The pathological stages of prostate cancer begin with abnormal epithelial proliferation and prostatic intraepithelial neoplasia with progression to invasive carcinoma and eventually metastatic disease. Recapitulating the progression of invasive prostate carcinoma in vivo could provide valuable information on understanding the genesis of the disease. My lab is particularly interested in how post-translational modifications of oncogenic proteins dictate their tumor initiation potential. The expression and activity of Src family kinases (SFKs) are highly elevated in numerous human cancers, including aggressive prostate cancer. In one of the on-going studies, we utilize genetic approaches and in complement small molecule inhibitors to define the role of posttranslational modifications of SFKs in their tumorigenic potential. Additionally, multiple genetic lesions have been revealed through the genomic screening of prostate cancer samples. The crosstalk of oncogenic signaling pathways will help us understand the initiation of invasive prostate cancer in vivo. Another on-going study focuses on how post-translational modifications regulate chromatin accessibility for initiation of tumor-propagating cells in prostate cancer. The long term goal of my lab is to interrogate the molecular mechanisms underlying advanced prostate carcinoma and provide the scientific rationale for using small molecule inhibitors in suppression of aggressive prostate cancer.
