Yong Chen Lab

 A causal role of genetic alterations in human cancer is well established. The genetic basis of prostate cancer, however, is still poorly defined. The PI3K/Pten/Akt pathway seems to be critical for the development of prostate cancer. The Pten tumor suppressor gene is the most frequently mutated gene in metastases of prostate cancer. A significant loss of Pten expression is also seen in primary prostate tumors. Homozygous deletion of Pten in mouse prostate results in prostate cancer development and metastasis. In addition, the phosphatidylinositol 3'-kinase (PI3K) appears to be a dominant growth factor-activated cell survival kinase in prostate tumor cells. It also stimulates the androgen pathway. Pten is a lipid phosphatase, PI3K is a lipid kinase, and Akt activation requires interactions with lipids (phosphatidylinositides). Therefore, lipid signaling plays a critical role in cancer of the prostate.

In addition to the genetic basis of cancer, the impact of epigenetic is increasingly being recognized. On the one hand, methylation, acetylation and other molecular mechanisms implicated in epigenetics are being studied intensively, but environmental factors causing these changes are largely unknown. On the other hand, factors such as diet are believed to affect cancer incidence, but molecular mechanisms have not been delineated.

My research focuses on two areas of prostate cancer; (1) genetic basis and lipid signaling in prostate cancer development, and (2) effect of dietary fat on prostate cancer development in genetically predisposed populations.

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Cancer Biology

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