A photo of Mohammed Azam.

Mohammad Azam, PhD


  • Member, Division of Experimental Hematology & Cancer Biology
  • Professor, UC Department of Pediatrics

About

PhD: Jawaharlal Nehru University, India.

Post-doc:
Whitehead Institute for Biomedical Research at MIT, 2001-2003.

Instructor:
Children’s Hospital of Boston and Harvard Medical School, 2006-2009.

Interests

Leukemia

Interests

Structure and function analysis of tyrosine kinases involved in the pathogenesis of leukemia; molecular basis of "oncogene addiction" modeling of human leukemia in mice using ES and patient derived iPS cells

Research Areas

Experimental Hematology and Cancer Biology, Cancer and Blood Diseases

Publications

Rational polypharmacological targeting of FLT3, JAK2, ABL, and ERK1 suppresses the adaptive resistance to FLT3 inhibitors in AML. Azhar, M; Kincaid, Z; Kesarwani, M; Menke, J; Schwieterman, J; Ansari, S; Reaves, A; Ahmed, A; Shehzad, R; Khan, A; et al. Blood Advances. 2023; 7:1460-1476.

Momelotinib is a highly potent inhibitor of FLT3-mutant AML. Azhar, M; Kincaid, Z; Kesarwani, M; Ahmed, A; Wunderlich, M; Latif, T; Starczynowski, D; Azam, M. Blood Advances. 2022; 6:1186-1192.

PLaCatinG AML1-ETO. Azam, M. Blood. 2022; 139:959-961.

Adaptive responses to mTOR gene targeting in hematopoietic stem cells reveal a proliferative mechanism evasive to mTOR inhibition. Fan, C; Zhao, C; Zhang, F; Kesarwani, M; Tu, Z; Cai, X; Davis, AK; Xu, L; Hochstetler, CL; Chen, X; et al. Proceedings of the National Academy of Sciences of USA. 2021; 118:e2020102118.

SWATH-Proteomics of Ibrutinib's Action in Myeloid Leukemia Initiating Mutated G-CSFR Signaling. Dwivedi, P; Chutipongtanate, S; Muench, DE; Azam, M; Grimes, HL; Greis, KD. Proteomics: Clinical Applications. 2020; 14:e1900144.

Phospho serine and threonine analysis of normal and mutated granulocyte colony stimulating factor receptors. Dwivedi, P; Muench, DE; Wagner, M; Azam, M; Grimes, HL; Greis, KD. Scientific Data. 2019; 6:21.

Targeted Inhibition of the Dual Specificity Phosphatases DUSP1 and DUSP6 Suppress MPNST Growth via JNK. Ramkissoon, A; Chaney, KE; Milewski, D; Williams, KB; Williams, RL; Choi, K; Miller, A; Kalin, TV; Pressey, JG; Szabo, S; et al. Clinical Cancer Research. 2019; 25:4117-4127.

The high NRF2 expression confers chemotherapy resistance partly through up-regulated DUSP1 in myelodysplastic syndromes. Lin, P; Ren, Y; Yan, X; Luo, Y; Zhang, H; Kesarwani, M; Bu, J; Zhan, D; Zhou, Y; Tang, Y; et al. Haematologica: the hematology journal. 2019; 104:485-496.

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