Mohammad Azam, PhD
- Member, Division of Experimental Hematology & Cancer Biology
- Professor, UC Department of Pediatrics
About
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
Services and Specialties
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
Publications
Selective degradation of oncogenic signaling nodes by momelotinib-based protacs exerts potent anti-leukemic response in B-ALL, AML, and MF while sparing normal cells. Blood. 2025; 146(Supplement 1):6108.
Novel BCR::ABL1 fusion alongside T315I reveals mechanism for dual ponatinib/asciminib resistance and proves sensitive to addition of axitinib. Blood. 2025; 146(Supplement 1):1501-1501.
Negative feedback regulation of nfkb, MAPK, and JAK-STAT drives adaptive resistance to gilteritinib in AML. Blood. 2025; 146(Supplement 1):1514-1514.
Momelotinib-mediated transcriptional reprogramming induces synthetic lethal interaction with calcineurin-NFAT signaling. Blood. 2025; 146(Supplement 1):756.
Enhanced antileukemic activity of momelotinib in combination with venetoclax and azacitidine compared to gilteritinib-based combination. Blood. 2025; 146(Supplement 1):7850-7850.
Targeting CDK16 Abrogates Growth-Factor Mediated TKI Resistance in AML. Blood. 2024; 144(Supplement 1):5786.
A Novel BCR::ABL1 Rearrangement Harboring the Gatekeeper Mutation Drives Hyper-Kinase Activity Conferring Resistance to Ponatinib and Asciminib Combination Therapy. Blood. 2024; 144(Supplement 1):4541-4541.
Enhanced Mitochondrial Priming By Momelotinib Confers Superior In Vivo Efficacy in Combination with Venetoclax Compared to Gilteritinib or Ruxolitinib. Blood. 2024; 144(Supplement 1):5814.
Enhanced MAPK signaling induced by CSF3R mutants confers dependence to DUSP1 for leukemic transformation. Blood advances. 2024; 8(11):2765-2776.
DUSP1 Specific Protac Selectively Targets the JAK2 V617F Expressing Cells. Blood. 2023; 142(Supplement 1):3156.
From the Blog
Research Reveals Potential Achille’s Heel in Treatment-Resistant MPN
Mohammad Azam, PhD8/21/2023
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