| | | Research | | Current Research Projects | | Andrew Kraft, M.D. | Our research has focused on three project areas. We have continued to study the ability of TRAIL to induce death of renal cancer. We find that renal cancers that are VHL negative are TRAIL-sensitive while those that are VHL positive are TRAIL-resistant. We are currently carrying out experiments to understand this effect at the biochemical level. The second project ongoing in the laboratory is to examine the role of the of the Pim proto-oncogene in regulating tumor growth. We find the Pim appears to control protein synthesis in the absence of the TOR pathway. This is a very important development suggesting that tumors may be resistant to rapamycin, a TOR inhibitor, in the clinic based on over-expression of Pim. Our final project is formed on the control of phosphorylation of AML1. We previously reported that AML1 is highly phosphorylated and mapped the sites of phosphorylation. Now we have shown that AML1 is phosphorylated by cyclin dependent kinase 1 at the G2M phase of the cell cycle. We also have found that AML1 is degraded at the G2M phase through an APC/C mediated degradation process. These results are reported in a poster presented at ASH in 2005. They are currently being compiled for submission and publication. | | Clifford W. Schweinfest, Ph.D. | We have determined that the oncogenic viral protein, E1A, can interfere with the growth arrest function of the tumor/growth suppressor gene, DRA and that the amino terminal portion of E1A is responsible for this interference. We have shown that the membrane associated protein, liprin, which co-regulates several important molecular pathways known to be perturbed in cancers, is necessary for DRA growth suppression function. | | M. Rita I. Young, Ph.D. | Collaborations established with Drs. Day and Gillespie (Otolaryngology – Head and Neck Surgery) and, more resently, with Drs. Neville and Chi (Development of Stomatology) have allowed determination of the feasibility of immunotherapeutic approaches by which to prevent recurrent premalignant oral lesions and squamous cell carcinoma of the head and neck (HNSCC). The strategy was to determine if premalignant oral lesions could be used to sensitize patients’ own blood cells against premalignant lesions or HNSCC. Results showed that oral premalignant lesions could stimulate patient lymphocytes to release IFN-Y in response to premalignant lesions and HNSCC, as well as to kill premalignant lesion cells and HNSCC cells. |
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