David S. Franklin, Ph.D.
Associate Professor of Biochemistry
Tulane Cancer Center Program Member
Address: 1430 Tulane Ave., Box SL-43, New Orleans, LA 70112-2699
Dr. Franklin received his Ph.D. in 1994 from Louisiana State University Medical Center (now LSUHSC). His research interests involve the human cancer syndrome multiple endocrine neoplasia (MEN). Using both tissue culture and in vivo mouse model systems, his lab studies the tumor suppressor MEN1 and proto-oncogene RET, whose mutations predispose patients to develop MEN tumors. Specifically, how do the MEN1 and RET gene products mediate normal cell cycle regulation? What are the effects of MEN tumor-specific mutations on the normal processes? In addition, the Franklin lab is involved in assessing the potential use of the Reishi mushroom as a complementary and alternative medicine in mouse models for breast and colon cancer.
Joshi PP, Kulkarni MV, Yu BK, Smith KR, Norton DL, Van Veelen W, Hoppener JWM, Franklin DS. Simultaneous down regulation of CDK inhibitors p18INK4c and p27KIP1 is required for MEN2A-RET mediated mitogenesis. Oncogene, 26:554-570, 2007.
Paris M, Wang WH, Franklin DS, Andrisani OM. The homeodomain transcription factor Phox2a, via cAMP-mediated activation, induces p27KIP1 transcription, coordinating neural progenitor cell cycle exit and differentiation. Mol Cell Biol, 26(23): 8826-8839, 2006.
Damo LA, Snyder PW, Franklin DS. Tumorigenesis in p27/p53- and p18/p53-double null mice: functional collaboration between the pRb and p53 pathways. Mol Carcinogenesis, 42:109, 2005.
Yuan Y, Shen H, Franklin DS, Scadden DT, Cheng, T. In vivo self-renewing divisions of hematopoietic stem cells are increased in the absence of the early G1-phase inhibitor, p18 INK4C. Nature Cell Biol, 6(5): 436-442, 2004.
Myers TK, Andreuzza S, Franklin DS. p18 INK4c and p27KIP1 are required for cell cycle arrest of differentiated myotubes. Exp Cell Res, 300(2): 365-378, 2004.