3 percent and .7 percent respectively. In addition, the therapy was well-tolerated and easily administered.
"Since most men with prostate cancer remain on androgen deprivation therapy for an indefinite amount of time, bone loss can be a serious and long-term side effect from therapy," said Joel Nelson, M.D., co-author of the study and professor and chairman of the department of urology at the University of Pittsburgh School of Medicine. "With more than 230,000 men being diagnosed with prostate cancer each year, the addition of alendronate therapy could help to prevent the incidence of debilitating bone fractures."
Androgen deprivation therapy works by depriving the body of testosterone, an androgen hormone that increases the growth of prostate tumors. However, testosterone also is essential to maintaining bone mass in men. While doctors have been using this type of therapy for more than a decade to treat men with late-stage metastatic prostate cancer, they have begun using it more recently in men with earlier-stage disease and for longer periods of time; this increased exposure increases the risk for developing osteoporosis.
"These results suggest to us that men who are under treatment for prostate cancer should be encouraged to get a bone density test and that those at risk could benefit greatly from bone-preserving therapy," said Dr. Greenspan.
Treatment For Prostate Cancer Helps Older Men Live Longer, Versus Observation
A new study shows older men with early stage prostate cancer survive longer if they are treated versus not being treated in favor of the "watchful waiting" approach advocated by many physicians for older men with other health problems. In addition, the study revealed a survival benefit for men treated with radiation therapy making it the first study to demonstrate a survival advantage in an older population. The study was presented by Fox Chase Cancer Center medical oncologist Yu-Ning Wong, M.D., at the 2006 Prostate Cancer Symposium Feb. 25 in San Francisco.
The study examines survival data of more than 48,606 men between 65 and 80 years old who survived at least one year after a diagnosis of localized prostate cancer (cancer that has not spread beyond the prostate).
Since the advent of the PSA (prostate-specific antigen) blood test about 20 years ago, many more cases of prostate cancer have been diagnosed at earlier stages.
"Some prostate cancers grow so slowly that they never become life-threatening, especially in elderly men who may die of other causes before the cancer causes problems," explained Wong. "But other men develop complications and die from their cancer making the decision to treat quite difficult."
It remains unclear whether detecting early prostate tumors translates into an equivalent benefit of saving lives and whether the benefits of early detection outweigh the risks of complications from follow up diagnostic tests and cancer treatments.
The cases examined in this study were diagnosed between 1991 and 1999. The men ranged from 65 to 80 years old at diagnosis. Median age at diagnosis was 72. A total of 34,046 men received treatment with either radiation therapy (19,948) or surgery--radical prostatectomy--to remove the prostate (14,098). The remaining 14,560 men were only observed (watchful waiting).
More than half the treated men were alive by the end of the study, with a median survival of 13 years. Median survival for the group receiving observation was about 10 years.
"This large, population-based study demonstrates a survival advantage for men treated with either radical prostatectomy or radiation therapy compared to observation," Wong said. "Eligible men should be considered for both treatment options."
The study examines survival data of more than 48,606 men between 65 and 80 years old who survived at least one year after a diagnosis of localized prostate cancer (cancer that has not spread beyond the prostate).
Since the advent of the PSA (prostate-specific antigen) blood test about 20 years ago, many more cases of prostate cancer have been diagnosed at earlier stages.
"Some prostate cancers grow so slowly that they never become life-threatening, especially in elderly men who may die of other causes before the cancer causes problems," explained Wong. "But other men develop complications and die from their cancer making the decision to treat quite difficult."
It remains unclear whether detecting early prostate tumors translates into an equivalent benefit of saving lives and whether the benefits of early detection outweigh the risks of complications from follow up diagnostic tests and cancer treatments.
The cases examined in this study were diagnosed between 1991 and 1999. The men ranged from 65 to 80 years old at diagnosis. Median age at diagnosis was 72. A total of 34,046 men received treatment with either radiation therapy (19,948) or surgery--radical prostatectomy--to remove the prostate (14,098). The remaining 14,560 men were only observed (watchful waiting).
More than half the treated men were alive by the end of the study, with a median survival of 13 years. Median survival for the group receiving observation was about 10 years.
"This large, population-based study demonstrates a survival advantage for men treated with either radical prostatectomy or radiation therapy compared to observation," Wong said. "Eligible men should be considered for both treatment options."
