Department of Cell Stress Biology
Assistant Professor of Oncology
Roswell Park Cancer Institute
BLSC 3319
Elm and Carlton Streets
Buffalo, New York 14263 USA
Tel: 716-845-4133 (office) 4758 & 4759 (lab)
Fax: 716-845-3944
E-mail: asoke.mal@roswellpark.org

Current Program

• The role of histone modifications in epigenetic reprogramming of skeletal muscle differentiation.
• Epigenetic mechanism regulating human rhabdomyosarcoma development.
• Identification of MyoD modulators by screening of a small molecules library.

Profile

Asoke K. Mal, PhD, joined the faculty of Roswell Park Cancer Institute (RPCI) in 2008 as an Assistant Professor of Oncology in the Department of Cell Stress Biology.

Dr. Mal came to RPCI from the Lerner Research Institute, Cleveland Clinic Foundation, OH, where he was on the faculty of the Department of Molecular Genetics. He earned his doctoral degree in 1992 in Biochemistry from the University of Calcutta, India.

Dr. Mal is a member of the American Association of Cancer Research and the American Association for the Advancement of Science. He has authored or co-authored several journal publications.

Area of Research Interest

The research program in Dr. Mal's laboratory is focused on broad but highly integrated areas of study. The epigenetic gene regulation program involves identifying the epigenetic changes and deciphering the mechanism as a potential target strategy for therapy. This program is aimed to identify the epigenetic mechanism regulating normal and perturb differentiation. Particularly, the research focuses on epigenetic modulation of gene expression regulating skeletal muscle differentiation during development and regeneration, as well as in muscle tumor rhabdomyosarcoma (RMS). The drug discovery program involves searching small molecule modulators that would activate the skeletal muscle differentiation program in multipotent muscle stem cells (satellite cells) and in RMS tumor cells. Both programs are aimed at therapeutic applications for skeletal muscle associated tumors and degenerative diseases.

Collaborators

Marc S. Penn, M.D., Ph.D.	Lerner Research Institute, Cleveland Clinic
Charles Keller, M.D.	Children's Cancer Research Institute, University of Texas Health Science Center

Publications

Mal AK. Histone Methyltransferase Suv39h1 represses MyoD-stimulated myogenic differentiation. EMBO J. 25 (14), 3323-3334 (2006).

Mal A, Harter ML. MyoD is functionally linked to the silencing of a muscle-specific regulatory gene prior to skeletal myogenesis. Proc. Natl. Acad. Sci. 100 (4), 1735-1739 (2003).

Mal A, Sturniolo M, Schiltz RL, Ghosh MK and Harter ML. A role for histone deacetylase HDAC1 in modulating the transcriptional activity of MyoD: inhibition of the myogenic program. EMBO J. 20, 1739-1753 (2001).

Chattopadhyay D, Mal A, Ghosh MK and Harter ML. Inactivation of p21 by E1A leads to the induction of apoptosis in DNA damaged cells. J. Virol. 75, 9844-9856 (2001).

Mal A, Chattopadhyay D, Ghosh MK, Poon RY, Hunter T and Harter ML. p21 and retinoblastoma protein control the absence of DNA replication in terminally differentiated muscle cells. J. Cell Biol. 149, 281-292 (2000).

Ravi R, Weber KE, McMahon MJ, Williams R, Baylin S, Mal A, Harter ML, Dillehay L E, Claudio PP, Giordano A, Nelkin BD and Marby M.. Activated Raf-1 causes growth arrest in human small lung cancer cells. J. Clin. Invest. 101, 153-159 (1998).

Mal A, Poon RY, Howe PH, Toyoshima H, Hunter T and Harter ML. Inactivation of p27Kip1 by the viral E1A oncoprotein in TGFβ-treated cells. Nature 380, 262-265 (1996).

Mal A, Piotrkowski A and Harter ML. Cyclin-dependent kinases phosphorylate the adenovirus E1A protein, enhancing its ability to bind pRb and disrupt pRb-E2F complexes. J. Virol. 70, 2911-2921 (1996).

Banerjee AC, Recupero AJ, Mal A, Piotrkowski A, Wang DM and Harter ML. The adenovirus 289R and 243R proteins inhibit the phosphorylation of p300. Oncogene 9, 1733-1737 (1994).

Mal A and Chatterejee IB. Hemoglobin: A scavenger of superoxide radical. J. Biosci., 16: 43-53 (1991).

Mal A and Chatterejee IB. Hemoglobin: A scavenger of superoxide radical. J. Biosci., 16: 55-70 (1991).