Golam Mohi
| Golam Mohi | |
|---|---|
 Golam Mohi headshot.png Mohi in 2024 | |
| Born | 1969 (age 56–57) Bangladesh |
| 🏫 Education | University of Dhaka (BSc, MSc) University of Tokyo (PhD) |
| 💼 Occupation | |
| Known for | Preclinical research on the PIM1 inhibitor TP-3654 (Nuvisertib) for myelofibrosis |
Golam Mohi (born 1969) is a Bangladeshi-American biochemist at the University of Virginia School of Medicine whose preclinical research on the PIM1 serine/threonine kinase formed the scientific basis for the development of Nuvisertib (TP-3654), an experimental drug for myelofibrosis that received Fast Track Designation from the U.S. Food and Drug Administration in 2025 and Orphan Drug Designation from the European Medicines Agency in the same year.[1][2]
Education and career
Mohi earned BSc (1991) and MSc (1993) degrees in biochemistry from the University of Dhaka and a PhD in molecular cell biology from the Institute of Medical Science of the University of Tokyo in 2001, where his dissertation work characterized Janus kinase 2 activation and was published in Molecular Biology of the Cell.[3]
He completed postdoctoral training in the laboratory of Benjamin G. Neel at Beth Israel Deaconess Medical Center and Harvard Medical School, joined the faculty of SUNY Upstate Medical University as Assistant Professor of Pharmacology in 2006, and moved to the University of Virginia School of Medicine as Professor of Biochemistry and Molecular Genetics in 2017. He is Co-Leader of the Hematologic Malignancies Translational Research Team at the UVA Cancer Center and has received continuous NIH funding for his myeloproliferative neoplasm research, including a 2025 R01 grant to study molecular mechanisms of disease progression.[4][5]
In April 2025, Mohi was honored by the Society of American Asian Scientists in Cancer Research (SAASCR) at the American Association for Cancer Research Annual Meeting in Chicago for his contributions to cancer research, alongside other senior researchers including Suresh S. Ramalingam and Manmeet Ahluwalia.[6][7]
Research
PIM1 inhibition and the development of Nuvisertib (TP-3654)
In a 2022 study published in Leukemia, Mohi's laboratory reported that genetic deletion or pharmacologic inhibition of the PIM1 kinase using TP-3654 reduced splenomegaly and bone marrow fibrosis in mouse models of myelofibrosis.[8] The work provided the preclinical rationale for the multinational Phase 1/2 clinical trial NCT04176198, sponsored by Sumitomo Pharma America, evaluating TP-3654 (later named Nuvisertib) in patients with myelofibrosis at more than 80 sites in eight countries.[9] Interim Phase 1/2 data presented at the American Society of Hematology Annual Meeting in 2024 showed durable clinical responses and sustained hematological improvement in patients with relapsed and refractory disease.[10] Nuvisertib received FDA Fast Track Designation in June 2025[1] and EMA Orphan Drug Designation in July 2025.[11]
Other contributions to leukemia and myeloproliferative neoplasm research
As a postdoctoral fellow in the Neel laboratory, Mohi was the first author of a 2005 Cancer Cell study identifying Shp2 as the first oncogenic protein tyrosine phosphatase, based on a mouse model in which somatic PTPN11 mutations associated with juvenile myelomonocytic leukemia produced a JMML-like myeloproliferative disease.[12]
After establishing his independent laboratory, Mohi developed an inducible JAK2V617F knock-in mouse in which the mutation produced a polycythemia vera-like disease that progressed to myelofibrosis (Blood, 2010). His group has subsequently identified CDK6 as a therapeutic target in myelofibrosis, with palbociclib and ruxolitinib showing combination activity in preclinical models;[13] and reported in Nature Communications in 2022 that the IL-1 pathway contributes to clonal expansion and bone marrow fibrosis in JAK2V617F-driven myeloproliferative neoplasms.[14] The laboratory also studies the U2AF1 splicing factor in myelodysplastic syndromes, and has reported that SRSF2 mutation alters the phenotype of JAK2V617F-driven MPN. In a 2019 collaboration with the laboratory of Kenneth Walsh published in JACC: Basic to Translational Science, Mohi co-authored work showing that JAK2V617F-driven clonal hematopoiesis accelerates pathological remodeling in murine heart failure, linking the mutation to cardiovascular disease.[15][16]
Selected publications
- Mohi MG, Williams IR, Dearolf CR, et al. (2005). "Prognostic, therapeutic, and mechanistic implications of a mouse model of leukemia evoked by Shp2 (PTPN11) mutations". Cancer Cell 7(2): 179–191. PMID 15710330.
- Akada H, Yan D, Zou H, Fiering S, Hutchison RE, Mohi MG (2010). "Conditional expression of heterozygous or homozygous Jak2V617F from its endogenous promoter induces a polycythemia vera-like disease". Blood 115(17): 3589–3597. PMID 20197548.
- Dutta A, Nath D, Yang Y, Le BT, et al., Mohi G (2022). "Genetic ablation of Pim1 or pharmacologic inhibition with TP-3654 ameliorates myelofibrosis in murine models". Leukemia 36(3): 746–759. PMID 34741118.
