Professor of Biochemistry & Molecular Biology
PO Box 980614
Richmond, VA 23298-0614
Email: sdeb@hsc.vcu.edu
Telephone: 804-828-9541
Web Site: www.people.vcu.edu/~sdeb/
Education
Ph.D., Calcutta University, 1982
Research
One fundamental problem of cancer cells is the loss
of proper regulation of cell growth. The primary
research interest of our laboratory is to understand
the molecular mechanism of cellular proliferation
and its control. In this regard we are currently
focusing on understanding the molecular biology of
the human tumor suppressor p53. p53 mutation is the
most frequently reported genetic defect in human
cancer. Unraveling the pathway used by p53 to control
cell proliferation may, therefore, lead to intervention
in a large number of human cancers.
Wild-type p53 inhibits the proliferation of transformed
cells, suppresses oncogene-mediated cell transformation,
and eliminates the tumorigenic potential of tumor-derived
cell lines. Tumor-derived mutants of p53, on the other
hand, immortalize primary cells and cooperate with
the ras oncogene to transform primary cells. Whereas
wild-type p53 can transcriptionally activate such genes
as p21, which negatively regulates cell cycle, we have
demonstrated that tumor-derived p53 mutants could specifically
transactivate promoters of growth-related genes such
as epidermal growth factor receptor (EGFR), and this
transactivation is directly related to mutant p53's
capablity to induce tumorigenicity in certain cell
systems. A part of our research is focused on the understanding
the mechanism of mutant p53-mediated transactivation
and establishing the pathway utilized by mutant p53
in enhancing tumorigenicity. For this purpose we are
using recombinant DNA technology, immunological tools
and cell biological approaches.
We are also working on the biological functions of
p73, a homologue of p53, as well as studying the role
of p53 and p73 in angiogenesis.
Publications
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