David M. Livingston, M.D.
Department of Genetics
Dana Farber Cancer Institute
44 Binney Street/Smith Bldg Room 870
Boston, MA 02115
Tel: (617) 632-3074
Fax: (617) 632-4381
13 postdoctoral fellows, 1 graduate student
The laboratory focuses on attempting to decipher molecular mechanisms that support the evolution of neoplastic and tumorigenic derivatives of normal human cells. In particular, we have a longstanding investment in how certain cell cycle-, differentiation-, and cell fate- controlling proteins such as the three members of the nuclear pocket protein family, p300/CBP, and the p400/TRRAP/TIP48/49 complex send signals that, when corrupted, lead normal primary human cells to acquire certain neoplastic characteristics. In addition, we also maintain a longstanding interest in the mechanisms that give rise to both hereditary and sporadic breast and ovarian cancer. In this regard, we are engaged in a longitudinal analysis of the in vivo functions of the BRCA1 and BRCA2 gene products and of certain BRCA1 and 2 partner proteins. Special focus has recently been placed on attempting to understand the heterochromatin maintenance function of BRCA1- containing multiprotein complexes and in their RNA interaction properties. We have traditionally utilized a variety of approaches-in particular, genetic, biochemical, and biological methods- to address specific problems in these focused areas of work.
- Eid JE, Kung AL, Scully R, Livingston DM. p300 interacts with the nuclear proto-oncoprotein, SYT, as part of the active control of cell adhesion. Cell 2000; 102:839-848.
- Fuchs M, Gerber J, Ikura T, Sif S, Drapkin R, Lane WS, Nakatani Y, Livingston DM. The p400 complex is an essential E1A transformation target. Cell 2001; 106: 297-307.
- Cantor SB, Bell DW, Ganesan S, Kass EM, Drapkin R, Grossman S, Wahrer DCR, Sgroi DC, Lane WS, Haber DA, Livingston DM. BACH1, a novel helicase-like protein, interacts directly with BRCA1 and contributes to its DNA repair function. Cell 2001; 105:149-160.
BBS webpage updated 12/02/2009