Source:  ScienceDaily; R. L. Vinall, J. Q. Chen, N. E. Hubbard, S. S. Sulaimon, M. M. Shen, R. W. DeVere White, A. D. Borowsky. Initiation of prostate cancer in mice by Tp53R270H, 2012

Researchers from University of California Davis, have found that a genetic mutation may play an important role in the development of prostate cancer.   The p53 (or Tp53) gene was previously thought to be a factor in late progression of prostate cancer, but until now has never been shown to act as an initiating factor. The findings may open new avenues for diagnosing and treating the disease.  Prostate cancer is the leading cancer diagnosis in men in the United States (Affecting 1 in 6 men). Although it is curable in about 80% of men with localized disease, the rate is much lower if the cancer is highly virulent and/0r has been diagnosed late after it has spread beyond the prostate gland.

So what did they find?  “Our team found a molecular pathway to prostate cancer that differs from the current conventional wisdom of how the disease develops,” said Alexander Borowsky, associate professor of pathology and laboratory medicine and principal investigator of the study. “With this new understanding, research can go in new directions to possibly develop new diagnostics and refine therapy.”   Investigators developed a mouse model genetically engineered to have a mutation in the “tumor suppressor” gene, p53 – in the cells of the prostate gland, itself.  These mice were significantly more likely to develop prostate cancer than control mice without the mutation, and provided the first indication that the p53 mutation could be involved in the initiation of prostate cancer.  Prior studies have associated p53 mutation with disease progression in prostate cancer, but this is the first to find that it can have a role in the early initiation of prostate cancer, as well. Until now, understanding of the role of p53 was that mutation occurred exclusively as a late event in the course of prostate cancer.  Based on the findings in the new mouse model that the researchers developed, p53 mutation not only can initiate prostate cancer but might also be associated with early progression toward more aggressive forms of the disease.

How does it work?  The p53 gene encodes for a protein that normally acts as a tumor suppressor, preventing the replication of cells that have suffered DNA damage. Mutation of the gene, which can occur through chemicals, radiation or viruses, causes cells to undergo uncontrolled cell division. Exactly how the p53 mutation promotes the initiation and progression of prostate cancer remains to be clarified and is a focus of current research by the UC Davis team. Genetic mutations can initiate cancers in a variety of ways. Those include promotion of uncontrolled cell growth and loss of the gene’s normal cell growth-suppressor functions.  “Knowing that prostate cancer can develop via p53 mutation opens new opportunities for researchers in the field,” said Borowsky. ”

Broader Reach?  The p53 mutation is also of intrest for other cancers, including breast, lung and esophageal cancers.  Another application of the discovery could be the development of a new diagnostic test for prostate cancer based on the presence of the p53 mutation as a biomarker.  According to Dr. Borowsky, “This is a game-changer in the understanding of prostate cancer.”

The Lewis Law Firm has a history of representing patients who have been misdiagnosed or diagnosed late with prostate cancer, breast cancer, cerivcal and ovarian cancer and pancreatic cancer.  If you or a loved one were misdiagnosed or diagnosed late with cancer, contact the Lewis Law Firm for a FREE consultation and case review today.

Posted by: Gayle R. Lewis, Esquire