Thursday, February 16, 2006
Vitamin supplements don’t prevent prostate cancer
Taking the vitamins E and C or the nutrient beta-carotene doesn’t protect against prostate cancer, says the latest study in the continuing, confusing quest to determine when supplements really help health.
The government research, published Tuesday in the Journal of the National Cancer Institute, is among many large studies examining whether these antioxidants play a role in prostate cancer when taken as pills - instead of when they’re consumed as part of an overall healthy diet.
The government research, published Tuesday in the Journal of the National Cancer Institute, is among many large studies examining whether these antioxidants play a role in prostate cancer when taken as pills - instead of when they’re consumed as part of an overall healthy diet.
Monday, February 13, 2006
Saw Palmetto Won't Ease Enlarged Prostate
Millions of older American men use the herbal supplement saw palmetto to treat an enlarged prostate, but a new study concludes the product doesn't work.
A few smaller studies had suggested the extract might be of limited benefit to men with enlarged prostate, clinically known as benign prostatic hyperplasia (BPH).
However, this controlled, blinded study of 225 men found that, "over a 12-month period, saw palmetto was no better than placebo in changing symptoms for this condition," said lead researcher Dr. Stephen Bent, an assistant professor of medicine at the University of California, San Francisco.
For more on benign prostatic hyperplasia, head to the U.S. National Institute of Diabetes and Digestive and Kidney Diseases.
Monday, February 06, 2006
High-risk Black Men Least Likely To Get Screening For Prostate Cancer
The men most at risk for aggressive prostate cancer - black men with a family history - are the least likely to get screening even during peak ages of risk, researchers say.
Only 25 percent of black men during peak ages of 60-69 are screened using the common blood test that measures prostate specific antigen levels and 36 percent get annual digital rectal exams, according to a study published in the Feb. 15 issue of Cancer.
Black males are diagnosed with prostate cancer at an average age of 65.
Just under 50 percent of all high-risk black males get blood tests and 38 percent get physical exams. Sixty-five percent of black males without a family history get the blood test and 45 percent get physical exams. By comparison, 81 percent of white males age 60-69 get blood tests and 68 percent get physical exams.
"Healthy black men who have several first-degree relatives with prostate cancer are much less likely to have ever gotten a prostate screening than black men without a family history and white men in the general population," says Dr. Sally Weinrich, a nursing professor and Georgia Cancer Coalition Distinguished Cancer Scholar. "However, these are the men who have a higher-than-average risk because of their positive family histories. Hereditary forms of prostate cancer are usually diagnosed at an earlier age than non-hereditary prostate cancer."
Dr. Weinrich and her husband, Dr. Martin Weinrich, an MCG biostatistician, identified black males with positive family histories through the national African American Hereditary Prostate Cancer Study, funded by the National Institutes of Health and concluded in 2004. Comparable black males and white males were identified through the Centers for Disease Control and Prevention's 1998 and 2000 National Health Interview Surveys.
Prior research has shown that black men have a 50 percent higher incidence of prostate cancer and more than double the mortality rate of white men. This research further suggests a glaring health disparity with access to health care and economics as key factors, Dr. Weinrich says.
"Black men have the right to be informed about prostate cancer screening options," she says. "We need additional research to study the reasons why black men with a positive family history have lower screening rates than black men in general."
Physicians should ask men specific questions about their family history. Men should also ask their families questions about who has had cancer and at what age they were diagnosed, experts say.
"While doctors cannot conclusively diagnose hereditary prostate cancer because no prostate cancer gene has been identified, answers to those questions are critical to our genetic revolution," says Dr. Weinrich.
Scientists are discovering more each day about the disease, she says. "People should also pay attention to the research. Thanks to genetic and scientific knowledge, we know more today about prostate cancer than we did five years ago and we will learn even more in the next five years."
Other co-authors on the study include Dr. Georgia Dunston, Howard University; Dr. Francis Collins, National Human Genome Research Institute; Dr. James Bennett, an Atlanta urologist; and other participants of the African American Hereditary Prostate Cancer Study.
"We at the School of Nursing are pleased that the Weinrichs have such depth in this area of much-needed research," says Dr. Lucy Marion, dean of the MCG School of Nursing. "They have a long history of research for detection of cancer among older African-American men."
