Prognosis Cancer

Over the past few decades the prognosis for prostate cancer has greatly improved. Commendably most (85%) prostate cancers are detected before they become invasive. Once the cancer is discovered at this stage the five year survival rate stands at an amazing 100 percent. The survival rates for black men is, unfortunately, much poorer than for whites in the U. S. Blacks are usually diagnosed with later stages of the disease. Further even within the stages the survival rate is significantly lower for blacks.

This may represent disparities in the type of access that blacks have to health care services and proper treatment. Current Research A number of research efforts are currently being undertaken into the study of cancers in general cancer and prostate cancer in particular. A longitudinal Prostate Cancer Prevention Trial was recently spearheaded by Coltman, Thompson and Feigl in order to determine the reaction of prostate cancer to finasteride. The results are still being awaited but indications are that finasteride is proving to be an effective means of inhibiting the growth of cancer cells.

The National Cancer Institute is also currently funding research by Jose Russo in Philadelphia into the possible link between four hydroxyestradiol mediates and the development of certain hormone related cancers such as breast cancer. The use of mobile phones has been brought into question in relation to its possible association with cancer. To this vein A. Swerdlow, at the British Institute of Cancer Research, is currently comparing mobile phone use and other radio-frequency exposure between a control and experimental group to determine a linkage particularly with leukemia.

Lan Qing, also at the National Cancer Institute is trying to determine the link between cancer and certain occupational elements such as Trichloroethylene and Chromosomal Aberrations. Until research begins to be conclusive the prognosis for cancer survival will continue to be dim and people will still greatly fear the disease and refrain from testing out of this fear. Dr. Arul Chinnaiyan serves as the S. P. Hicks Endowed Professor of Pathology and Director of Cancer Bioinformatics at the University of Michigan in Ann Arbor, Mich.

He received awards in 2005 and 2006 from the Prostate Cancer Foundation Competitive Award. This is as a result of his continuing research into prostate cancer. In 2005, Dr. Chinnaiyan and his colleagues at the University of Michigan discovered a chromosomal translocation that is unique to prostate cancer. It appears segments of two chromosomes swap places with each other. This translocation causes two unrelated genes — known as TMPRSS2 and ERG — to now be adjacent to each other and to fuse together.

Genes are small segments of chromosomes that contain specific instructions on how the cell is supposed to behave. Because instructions in the genes are so specific, investigators can look at abnormal cell processes and track back to how and why the mistake occurred. Because the TMPRSS2 and ERG gene fusion can be easily detected and is unique to prostate cancer, it is a perfect target for cancer-killing therapies. If a therapy can be engineered to seek out cells that harbor this gene fusion, physicians will be able to directly kill prostate cancer cells without damaging healthy cells.

Dr. Chinnaiyan and his team are now developing a system to screen hundreds of molecules that might inhibit activity of ERG and prevent it from binding to TMPRSS2. It is hoped that blocking the formation of the TMPRSS2:ERG gene fusion will slow and/or stop the progression of prostate cancer. Dr. Robert E. Carraway is Professor of Physiology at the University of Massachusetts Medical School in Worcester, Mass. He was a recipient of a 2005 Prostate Cancer Foundation Competitive Award.

This unique program supports innovative prostate cancer research projects directed by leading scientists around the world and enables them to forge ahead with their crucial work. His project is entitled “Blood fatty acids regulate prostate tumor growth: animal and human studies. ” Studies have shown that the risk of developing prostate cancer correlates with dietary fat intake, especially in regard to the amount of fatty acid (FA) in the diet. Although FAs are known to directly stimulate prostate cancer growth, new research has shown that they can also affect prostate cancer growth in other ways.

As FAs enter the intestines, the hormone neurotensin (NT) is released. NT enhances fat digestion and absorption, increasing the delivery of FAs to the tumor and stimulating the growth of prostate cancer cells. Dr. Carraway and his colleagues are testing the hypothesis that NT affects prostate cancer cells by stimulating the growth of new blood vessels within and surrounding the tumor, thereby enabling the tumor cells to increase FA absorption. In theory, interrupting this process and diminishing NT’s effects on fat absorption and blood vessel growth will lead to decreased tumor growth in men with prostate cancer.

One important clue to how NT affects blood vessel growth and FA delivery to tumor sites might be found in yet another corner: NT stimulates the release of mast cells, whose presence in around the tumor is known to negatively correlate with patient survival. Dr. Carraway’s research is focusing on the idea that these two processes are linked and that NT enhances FA absorption into tumors via its actions on mast cells. It is hoped that the findings from this project will lead to the development of new strategies to inhibit prostate cancer growth.

Dr. Jay H. Fowke is Assistant Professor and Cancer Epidemologist at Vanderbilt University Medical Center in Nashville, Tenn. He was a recipient of a 2005 Prostate Cancer Foundation Competitive Award. This unique program supports innovative prostate cancer research projects directed by leading scientists around the world and enables them to forge ahead with their crucial work. Dr. Fowke’s project is entitled Glitazones and prostate cancer risk in a large cohort of men with Type 2 Diabetes.

” The goal of this project is to investigate the relationship between thiazolidinedione (TZD) use and the risk of developing prostate cancer. TZDs, or glitazones, target a receptor found on the surface of cells known as the peroxisome proliferator-activated receptor-gamma (PPAR? ) receptor and are approved by the FDA to control insulin in people with type 2 diabetes. But PPAR? also plays an important role in regulating the differentiation of cells, and earlier research showed that activating PPAR? inhibits cell proliferation and induces cell death in the prostate.

The combination of these factors led to the hypothesis that men who are using TZDs to control their diabetes might also be at lower risk for developing prostate cancer. Dr. Fowke and his colleagues are investigating the relationship between TZD use and prostate cancer risk using data derived from over 9 million active or retired members of the U. S. military. Computerized medical records were accessed to identify TZD use and prostate cancer diagnoses among 275,405 men over the age of 40 who had been diagnosed with type 2 diabetes.

Preliminary results suggest that TZD use is associated with a lower rate of prostate cancer detection. Dr. Fowke’s research over the coming months will focus on determining how this relationship might be affected by prostate cancer screening practices and on defining the impact of TZD on men with low-grade versus high-grade prostate cancer. It is hoped that the final results from this project will lead to the evaluation of TZDs as preventative agents in men at risk for developing prostate cancer.

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