Prostate Cancer

Moderate amounts of regular exercise may lower mortality rates for prostate cancer survivors, according to a study presented at the American Association for Cancer Research Frontiers in Cancer Prevention Research Conference.

The study's authors explained that previous investigations focused on how exercise affected the risk of developing prostate cancer but failed to identify the exact molecular effects that exercise had on prostate cancer.

To examine exercise in relation to overall survival rates in prostate cancer survivors, lead author, Stacey Kenfield, ScD, epidemiology research associate at the Harvard School of Public Health, and colleagues assessed physical activity levels for 2686 males with prostate cancer before and after diagnosis.

Researchers found that men who engaged in 3 or more hours of Metabolic Equivalent Tasks (MET) a week—equivalent to jogging, biking, swimming, or playing tennis for about a half-hour per week—had a 35% lower risk of overall mortality. Furthermore, men who walked ≥90 minutes at a normal to brisk pace had a 51% lower risk of all-cause mortality compared to men who walked <90 minutes at an easy walking pace.

“We saw benefits at very attainable levels of activity,” said Kenfield. “Our data indicate that for prostate cancer survivors, a moderate amount of regular exercise may improve overall survival, while ≥5 hours per week of vigorous exercise may decrease the death rate due to prostate cancer specifically.”

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AFP - WASHINGTON — US researchers have found an antibody that hunts down prostate cancer cells in mice and can destroy the killer disease even in an advanced stage, a study showed Monday.

The antibody, called F77, was found to bond more readily with cancerous prostate tissues and cells than with benign tissue and cells, and to promote the death of cancerous tissue, said the study published in the Proceedings of the National Academy of Science (PNAS).

When injected in mice, F77 bonded with tissue where prostate cancer was the primary cancer in almost all cases (97 percent) and in tissue cores where the cancer had metastasized around 85 percent of the time.

It recognized even androgen-independent cancer cells, present when prostate cancer is incurable, the study by researchers at the University of Pennsylvania showed.

F77 "initiated direct cell death of prostate cancer cells... and effectively prevented tumor outgrowth," it said.

But it did not target normal tissue, or tumor tissues in other parts of the body including the colon, kidney, cervix, pancreas, lung, skin or bladder, the study showed.
he antibody "shows promising potential for diagnosis and treatment of prostate cancer, especially for androgen-independent metastatic prostate cancer," which often spreads to the bones and is difficult to treat, the researchers wrote in PNAS.

Currently, the five-year survival rate for metastatic prostate cancer is just 34 percent, according to the study.

Prostate cancer is the second most common cancer among men, claiming half a million lives each year worldwide, according to the World Health Organisation (WHO).

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Being diagnosed with prostate cancer may raise men's risk of having a heart attack or stroke, especially in the first week after diagnosis. Researchers found an increased risk of about 30 percent during the year after prostate cancer diagnosis. The risk of suicide during this time also increased, although this was much less common than heart problems.

What do we know already?
The numbers of men being diagnosed with prostate cancer are increasing, especially now that a blood test (called prostate-specific antigen, or PSA) that can help detect potential prostate cancer is more widely used. This may mean that more men are diagnosed early, and some may have a better chance of being treated and surviving their cancer.

However, we're not sure that all men with prostate cancer benefit from treatment. The research isn't clear. Part of the trouble is that many prostate cancers grow very slowly, and might never have caused any trouble if they'd not been picked up. Others grow much more quickly. It's hard to tell which cancers are likely to need treatment, and which are best left alone.

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Teva Pharmaceutical Industries Ltd. ( TEVA) headquartered in Israel and OncoGenex Pharmaceuticals, Inc. (NASDAQ: OGXI) announced on Dec 21 that they have entered a licensing agreement under which both companies will further develop and commercialize OGX-011, an anticancer drug that may be enlisted to treat advanced prostate cancer, lung cancer and breast cancer, and Teva will purchase shares in OncoGenex.

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The prostate, an androgen-regulated exocrine gland, is an integral part of the male reproductive system which has an essential function in sperm survival and motility in its long hostile route to meet and fertilise the egg in the Fallopian tube.

Testosterone is known to be the key, obligatory regulator of the prostate that promotes the development and progression of prostate cancer (PCa). Yet, the pathophysiological mechanism of PCa remains unclear and its causal relation to serum testosterone has not been established. Here, we report on the discovery of a previously unrecognized route of flow of free testosterone (FT), at a concentration of 130 times the physiological levels, reaching the prostate via the testicular and prostate venous drainage systems, bypassing the systemic circulation.

This condition results from the malfunction of the vertically oriented testicular venous drainage system in humans, a phenomenon with a prevalence that increases rapidly with age, which causes deviation of the testicular venous flow from its normal route. Early results of an interventional radiological procedure, super-selective intraprostatic androgen deprivation therapy are discussed.

This treatment has resulted in decrease in prostate volume, and serum PSA, with disappearance of cancerous cells on repeat biopsies in five of six patients. Some of the unresolved biological enigmatic questions associated with PCa are discussed.

We conclude that pathological flow of FT from the testes directly to the prostate in an extremely high concentration via the testicular-prostate venous drainage systems was identified may explain the mechanism for the development of PCa. We suggest a time-window for eradication of localised, androgen-sensitive, PCa cells. We anticipate that this treatment may retard, stop or even reverse the development of the disease. A mechanism for the evolution of PCa is discussed.

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