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M Golam Mohi, Ph.D. Assistant Professor, Pharmacology 3319 Weiskotten Hall Upstate Medical University 750 East Adams Street Syracuse, NY 13210 315-464-9861

Education and Clinical Training

Research Program and Department Affiliations

Research Interests

Research Abstract

Molecular Mechanism of Leukemogenesis

Normal development of blood cells requires precise control of cell proliferation, differentiation, and death. Abnormal regulation of these processes can cause excessive proliferation or block in differentiation of blood cells ultimately resulting in myeloproliferative disorders (MPD), myelodysplastic syndrome (MDS), or leukemia. Translocations or mutations in protein tyrosine kinases (PTKs) play important roles in MPDs and leukemias. Most chronic myeloid leukemias are caused by translocations that generate fusion-PTKs. For example, BCR/ABL is the product of Philadelphia chromosome translocation in chronic myeloid leukemia (CML); other translocations involve fusion of Ets family transcription factor Tel to various PTKs, including Jak2 and PDGFRβ. Internal tandem duplication (ITD) mutation in the receptor tyrosine kinase FLT3 has been found in ~30% cases of acute myeloid leukemia (AML). Point mutations in PTKs also can cause MPD, e.g., a single point mutation (V617F) in JAK2 has been found in most cases of polycythemia vera (PV), as well as a significant percentage of primary idiopathic myelofibrosis (PMF) and essential thrombocytosis (ET). These abnormal PTKs subvert normal cytokine and/or growth factor signaling and lead to constitutive activation of a number of signaling molecules and/or pathways. For example, Gab2, Shp2 and Stat5 signaling molecules, which are normally activated by growth factors/cytokines, are constitutively activated by several leukemia-associated oncogenic PTKs. The long-term research goal of my laboratory is to elucidate the molecular mechanism of MPD/leukemia. Currently, our research projects are focused on the following areas:

1. Investigate of the role of different signaling pathways in hematopoietic transformation mediated by mutant PTKs and identify the critical signaling molecule(s) required for transformation.
   
   
2. Study the role of JAK2 mutations in the pathogenesis of MPDs (e.g., PV, ET and PMF). Test the efficacy of JAK2 inhibitors with a potential role in the treatment of PV, ET and PMF.

These studies would allow us to better understand the biology and the mechanism of MPDs/leukemias. Moreover, the results of these studies should identify novel targets/therapies for MPDs/leukemias.

Publications - link to PubMed

This profile was last updated on 05/08/2008

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