(SACRAMENTO, Calif.) A team of UC Davis investigators has found that a genetic mutation may play an important role in the development of prostate cancer. The mutation of the so-called p53 (or Tp53) gene was previously implicated in late disease progression, 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.
The study was published online in the journal Disease Models & Mechanisms and will appear in the November 2012 print edition in an article titled, "Initiation of prostate cancer in mice by Tp53R270H: Evidence for an alternate molecular progression," and is available online.
"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."
Prostate cancer is the leading cancer diagnosis in men in the United States. Although it is curable in about 80 percent of men with localized disease, the rate is much lower if the cancer is highly virulent and has spread beyond the prostate gland.
The investigators developed a mouse model genetically engineered to have a mutation in the "tumor suppressor" gene, p53, specifically in the cells of the prostate gland. 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. They also note that the mutation of p53 in the prostate differs from loss or "knock-out" of the gene, which suggests that the mechanism is more complicated than simply a "loss of tumor suppression" and appears to involve an actively oncogenic function o
|Contact: Dorsey Griffith|
University of California - Davis Health System