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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.

UVASchool of Medicine
UVACancer Center

Personal statement

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.
Golam Mohi, PhD · UVA Medicine in Motion · 2025
  • 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.

Education

  1. 2001

    Ph.D., Molecular Cell Biology

    University of Tokyo, Japan

    Univ. ofTOKYO
  2. 2005

    Postdoctoral Fellow, Cancer Biology

    Harvard Medical School (Beth Israel Deaconess, Benjamin Neel Lab)

    HARVARDMedical School

Career

  1. 2001–2005

    Postdoctoral Fellow

    Beth Israel Deaconess / Harvard Medical School

    HARVARDMedical School
  2. 2005–2006

    Instructor, Cancer Biology Program

    Beth Israel Deaconess / Harvard Medical School

    HARVARDMedical School
  3. 2006–2012

    Assistant Professor of Pharmacology

    SUNY Upstate Medical University

    SUNYUpstate
  4. 2012–2017

    Associate Professor of Pharmacology, with tenure

    SUNY Upstate Medical University

    SUNYUpstate
  5. 2017 (Mar–Aug)

    Professor of Pharmacology

    SUNY Upstate Medical University

    SUNYUpstate
  6. 2017–present

    Professor of Biochemistry & Molecular Genetics

    University of Virginia School of Medicine

    UVASchool of Medicine
  7. 2023–present

    Co-Leader, Hematologic Malignancies Translational Research Team

    UVA Cancer Center

    UVACancer Center

Awards & honors

Active grants

  1. NIHR01

    Molecular Basis for Progression of Myeloproliferative Neoplasms Induced by JAK2V617F

    NIHInstitutes of Health

  2. NIH NHLBIR01

    Molecular basis for myelodysplasia induced by U2AF1 mutations

    NHLBIHeart · Lung · Blood

Memberships & service

Memberships

  • 2023–present

    ASH Scientific Committee on Myeloid Neoplasia

    Member

    ASHSociety of Hematology
  • 2009–present

    American Association for Cancer Research

    Member

    AACRCancer Research
  • 2004–present

    American Society of Hematology

    Member

    ASHSociety of Hematology
  • 2003–present

    American Association for the Advancement of Science

    Member

    AAASScience

Contributions to science

  1. 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

  2. 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

  3. 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

  4. 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

For the complete bibliography, theme essays, and lab roster.

Research themesAll publicationsContact →