- Rahman MF, Yang Y, Le BT, Dutta A, et al., Mohi G (2022). "Interleukin-1 contributes to clonal expansion and progression of bone marrow fibrosis in JAK2V617F-induced myeloproliferative neoplasm". Nature Communications 13: 5347. PMID 36100596.
References
- ↑ 1.0 1.1 Ryan, Chris (June 13, 2025). "FDA Grants Fast Track Designation to Nuvisertib for Myelofibrosis". OncLive. Retrieved May 10, 2026.
- ↑ "Sumitomo Pharma America Announces that Nuvisertib (TP-3654) Has Received FDA Fast Track Designation for the Treatment of Myelofibrosis" (Press release). Sumitomo Pharma America. June 12, 2025.
- ↑ Mohi, MG; Arai, K; Watanabe, S (1998). "Activation and Functional Analysis of Janus Kinase 2 in BA/F3 Cells Using the Coumermycin/Gyrase B System". Molecular Biology of the Cell. 9 (12): 3299–3308. doi:10.1091/mbc.9.12.3299. PMC 25626.
- ↑ Wallace, David (January 2025). "UVA Researcher Receives $2.4M For MPN Progression Study". PV Reporter. Retrieved May 10, 2026.
- ↑ "Golam Mohi, PhD". University of Virginia School of Medicine. Retrieved May 10, 2026.
- ↑ "SAASCR Honors Leading Asian American Cancer Researchers". India-West. May 12, 2025. Retrieved May 10, 2026.
- ↑ "Indian American Cancer Scientists Honored With Prestigious Awards For Groundbreaking Discoveries". India Post. 2025. Retrieved May 10, 2026.
- ↑ Dutta, A; Nath, D; Yang, Y; Le, BT; Mohi, G; et al. (2022). "Genetic ablation of Pim1 or pharmacologic inhibition with TP-3654 ameliorates myelofibrosis in murine models". Leukemia. 36 (3): 746–759. doi:10.1038/s41375-021-01464-2. PMID 34741118 Check
|pmid=value (help). - ↑ "A Study to Evaluate the Safety and Efficacy of TP-3654 in Patients With Myelofibrosis (NCT04176198)". ClinicalTrials.gov. Retrieved May 10, 2026.
- ↑ "Nuvisertib (TP-3654), an Investigational Selective PIM1 Kinase Inhibitor, Showed Durable Clinical Response and Sustained Hematological Improvement in Relapsed/Refractory Myelofibrosis Patients". Blood. 144 (Supplement 1): 655. 2024.
- ↑ "Sumitomo Pharma America Announces that the European Medicines Agency Has Granted Orphan Drug Designation to Nuvisertib (TP-3654) for the Treatment of Myelofibrosis" (Press release). PR Newswire. July 2025.
- ↑ Mohi, MG; Williams, IR; et al. (2005). "Prognostic, therapeutic, and mechanistic implications of a mouse model of leukemia evoked by Shp2 (PTPN11) mutations". Cancer Cell. 7 (2): 179–191. doi:10.1016/j.ccr.2005.01.010. PMID 15710330.
- ↑ Seymour, Caroline (August 19, 2021). "Palbociclib/Ruxolitinib Combo Shows Preclinical Promise in Myelofibrosis". OncLive. Retrieved May 10, 2026.
- ↑ Rahman, MF; Yang, Y; Le, BT; Dutta, A; Mohi, G; et al. (2022). "Interleukin-1 contributes to clonal expansion and progression of bone marrow fibrosis in JAK2V617F-induced myeloproliferative neoplasm". Nature Communications. 13: 5347. doi:10.1038/s41467-022-32928-3. PMID 36100596 Check
|pmid=value (help). - ↑ Sano, S; Wang, Y; Yura, Y; Mohi, MG; Walsh, K; et al. (2019). "JAK2V617F-Mediated Clonal Hematopoiesis Accelerates Pathological Remodeling in Murine Heart Failure". JACC: Basic to Translational Science. 4 (6): 684–697. doi:10.1016/j.jacbts.2019.05.013. PMID 31709318.
- ↑ Yang, Y; Akada, H; Le, BT; Dutta, A; Mohi, G; et al. (2023). "SRSF2 mutation reduces polycythemia and impairs hematopoietic progenitor functions in JAK2V617F-driven myeloproliferative neoplasm". Blood Cancer Journal. 13: 171. doi:10.1038/s41408-023-00947-y.
External links
- Faculty profile, University of Virginia School of Medicine
- Golam Mohi publications indexed by Google Scholar
- Entry at ORCID
- Clinical trial NCT04176198 at ClinicalTrials.gov
Category:1969 births
Category:Living people
Category:21st-century American biologists
Category:Bangladeshi emigrants to the United States
Category:Bangladeshi biochemists
Category:American biochemists
Category:American hematologists
Category:American cancer researchers
Category:University of Dhaka alumni
Category:University of Tokyo alumni
Category:Harvard Medical School people
Category:State University of New York Upstate Medical University faculty
Category:University of Virginia School of Medicine faculty
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