Virology
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David M. Livingston, M.D.

Emil Frei Professor of Medicine

Dana Farber Cancer Institute
44 Binney St.
Smith Building Rm. 870
Boston, MA 02115
Tel: 617-632-3074
Fax: 617-632-4381
david_livingston@dfci.harvard.edu
20 postdoctoral fellows, 1 graduate students

 David Livingston

Our laboratory focuses on the molecular mechanisms that underlie transformation of normal cells to a fully neoplastic state. In addition, we are beginning to study events in tumor progression for which molecular signatures and mechanisms can now be deciphered. The core thrust of the work emanates from knowledge that the transforming and tumor inducing behavior of certain DNA tumor viruses - e.g., the papovaviruses and the human adenoviruses - is a product of the perturbation by certain viral oncoproteins of the functions of several sets of cellular proteins, the operations of which normally suppress the emergence of a neoplastic phenotype. In particular, we are working on how the nuclear pocket proteins (pRB, p107, and p130) and their E2F family transcription factor targets contribute to cell proliferation and genome integrity control. Analogous questions are being posed for the p300/CBP and the p400/TRRAP families of nuclear signal integrating molecules. Finally, the laboratory is interested in the molecular biology of breast cancer development and is invested in an effort to understand how BRCA1 and 2 act as breast cancer tumor suppressing molecules. In most cases, a combination of cell and molecular biological, virological, and mouse genetic experiments are in progress in an effort to answer the questions at hand.

 

References:

  1. Kanellopoulou C, Muljo SA, Kung AL, Ganesan S, Drapkin R, Jenuwein T, Livingston DM, Rajewsky K. Dicer-deficient mouse embryonic stem cells are defective in differentiation and centromeric silencing. Genes Dev 2005, 19:489-501
  2. Richardson AL, Wang ZC, De Nicolo A, Lu X, Brown M, Miron A, Liao X, Iglehart JD, Livingston DM, Ganesan S. X chromosomal abnormalities in basal-like, human breast cancer. Cancer Cell 2006; 9:121-132.
  3. Bing X, Sheng Q, Fryer JP, Nakanishi K, Ohashi A, Christ N, Liu X, Jasin M, Couch FJ, Livingston, DM. Control of BRCA2 cellular and clinical functions by a nuclear partner, PALB2. Mol Cell 2006, in press