Androgen ablation has been the cornerstone of treatment for metastatic prostate cancer for decades. Although this treatment has a rapid and dramatic effect, it is short lived. Eventually all the patients develop disease that grows despite the absence of male hormones.
Many mechanisms are thought to be responsible for prostate cancer¿s ability to grow despite the absence of androgens. Our laboratory has identified the presence of genetic mutations in an oncogene called [BETA]-catenin. These mutations have been shown to be important in colon cancer formation as well as in other cancers (ovarian, melanoma). Since the gain of hormone independence appears to be such a pervasive event in the progression of prostate cancer, we asked whether this oncogene could be involved. Indeed, we have found that the abnormal proteins produced by certain genetic mutations are able to increase the activity of genes that are under the control of the male hormones and their receptors. It is possible that these abnormal proteins might also help the cells to survive through the ¿starvation¿ imposed by androgen ablation. We are planning to investigate in detail the function of the oncogene [BETA]-catenin in the progression of prostate cancer. | 