Only 25 percent of black men during peak ages of 60-69 are screened using the common blood test that measures prostate specific antigen levels and 36 percent get annual digital rectal exams, according to a study published in the Feb. 15 issue of Cancer.
Black males are diagnosed with prostate cancer at an average age of 65.
Just under 50 percent of all high-risk black males get blood tests and 38 percent get physical exams. Sixty-five percent of black males without a family history get the blood test and 45 percent get physical exams. By comparison, 81 percent of white males age 60-69 get blood tests and 68 percent get physical exams.
"Healthy black men who have several first-degree relatives with prostate cancer are much less likely to have ever gotten a prostate screening than black men without a family history and white men in the general population," says Dr. Sally Weinrich, a nursing professor and Georgia Cancer Coalition Distinguished Cancer Scholar. "However, these are the men who have a higher-than-average risk because of their positive family histories. Hereditary forms of prostate cancer are usually diagnosed at an earlier age than non-hereditary prostate cancer."
Dr. Weinrich and her husband, Dr. Martin Weinrich, an MCG biostatistician, identified black males with positive family histories through the national African American Hereditary Prostate Cancer Study, funded by the National Institutes of Health and concluded in 2004. Comparable black males and white males were identified through the Centers for Disease Control and Prevention's 1998 and 2000 National Health Interview Surveys.
Prior research has shown that black men have a 50 percent higher incidence of prostate cancer and more than double the mortality rate of white men. This research further suggests a glaring health disparity with access to health care and economics as key factors, Dr. Weinrich says.
"Black men have the right to be informed about prostate cancer screening options," she says. "We need additional research to study the reasons why black men with a positive family history have lower screening rates than black men in general."
Physicians should ask men specific questions about their family history. Men should also ask their families questions about who has had cancer and at what age they were diagnosed, experts say.
"While doctors cannot conclusively diagnose hereditary prostate cancer because no prostate cancer gene has been identified, answers to those questions are critical to our genetic revolution," says Dr. Weinrich.
Scientists are discovering more each day about the disease, she says. "People should also pay attention to the research. Thanks to genetic and scientific knowledge, we know more today about prostate cancer than we did five years ago and we will learn even more in the next five years."
Other co-authors on the study include Dr. Georgia Dunston, Howard University; Dr. Francis Collins, National Human Genome Research Institute; Dr. James Bennett, an Atlanta urologist; and other participants of the African American Hereditary Prostate Cancer Study.
"We at the School of Nursing are pleased that the Weinrichs have such depth in this area of much-needed research," says Dr. Lucy Marion, dean of the MCG School of Nursing. "They have a long history of research for detection of cancer among older African-American men."
Thursday, February 02, 2006
Better Prostate Cancer Detection
BACKGROUND: According to the American Cancer Society, more than 232,000 men in the United States will be diagnosed with prostate cancer this year. More than 30,300 men will die from the disease. While one man in six will get prostate cancer during his lifetime, only one man in 34 will die from it. If a man is suspected of having prostate cancer with an abnormal PSA test or by a digital rectal exam, doctors will then do a transrectal ultrasound-guided biopsy (TRUS). A TRUS biopsy - which is the current standard - removes a few samples of the prostate to determine whether cancer is present.
CAN YOU TRUST THE TRUS?
Gary Onik, M.D., the Director of Florida Hospital/Celebration Health's Prostate Cancer Research Program, says, "Unfortunately, we're finding that [the TRUS biopsy] is really not very effective at all. When you look at the statistics of a normal size gland ... the chances of actually finding that tumor are about 15 percent. So, 85 percent of patients by that biopsy method may be missing their cancer." You might be asking -- how can this possibly be the gold standard? Dr. Onik says, "Because we didn’t have any other way of knowing that we were doing it incorrectly." Now, there is a new, much more reliable way to get an accurate diagnosis.
3D MAPPING
A new biopsy method, called 3D mapping, uses a grid placed over the prostate to determine exactly how much cancer there is and exactly where it is in the prostate. Dr. Onik explains, "It's like playing Battleship with the prostate. Every hole that we have has a coordinate, and we can place the needle through that. We have a picture that overlays and shows us the prostate and where that biopsy's being taken from. Then, we can basically look at the picture when we get a positive biopsy back and see exactly where the cancer is in the gland.” In a TRUS biopsy, the samples are taken through the rectum, so doctors can only get about 12 samples. With the new 3D mapping method, biopsies are taken through the skin so doctors are able to get many more -- even up to 100 -- samples. By getting so many more samples, doctors can determine how widespread the cancer is. If only one or two samples out of 100 come back with a slight percentage of cancer, it could be a much different prognosis and treatment regimen than if half of the samples came back showing significant cancer.
