Samuel G. Katz M.D., Ph.D.

Assistant Professor of Pathology


Research Summary

The goal of the Katz laboratory is to selectively control the cell death machinery for therapeutic benefit. Toward that end a multidisciplinary approach is applied to understand how mammalian cells are conditioned to expire, and how mutations in essential apoptotic regulators lead to developmental defects or malignancy. In particular, BCL-2 family proteins are vital regulators of mitochondrial integrity and have been implicated in the development, maintenance and chemoresistance of numerous cancers. While the basic mode of BCL-2 family action is established, how this pathway is integrated in the context of various cellular programs, including alternate survival and death pathways, is not nearly as well understood.

Thus, we focus on:

  1. severe apoptotic blockades in cancer stem cells;
  2. loss of pro-apoptotic BCL-2 family members in mantle cell lymphoma as well as other cancers; and
  3. the mechanism of key understudied family members.


Selected Publications

  • Katz SG, Fisher JK, Correll M, Bronson RT, Ligon KL, Walensky LD. Brain and testicular tumors in mice with progenitor cells lacking BAX and BAK. Oncogene, in press.
  • LaBelle JL, Katz SG, Bird GH, Gavathiotis E, Stewart ML, Lawrence C, Fisher JK, Godes M, Pitter K, Kung AL, Walensky LD. A Stapled BIM peptide overcomes apoptotic resistance in hematologic cancers. Journal of Clinical Investigation 2012, 122(6):2018-2031.
  • Gavathiotis E, Suzuki M, Davis ML, Pitter K, Bird GH, Katz SG, Tu H-C, Kim H, Cheng EH-Y., Tjandra N, Walensky LD. BAX activation is initiated at a novel interaction site. Nature 2008; 455:1076-1081.
  • Katz SG, Williams A, Yang J, Fujiwara Y, Tsang AP, Epstein JA, Orkin SH. Endothelial lineage mediated loss of the GATA cofactor FOG-1 impairs cardiac development. PNAS 2003; 100:14030-14035.
  • Katz SG*, Cantor AB*, Orkin SH. Interaction between FOG-1 and the corepressor C-terminal binding protein is dispensable for normal erythropoiesis in vivo. Mol Cell Biol 2002; 22:3121-3128.

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