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School of Medicine
Johns Hopkins prostate cancer experts lead the world in surgical, medical, radiation and experimental treatments for prostate cancer. Our experts have identified genetic culprits to hereditary and sporadic prostate cancer, defined and perfected the surgical techniques for preserving function, created ways to detect and monitor prostate cancer, led tests of life-extending drugs now used as standard care for prostate cancer and conduct groundbreaking research on sensitizing prostate cancer cells to treatments. In addition, Johns Hopkins leads the world's largest active surveillance program to keep low-grade, low-risk prostate cancer in check.
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Prostate Cancer Experts
Prostate cancer experts from the Brady Urological Institute and Kimmel Cancer Center collaborate to provide world-class care and conduct innovative research, pushing the boundaries of current care to develop new and better ways to fight prostate cancer. Consultations with a multidisciplinary group of experts is available through a single-day clinic.
About Prostate Cancer
Most men over the age of 50 will have some experience with prostate disease -- with either an enlarged prostate or cancer. Prostate cancer is among the most common types of cancer diagnosed each year in the U.S.
African American men have the highest prostate cancer incidence in the world. Another important risk factor is a positive family history. If a man has a father or brother with the disease, his risk for developing it is twice that of a man with no family history. International studies suggest that dietary fat also may play a role in the development of the cancer. Learn more about prostate cancer prevention and screening.
Physicians hope to learn more about the incidence and risks of the disease through a registry of all Johns Hopkins prostate cancer patients, which has been initiated and maintained at Johns Hopkins. Scientists from The Johns Hopkins Brady Urological Institute and Kimmel Cancer Center were the first to link a gene, called HPC-1, to susceptibility to prostate cancer. Although hereditary prostate cancer affects less than 10 percent of men with the disease, researchers are studying additional genetic determinants of hereditary prostate cancer and benign prostate enlargement. Recently, Johns Hopkins led genomic sequencing studies that identified a mutation in the HOXB13 gene that increases risk of prostate cancer by 10 to 20 times.
Finally, in a 10-year study of more than 30,000 health professionals, epidiology researchers at Johns Hopkins and Harvard found that the longer men take cholesterol-lowering drugs such as statins, the far less likely they are to develop advanced prostate cancer. Results indicate that statin-takers cut their risk for advanced disease in half. The researchers caution that data are not conclusive enough to warrant prescribing the drug to reduce cancer risk alone because many questions still linger, such as how they might contribute to delaying the cancer process more effectively than non-statins. They say that additional large studies may help confirm these results.
Prostate Cancer Symptoms
Early prostate cancer does not often cause symptoms, but some of the following problems may occur:
- A need to urinate frequently, especially at night
- Difficulty starting urination or holding back urine
- Inability to urinate
- Weak or interrupted flow of urine
- Painful or burning urination
- Painful ejaculation
- Blood in urine or semen
- Frequent pain or stiffness in the lower back, hips, or upper thighs
Physicians at the Kimmel Cancer Center use a computer to define prostate cancer cells mathematically under the microscope and identify the cancerous shapes at a much earlier stage of diagnosis, ensuring the best outcomes. This augments standard diagnostic tests including prostate specific antigen (PSA) measured in the blood, the Gleason score (a scale used to describe the aggressiveness of the tumor cell) and physical examination by a urologist. Scientists at Johns Hopkins are studying the relevance of various forms of PSA and have tracked the effectiveness of PSA velocity (the rate of change in PSA) in determining prostate cancer development. The well-known Partin Tables were created by current Brady Urological Institute director Alan Partin and Patrick Walsh using PSA levels, Gleason scores and estimated clinical stage to determine the stage of cancer and best treatment options. Most recently, researchers at Johns Hopkins and The Brady Urological Institute have identified three risk factors and developed a simple reference tool that doctors can use to determine who is at high risk of death after prostate cancer recurrence following surgery. The new tool, a set of tables that assess a combination of blood tests, the surgical pathology results, and time following surgery can be used to tell which men with recurring cancer after surgery are most likely to die from their renewed disease and would benefit from further treatment.
Two recent studies in the New England Journal of Medicine regarding the effectiveness of PSA in decreasing prostate cancer deaths had contradictory findings.
Environmental Factors Influencing Prostate Cancer
Epidemiological evidence points to environment, and specifically dietary factors, as a culprit in the initiation of prostate cancer. Japanese men living in Japan enjoy very low rates of the disease, says Kimmel Cancer Center director and clinician-scientist William Nelson, M.D., Ph.D. However, if these same men move to the U.S. and adopt a western diet, over time their prostate cancer rate equals those of American men.
In fact, Nelson says, men actually begin to develop prostate cancer lesions in their twenties and thirties, and it is likely there is something in the environment that fosters these molecular assaults. The early form of this disease is characterized by genetic changes known as translocations. They begin early in a man's life, accumulating over time, so that by the time he reaches his seventies, there are so many that the prostate genome looks like a jigsaw puzzle that has been put together improperly. Nelson and his colleagues suspect this genetic instability may be the first step in prostate cancer development.
Investigators at Hopkins are currently studying a gene called GSTP1 that may serve to protect prostate cancer cells against environmental damage from smoke and other chemicals. When functioning properly, the gene appears to detoxify carcinogens. In prostate cancer patients, this gene had probably been deactivated through a cellular process known as hypermethylation. Methylation is like a cellular punctuation mark, and when it is too low, or in this case, too high, affected genes no longer function properly. The inactivation of GTSP1 may cause the prostate to stop producing critical protective enzymes, and as a result, is defenseless to an ongoing onslaught of carcinogens that eventually results in prostate cancer.
Nelson and colleagues are exploring an infectious disease or inflammation as another potential origin of prostate cancer. New discoveries have revealed inflammatory prostate lesions known as PIA (proliferative inflammatory atrophy) as a very early cause of cell damage. The researchers believe these lesions progress to another condition called PIN (prostate intraepithelial neoplasia), funny looking cells which are not cancerous themselves but are strongly linked to prostate cancer and considered by some to be precancers that eventually progress to prostate cancer. The investigators believe these inflammatory cells activate oxygen and damage prostate cells. Certain dietary chemicals released when charbroiling meats are believed to bind to cell DNA and damage prostate cells. In the absence of GTSP1 protection, the prostate cell is unable to repair this damage.
These scientists are now exploring the possibility of therapeutically inducing protective enzymes that would replace the lost function of GTSP1. Many of these protective substances are present in cruciferous vegetables and may explain why cultures with diets high in vegetables experience lower prostate cancer rates than Americans. By protecting prostate cells from early events such as chronic inflammation and environmental assaults, the investigators are hoping to prevent the genomic hodgepodge that results in prostate cancer.