BENEFITS FOR PATIENTS
Dr. Onik says, "A lot of patients are being treated inappropriately with the wrong therapies because they’re either under-diagnosed or over-diagnosed." He says many men who choose watchful waiting as a therapy may be doing so with a very inaccurate diagnosis. He says, "When we biopsy them [with 3D mapping], we find that a lot of them have very significant cancer that needs to be treated but wouldn’t have been treated unless we had done this biopsy." On the other hand, Dr. Onik says some men may get an inaccurate or incomplete diagnosis with a TRUS biopsy and decide to have a radical prostatectomy. He says, "Sometimes, we see patients who are ready to have their prostate gland and everything removed, and we do this [3D mapping] biopsy, and we can’t even find their tumor."
WHERE IS IT?
Currently, Dr. Onik says there are about five centers in Florida doing the 3D mapping biopsy method. More studies are planned, and Dr. Onik expects that this method will become widespread across the country within a few years. He adds, "This is one of those times where I think this will possibly change the way we look at prostate cancer."
FOR MORE INFORMATION
http://www.hopeforprostatecancer.com/
CAN YOU TRUST THE TRUS?
Gary Onik, M.D., the Director of Florida Hospital/Celebration Health's Prostate Cancer Research Program, says, "Unfortunately, we're finding that [the TRUS biopsy] is really not very effective at all. When you look at the statistics of a normal size gland ... the chances of actually finding that tumor are about 15 percent. So, 85 percent of patients by that biopsy method may be missing their cancer." You might be asking -- how can this possibly be the gold standard? Dr. Onik says, "Because we didn’t have any other way of knowing that we were doing it incorrectly." Now, there is a new, much more reliable way to get an accurate diagnosis.
3D MAPPING
A new biopsy method, called 3D mapping, uses a grid placed over the prostate to determine exactly how much cancer there is and exactly where it is in the prostate. Dr. Onik explains, "It's like playing Battleship with the prostate. Every hole that we have has a coordinate, and we can place the needle through that. We have a picture that overlays and shows us the prostate and where that biopsy's being taken from. Then, we can basically look at the picture when we get a positive biopsy back and see exactly where the cancer is in the gland.” In a TRUS biopsy, the samples are taken through the rectum, so doctors can only get about 12 samples. With the new 3D mapping method, biopsies are taken through the skin so doctors are able to get many more -- even up to 100 -- samples. By getting so many more samples, doctors can determine how widespread the cancer is. If only one or two samples out of 100 come back with a slight percentage of cancer, it could be a much different prognosis and treatment regimen than if half of the samples came back showing significant cancer.
BENEFITS FOR PATIENTS
Dr. Onik says, "A lot of patients are being treated inappropriately with the wrong therapies because they’re either under-diagnosed or over-diagnosed." He says many men who choose watchful waiting as a therapy may be doing so with a very inaccurate diagnosis. He says, "When we biopsy them [with 3D mapping], we find that a lot of them have very significant cancer that needs to be treated but wouldn’t have been treated unless we had done this biopsy." On the other hand, Dr. Onik says some men may get an inaccurate or incomplete diagnosis with a TRUS biopsy and decide to have a radical prostatectomy. He says, "Sometimes, we see patients who are ready to have their prostate gland and everything removed, and we do this [3D mapping] biopsy, and we can’t even find their tumor."
WHERE IS IT?
Currently, Dr. Onik says there are about five centers in Florida doing the 3D mapping biopsy method. More studies are planned, and Dr. Onik expects that this method will become widespread across the country within a few years. He adds, "This is one of those times where I think this will possibly change the way we look at prostate cancer."
FOR MORE INFORMATION
http://www.hopeforprostatecancer.com/
Waistline Protection for the Prostate
New studies claim prostate cancer can be predicted by a man's waist size
Highlight:
Registered dietitian Karen Collins looks at recent studies that have suggested waist size is an effective predictor of prostate cancer.
Highlight:
Registered dietitian Karen Collins looks at recent studies that have suggested waist size is an effective predictor of prostate cancer.
