Principal Investigator
Golam Mohi,
PhD.
Professor of Biochemistry & Molecular Genetics at the University of Virginia School of Medicine. Co-Leader of the Hematologic Malignancies Translational Research Team at the UVA Cancer Center. Working on the molecular pathogenesis of myeloproliferative neoplasms and myelodysplastic syndromes — from a single mutation to a clinical trial.
We are interested in understanding how different mutations associated with blood cancer contribute to the disease. Our ultimate goal is to find new therapeutic targets and develop novel therapies for leukemias.
- 01.
Long-term goal: understand the molecular pathogenesis of MPN and MDS — and translate that understanding into new therapeutic targets.
- 02.
Track record at UVA: 8 articles in Blood, 5 in Leukemia, plus papers in Cancer Research and Nature Communications, in MPN alone.
- 03.
Bench-to-clinic example: lab’s PIM1 work motivated the multicenter Phase 1/2 trial NCT04176198 (TP-3654 / Nuvisertib) — UVA Cancer Center is a major site.
- 1991
B.S., Biochemistry
University of Dhaka, Bangladesh
University ofDhaka - 1993
M.S., Biochemistry
University of Dhaka, Bangladesh
University ofDhaka - 2001
Ph.D., Molecular Cell Biology
University of Tokyo, Japan
University ofTokyo - 2005
Postdoctoral Fellow, Cancer Biology
Harvard Medical School (Beth Israel Deaconess, Benjamin Neel Lab)
HarvardMedical School
- 1993–1995
Research Fellow / Officer, Immunology Laboratory
ICDDR,B (Bangladesh)
ICDDR,B - 1995–2001
Lecturer, Department of Biochemistry
University of Dhaka
University ofDhaka - 2001–2005
Postdoctoral Fellow
Beth Israel Deaconess / Harvard Medical School
HarvardMedical School - 2005–2006
Instructor, Cancer Biology Program
Beth Israel Deaconess / Harvard Medical School
HarvardMedical School - 2006–2012
Assistant Professor of Pharmacology
SUNY Upstate Medical University
SUNYUpstate - 2012–2017
Associate Professor of Pharmacology, with tenure
SUNY Upstate Medical University
SUNYUpstate - 2017 (Mar–Aug)
Professor of Pharmacology
SUNY Upstate Medical University
SUNYUpstate - 2017–present
Professor of Biochemistry & Molecular Genetics
University of Virginia School of Medicine
UVASchool of Medicine - 2023–present
Co-Leader, Hematologic Malignancies Translational Research Team
UVA Cancer Center
UVACancer Center
- 2013–2018
Leukemia & Lymphoma Society Scholar Award
LLSLeukemia & Lymphoma - 2012
SUNY Upstate President’s Award for Excellence in Basic Research
SUNYUpstate - 2005–2008
American Society of Hematology Scholar Award
ASHHematology - 2001–2004
Leukemia & Lymphoma Society Postdoctoral Fellowship
LLSLeukemia & Lymphoma - 1996–2001
Japanese Ministry of Education Scholarship for doctoral studies
- 1992–1993
University Grants Commission Merit Scholarship for Excellence
- 1991, 1993
Gold medals — first position in B.S. and M.S.
University ofDhaka
- 2025–present
R01 $2.4M active
Molecular Basis for Progression of Myeloproliferative Neoplasms Induced by JAK2V617F
NIHNational Inst. of Health - 2023–present
R01 active
Molecular basis for myelodysplasia induced by U2AF1 mutations
NHLBINIH - 2023–present
R21 active
Pharmacologic inhibition of IL-1 signaling in pre-clinical models of myelofibrosis
NCINational Cancer Inst. - 2020–2023
R01HL149893 completed
The Role of PTPN11 in Myelofibrosis
NHLBINIH - 2009–2022
R01HL095685 completed
Role of JAK2V617F in the Pathogenesis of Myeloproliferative Neoplasms
NHLBINIH
Memberships
- 2023–present
ASH Scientific Committee on Myeloid Neoplasia
Member
ASHHematology - 2009–present
American Association for Cancer Research
Member
AACRCancer Research - 2004–present
American Society of Hematology
Member
ASHHematology - 2003–present
American Association for the Advancement of Science
Member
AAASScience
Twenty-one panels and study sections served (2010–2023), spanning NIH/NHLBI, NIH/NIDDK, NIH MCH, NIH SEPs, plus the Medical Research Council UK, the Austrian Science Fund, and the American Cancer Society IRG.