In one of the new studies that show the risk from excessive body fat, among men treated for prostate cancer, those who had gained more than about three-and-a-half pounds a year between the ages of 25 and 40 were twice as likely to have this cancer recur as men who gained less weight. According to this study, men who were obese when diagnosed with prostate cancer were more likely to have the cancer return than leaner men. The impact on recurrence was even stronger if they were obese by age 40.
Original source:
http://www.infozine.com/news/stories/op/storiesView/sid/12085/
Fatty Acid: Link to Prostate Cancer?
Prostate cancer tumors may get a growth spurt from omega-6 fatty acids, scientists report in Cancer Research.
In lab tests, researchers exposed human prostate cancer cells to arachidonic acid, a common type of omega-6 fatty acid. Those cells grew about twice as quickly as prostate cancer cells not exposed to arachidonic acid.
Full article here.
In lab tests, researchers exposed human prostate cancer cells to arachidonic acid, a common type of omega-6 fatty acid. Those cells grew about twice as quickly as prostate cancer cells not exposed to arachidonic acid.
Full article here.
Tuesday, January 31, 2006
New Guidelines for Cancer Screening: What Tests to Get When
Confused about what cancer tests you need? The American Cancer Society (ACS) has released new guidelines for cancer screening.
The ACS updates its screening guidelines every year. This year’s list covers a wide range of cancers, including cancer of the breast, prostate, colon, rectum, cervix, and endometrium (the lining of the uterus).
Many people aren’t getting screened for cancer, write experts Robert Smith, PhD, and colleagues. Smith is the ACS director of cancer screening. Their report appears in CA: A Cancer Journal for Clinicians.
The chances of surviving cancer are often better with early detection. Routine tests can make a big difference, even for people who aren’t at high risk of cancer.
New Guidelines
The new guidelines touch on hot topics in cancer screening.
Digital mammography gets mentioned as a tool that may prove helpful, needs more study, and isn’t yet widely available. No cancer test is perfect, including mammography, but nondigital mammograms may still help, says the ACS.
Regarding prostate cancer, a prostate-specific antigen (PSA) test should be available to all men age 50 and older with a life expectancy of at least 10 more years, the guidelines state.
However, men should be told about the PSA test’s benefits and limits, and better tests for prostate cancer should be created, says the ACS.
The guidelines don’t require women to do regular breast self-exams. Such tests can be helpful, but not all cancers can be felt early on, and many breast lumps aren’t cancerous, so a doctor’s exam is a must for any new breast symptoms.
What Tests, and When
Here’s a quick look at the guidelines, which target people at average risk for cancer. Those with a higher cancer risk many need earlier screening.
Special appointments aren’t necessary to check for some cancers. Doctors can screen for skin cancer, oral cancers, and thyroid cancers anytime instead of requiring an extra appointment, the ACS notes.
Falling Short
America’s record on cancer screening has room for improvement, the ACS notes.
Consider these 2004 ACS statistics, published along with the guidelines:
Fewer than six in 10 women aged 40 and older got a mammogram in the last year. Half of men aged 50 and older got a digital rectal exam in the past year. Barely half (52 percent) of adults aged 50 and older got tested for colon cancer in the past five years.
The most utilized test was the Pap test, which checks for irregularities in the cervix that may (or may not) be cancerous. More than eight in 10 eligible women got a Pap test in 2004, reports the ACS.
Those numbers are based on a national health survey.
By Miranda Hitti, reviewed by Louise Chang, MD
SOURCES: Smith, R. CA: A Cancer Journal for Clinicians, January/February 2006; vol 56: pp 11-25. News release, American Cancer Society.
The ACS updates its screening guidelines every year. This year’s list covers a wide range of cancers, including cancer of the breast, prostate, colon, rectum, cervix, and endometrium (the lining of the uterus).
Many people aren’t getting screened for cancer, write experts Robert Smith, PhD, and colleagues. Smith is the ACS director of cancer screening. Their report appears in CA: A Cancer Journal for Clinicians.
The chances of surviving cancer are often better with early detection. Routine tests can make a big difference, even for people who aren’t at high risk of cancer.
New Guidelines
The new guidelines touch on hot topics in cancer screening.
Digital mammography gets mentioned as a tool that may prove helpful, needs more study, and isn’t yet widely available. No cancer test is perfect, including mammography, but nondigital mammograms may still help, says the ACS.
Regarding prostate cancer, a prostate-specific antigen (PSA) test should be available to all men age 50 and older with a life expectancy of at least 10 more years, the guidelines state.
However, men should be told about the PSA test’s benefits and limits, and better tests for prostate cancer should be created, says the ACS.
The guidelines don’t require women to do regular breast self-exams. Such tests can be helpful, but not all cancers can be felt early on, and many breast lumps aren’t cancerous, so a doctor’s exam is a must for any new breast symptoms.
What Tests, and When
Here’s a quick look at the guidelines, which target people at average risk for cancer. Those with a higher cancer risk many need earlier screening.
- Breast cancer: Women should get a clinical breast exam at least every three years, starting in their 20s, and get an annual mammogram starting at 40. Breast self-exams are optional. See a doctor about any breast symptoms.
- Colorectal cancer: Starting at age 50, men and women should get colonoscopy every 10 years or other tests more often (double-contrast barium enema every five years; annual fecal occult blood test or fecal immunochemical test; flexible sigmoidoscopy every five years, with or without a fecal occult blood test or fecal immunochemical test).
- Prostate cancer: Digital rectal exam and prostate-specific antigen (PSA) test should be available annually for men age 50 and older with a life expectancy of at least 10 more years. Doctors and patients should discuss the pros and cons of the PSA test.
- Cervical cancer: Women should get annual Pap tests starting about three years after first vaginal intercourse or by age 21, whichever comes first. At or after age 30, women who have three normal Pap tests may get screened every two or three years. After 70, screening may stop for women who’ve had three normal Pap tests in a row and no abnormal Pap tests for a decade.
- Endometrial (uterine) cancer: At menopause, women should be told about endometrial cancer’s warning signs and urged to tell their doctors if they have any unexpected bleeding or spotting.
Special appointments aren’t necessary to check for some cancers. Doctors can screen for skin cancer, oral cancers, and thyroid cancers anytime instead of requiring an extra appointment, the ACS notes.
Falling Short
America’s record on cancer screening has room for improvement, the ACS notes.
Consider these 2004 ACS statistics, published along with the guidelines:
Fewer than six in 10 women aged 40 and older got a mammogram in the last year. Half of men aged 50 and older got a digital rectal exam in the past year. Barely half (52 percent) of adults aged 50 and older got tested for colon cancer in the past five years.
The most utilized test was the Pap test, which checks for irregularities in the cervix that may (or may not) be cancerous. More than eight in 10 eligible women got a Pap test in 2004, reports the ACS.
Those numbers are based on a national health survey.
By Miranda Hitti, reviewed by Louise Chang, MD
SOURCES: Smith, R. CA: A Cancer Journal for Clinicians, January/February 2006; vol 56: pp 11-25. News release, American Cancer Society.
Saturday, January 28, 2006
Screening For Prostate Cancer May Not Reduce Men's Risk Of Death
Screening men for prostate cancer may not reduce their risk for dying, according to a new study in the January 9 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
More men will have been diagnosed with prostate cancer than any other cancer in 2005 and more than 30,000 men will have died from the disease, according to background information in the article. Men can be screened for prostate cancer by measuring prostate-specific antigen (PSA) levels in the blood and performing digital rectal examination. However, there is little evidence of these tests' effectiveness in reducing death, the authors report. In this context, medical groups differ on screening guidelines; for instance, the American Cancer Society states that doctors should offer the PSA blood test and digital rectal exam annually to men age 50 years or older, whereas the U.S. Preventive Services Task Force has found insufficient evidence to recommend screening and the American College of Physicians advises physicians to counsel men about its benefits and risks.
John Concato, M.D., M.P.H., from the Veterans Affairs (VA) Connecticut Healthcare System, West Haven, and Yale University, New Haven, and colleagues conducted a study to address the question of whether screening improves the chances of survival. From approximately 72,000 veterans receiving health care at any of 10 VA medical centers in New England, they identified 501 men age 50 years and older who were diagnosed with prostate cancer between 1991 and 1995 and had died by the end of 1999. A comparison group of 501 living men was also identified; each man in this control group was matched, for age and treatment at the same center, to a man with prostate cancer who had died. Medical records were reviewed to determine whether men in either group had been screened for prostate cancer.