- 2023NIHNational Inst. of Health
NIH GRIC Study Section
Reviewer / Ad hoc
- 2023NHLBINIH
NIH/NHLBI R61/R33 ZHL1 CSR-F (M1)
Reviewer
- 2022NIHNational Inst. of Health
NIH/NIDDK RC2 Panel ZDK1 GRB-9 (J2)
Reviewer
- 2022NIHNational Inst. of Health
NIH SEP ZCA1 SRB-K O2-SEP6
Reviewer
- 2021NHLBINIH
NIH/NHLBI Program Project Grant
Reviewer
- 2021NIHNational Inst. of Health
NIH SEP ZCA1 SRB-K M2-SEP6
Reviewer
- 2021NIHNational Inst. of Health
NIH SEP HLBP (7)
Reviewer
- 2020NIHNational Inst. of Health
NIH/NIDDK RC2 Panel
Reviewer
- 2020NIHNational Inst. of Health
NIH SEP ZDK1-GRB (J4)
Reviewer
- 2019NIHNational Inst. of Health
NIH SEP ZRG1 OBT-C (02) M
Reviewer
- 2019
Medical Research Council, UK
Reviewer
- 2018NIHNational Inst. of Health
NIH MCH Study Section
Reviewer (Feb & Oct)
- 2018NIHNational Inst. of Health
NIH SEP ZRG1 VH-J 90 S
Reviewer
- 2017NIHNational Inst. of Health
NIH SEP ZRG1VH-B(03)
Co-Chair
- 2016NHLBINIH
NIH/NHLBI PPG HLBP workgroup
Reviewer
- 2015
Austrian Science Fund
Reviewer
- 2014NIHNational Inst. of Health
NIH MCH Study Section
Reviewer
- 2013NIHNational Inst. of Health
NIH SEP ZRG1 BDCN-L(60)R
Reviewer
- 2011–13
American Cancer Society IRG
Reviewer
- 2011NIHNational Inst. of Health
NIH SEP ZRG1VH-F(80)
Reviewer
- 2010NIHNational Inst. of Health
NIH MCH Study Section
Reviewer
01.Contribution
Postdoctoral work on BCR/ABL and Shp2 (PTPN11)
As a postdoctoral fellow in Ben Neel’s lab at Harvard, established that GAB2 is essential for hematopoietic transformation by BCR/ABL — the CML driver — through both PI3K/Akt and Erk/MAPK arms. Showed that mTOR inhibitor rapamycin synergizes with imatinib against BCR/ABL- and FLT3-driven leukemias, including imatinib-resistant variants. Demonstrated that leukemia-associated PTPN11/Shp2 mutants are gain-of-function and more activating than the Noonan-syndrome variants, and that expressing leukemia-associated Shp2 E76K in hematopoietic progenitors generates a JMML-like MPN. Co-authored the PTPN11 D61G knock-in mouse model of Noonan syndrome. Established Shp2 as the first oncogenic protein tyrosine phosphatase.
Anchor papersPMID 12124177PMID 14976243PMID 15273746PMID 15710330
02.Contribution
JAK2V617F MPN — foundation
Built the inducible JAK2V617F knock-in mouse expressing the mutation from its endogenous promoter — the first model where heterozygous expression alone produced PV-like disease and homozygous expression accelerated progression to myelofibrosis. Demonstrated that Stat5 is critical for JAK2V617F-induced PV, while Stat3 is dispensable. Showed Tyrosine 201 of JAK2V617F is required for constitutive activation and efficient induction of MPN. These models are now standard tools across the field.
Anchor papersPMID 20197548PMID 22144185PMID 22408262PMID 22837531
03.Contribution
JAK2V617F phenotypic diversity
Showed loss of EZH2 cooperates with JAK2V617F in myelofibrosis pathogenesis (Blood 2016); HMGA2 is overexpressed in MF patients and drives MF in JAK2V617F mice through TGF-β1 and CXCL12 (Blood 2017); STAT3 is dispensable for PV (Leukemia 2015); and PIM1 plays an essential role in MF, with TP-3654 ameliorating disease (Leukemia 2022) — directly motivating the multicenter Phase 1/2 trial NCT04176198 of TP-3654 / Nuvisertib in myelofibrosis patients.
Anchor papersPMID 27081096PMID 28637665PMID 26044284PMID 34741118
04.Contribution
Wild-type JAK2, PTP1B, and U2AF1 in hematopoiesis
Through a conditional Jak2 knockout, established that wild-type Jak2 is essential for adult hematopoietic-stem-cell maintenance and function. Loss of WT Jak2 in JAK2V617F mice worsens MPN and accelerates fibrosis. Genetic ablation of PTPN1 (PTP1B) expands HSC/progenitors and produces an MPN-like phenotype. Most recently, showed RNA splicing factor U2AF1 is required for HSPC survival and function — anchoring the lab’s MDS splicing-factor program.
Anchor papersPMID 24677703PMID 24480985PMID 28111468PMID 33414485
The full archive