Seventy - or 14 percent - of the men who died of prostate cancer and 65 (13%) of the men in the control group were screened with PSA. If prostate cancer screening prevented death, fewer men who died would have received screening compared to the men who were living, the authors report. In addition, screening was not found to reduce mortality among men who were younger or healthier or when digital rectal exams were also considered. According to the authors, screening tests can increase the detection of cancer, even at earlier stages, but not necessarily prolong survival.
"Optimal clinical strategies for diagnosing and treating prostate cancer remain uncertain and in need of additional investigation," they write. "Based on available evidence, including the present study, recommendations regarding screening for prostate cancer should not endorse routine testing of asymptomatic men to reduce mortality. Rather, the uncertainty of screening should be explained to patients in a process of 'verbal informed consent,' promoting informed decision making."
More men will have been diagnosed with prostate cancer than any other cancer in 2005 and more than 30,000 men will have died from the disease, according to background information in the article. Men can be screened for prostate cancer by measuring prostate-specific antigen (PSA) levels in the blood and performing digital rectal examination. However, there is little evidence of these tests' effectiveness in reducing death, the authors report. In this context, medical groups differ on screening guidelines; for instance, the American Cancer Society states that doctors should offer the PSA blood test and digital rectal exam annually to men age 50 years or older, whereas the U.S. Preventive Services Task Force has found insufficient evidence to recommend screening and the American College of Physicians advises physicians to counsel men about its benefits and risks.
John Concato, M.D., M.P.H., from the Veterans Affairs (VA) Connecticut Healthcare System, West Haven, and Yale University, New Haven, and colleagues conducted a study to address the question of whether screening improves the chances of survival. From approximately 72,000 veterans receiving health care at any of 10 VA medical centers in New England, they identified 501 men age 50 years and older who were diagnosed with prostate cancer between 1991 and 1995 and had died by the end of 1999. A comparison group of 501 living men was also identified; each man in this control group was matched, for age and treatment at the same center, to a man with prostate cancer who had died. Medical records were reviewed to determine whether men in either group had been screened for prostate cancer.
Seventy - or 14 percent - of the men who died of prostate cancer and 65 (13%) of the men in the control group were screened with PSA. If prostate cancer screening prevented death, fewer men who died would have received screening compared to the men who were living, the authors report. In addition, screening was not found to reduce mortality among men who were younger or healthier or when digital rectal exams were also considered. According to the authors, screening tests can increase the detection of cancer, even at earlier stages, but not necessarily prolong survival.
"Optimal clinical strategies for diagnosing and treating prostate cancer remain uncertain and in need of additional investigation," they write. "Based on available evidence, including the present study, recommendations regarding screening for prostate cancer should not endorse routine testing of asymptomatic men to reduce mortality. Rather, the uncertainty of screening should be explained to patients in a process of 'verbal informed consent,' promoting informed decision making."
Wednesday, January 25, 2006
Spicing up protection of the prostate
Here's another way to spice up your health: Researchers from Rutgers University have found that turmeric, a spice used in curry dishes, stops prostate cancer cells from dividing in animals.
"We wanted to see whether there was a link between diet and prostate cancer," said Ah-Ng Tony Kong, a professor of pharmaceutics at Rutgers, the State University of New Jersey. Indeed, the researchers found that one month of treatment with turmeric, also known as curcumin, along with phenethyl isothiocyanate (also known as PEITC), was enough to reduce prostate tumors by 60 to 70 percent.
Each substance worked to stop the cancer growth, but they offered the most benefit together. The researchers are now designing a clinical trial to test this combination in men with prostate cancer.
"It is too early to know how much is necessary to have an effect," Kong said. Curry has also popped up in other research laboratories, where it has been tested with positive results against skin cancer cells, breast cancer cells and the sticky plaque that builds up between brain cells in patients with Alzheimer's disease in laboratory studies.
Foods that are high in PEITC include watercress, cabbage, broccoli, Brussels sprouts, kale, cauliflower, kohlrabi and turnips. "The bottom line is that PEITC and curcumin, alone or in combination, demonstrate significant cancer-preventive qualities in laboratory mice, and the combination of PEITC and curcumin could be effective in treating established prostate cancers," Kong said.
The findings were published in the latest issue of the journal Cancer Research.
The researchers injected the mice with curcumin or PEITC, alone or in combination, three times a week for four weeks, beginning a day before the introduction of the prostate cancer cells. The nutrient treatment had no effect, however, on the tumor growth in animals with advanced disease.
"We wanted to see whether there was a link between diet and prostate cancer," said Ah-Ng Tony Kong, a professor of pharmaceutics at Rutgers, the State University of New Jersey. Indeed, the researchers found that one month of treatment with turmeric, also known as curcumin, along with phenethyl isothiocyanate (also known as PEITC), was enough to reduce prostate tumors by 60 to 70 percent.
Each substance worked to stop the cancer growth, but they offered the most benefit together. The researchers are now designing a clinical trial to test this combination in men with prostate cancer.
"It is too early to know how much is necessary to have an effect," Kong said. Curry has also popped up in other research laboratories, where it has been tested with positive results against skin cancer cells, breast cancer cells and the sticky plaque that builds up between brain cells in patients with Alzheimer's disease in laboratory studies.
Foods that are high in PEITC include watercress, cabbage, broccoli, Brussels sprouts, kale, cauliflower, kohlrabi and turnips. "The bottom line is that PEITC and curcumin, alone or in combination, demonstrate significant cancer-preventive qualities in laboratory mice, and the combination of PEITC and curcumin could be effective in treating established prostate cancers," Kong said.
The findings were published in the latest issue of the journal Cancer Research.
The researchers injected the mice with curcumin or PEITC, alone or in combination, three times a week for four weeks, beginning a day before the introduction of the prostate cancer cells. The nutrient treatment had no effect, however, on the tumor growth in animals with advanced disease.
Dogs Get Prostate Cancer, Too
It turns out that man's best friend suffers from an affliction that strikes many men: prostate cancer.
In fact, canine cases of the disease are helping scientists learn some new tricks about treating the second deadliest cancer among men.
Rosol has been studying prostate cancer in dogs to learn how advanced cases metastasize, or spread, to the bones. Until now, there hasn't been a good way to study that process.
Click here to find out more!
By using cancer cells taken from dogs, Rosol's research team created a new cell line - the first that closely mimics prostate cancer cells in humans, which could someday give them insights into new treatments.
Preventing metastasis would be especially valuable for people like Jim Strecker. He's been battling prostate cancer for seven years, but he never felt any pain from it until it spread to his bones. At that point, the pain grew so severe that he couldn't sleep or enjoy his artwork.
Strecker eventually found a treatment that makes his condition less painful. But someday doctors may be able to do more than just ease the pain. With the help of man's best friend, they might be able to sculpt a treatment that stops prostate cancer in the first place.
The new cell line is significant because it allows researchers to test new prostate cancer treatments the lab, which is much faster and easier than in humans.
Source: http://www.prostate-search.com/news/prostate-cancer/key-prostate-cancer.php
In fact, canine cases of the disease are helping scientists learn some new tricks about treating the second deadliest cancer among men.
"The only animal that gets prostate cancer, in addition to men, are dogs," said Dr. Thomas Rosol, of the Ohio State University Comprehensive Cancer Center. "And the disease is very similar in dogs as it is in men."
Rosol has been studying prostate cancer in dogs to learn how advanced cases metastasize, or spread, to the bones. Until now, there hasn't been a good way to study that process.
Click here to find out more!
By using cancer cells taken from dogs, Rosol's research team created a new cell line - the first that closely mimics prostate cancer cells in humans, which could someday give them insights into new treatments.
"That would be really tremendous, if down the road, we can actually inhibit the bone metastasis," said Rosol. "This would be an enormous breakthrough for human medicine."
Preventing metastasis would be especially valuable for people like Jim Strecker. He's been battling prostate cancer for seven years, but he never felt any pain from it until it spread to his bones. At that point, the pain grew so severe that he couldn't sleep or enjoy his artwork.
"Even doing my sculpture downstairs, my back would get so tired and so painful that I had to stop from time to time," Strecker said.
Strecker eventually found a treatment that makes his condition less painful. But someday doctors may be able to do more than just ease the pain. With the help of man's best friend, they might be able to sculpt a treatment that stops prostate cancer in the first place.
The new cell line is significant because it allows researchers to test new prostate cancer treatments the lab, which is much faster and easier than in humans.
Source: http://www.prostate-search.com/news/prostate-cancer/key-prostate-cancer.php
Subscribe to:
Posts (Atom)