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The Mohi LabMohiLAB
IL-1IL-1RIRAKNF-κBJAK2STAT5STAT3EZH2HMGA2TGF-β1PIM1CDK6U2AF1SRSF2Inflammation armJAK / STATEpigenetic / TFSplicing factor clusterTherapeutic targetsFig. 0 · Lab signaling map

Chapter I  ·  The cell

A research lab at UVA studying JAK2-driven myeloproliferative neoplasms, splicing-factor mutations in MDS, AML progression, IL-1 inflammation, PIM kinases, and triple-negative breast cancer — with a single throughline: find what to target next.

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Thesis
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
The work

Bench science with the patient still in view.

A working philosophy in three movements.

i.The questions

We work at the intersection of three big questions in blood cancer: how single mutations like JAK2V617F drive the diverse spectrum of myeloproliferative neoplasms; how splicing-factor errors in U2AF1, SRSF2, and SF3B1 collapse hematopoiesis in MDS; and how chronic inflammation cooperates with these genetic lesions to push disease forward.

ii.The approach

Inducible knock-in mouse models, conditional knockouts, patient samples, and pharmacologic tools — used together to ask what each piece of biology contributes, and what would happen if we removed it. Findings that hold at the bench have to hold in trials. The lab’s PIM1 work moved from murine myelofibrosis models into NCT04176198, the Phase 1/2 trial of TP-3654 (Nuvisertib) — now active at UVA Cancer Center.

iii.The goal

What we’re after is the next therapeutic target — the one that doesn’t yet have a trial behind it. Every paper, every graduate project, every grant in this lab is a wager on which mechanism will translate.

Where the lab publishes & who funds the science

Research fronts

Six fronts.
One signaling network.

Each theme below is a working hypothesis — what to validate next, what models to build, what trials to anchor. Click for the long-form essay.

Selected publications

Three papers,
three working theses.

A short selection from the lab’s recent work. Each anchors a different theme on the research index — and a different active grant or trial.

№ 01 / 032022Nature Communications

Interleukin-1 contributes to clonal expansion and progression of bone marrow fibrosis in JAK2V617F-induced myeloproliferative neoplasm

Rahman MF, Yang Y, Le BT, Dutta A, Posyniak J, Faughnan P, Sayem MA, Aguilera NS, Mohi G

We show that IL-1 signaling drives clonal expansion of JAK2V617F-mutant hematopoietic cells and accelerates bone marrow fibrosis. Genetic and pharmacologic inhibition of IL-1 ameliorates myelofibrosis in murine models — implicating the IL-1 pathway as a therapeutic target in MPN.

DOI: 10.1038/s41467-022-32928-3 ↗PMID: 36100596 ↗

№ 02 / 032022Leukemia

Genetic ablation of PIM1 or pharmacologic inhibition with TP-3654 ameliorates myelofibrosis in murine models

Dutta A, Nath D, Yang Y, Le BT, Rahman MF, Faughnan P, Wang Z, Stuver M, He R, Tan W, Hutchison RE, Foulks JM, Warner SL, Zang C, Mohi G

Genetic ablation of PIM1 or treatment with the PIM1 inhibitor TP-3654 reduces splenomegaly, normalizes blood counts, and lowers bone marrow fibrosis in JAK2V617F-driven myelofibrosis models. The work is the translational basis for the Phase 1/2 trial NCT04176198 (Nuvisertib) — now active at UVA Cancer Center.

DOI: 10.1038/s41375-021-01464-2 ↗PMID: 34741118 ↗

№ 03 / 032021Leukemia

U2af1 is required for survival and function of hematopoietic stem/progenitor cells

Dutta A, Yang Y, Le BT, Zhang Y, Abdel-Wahab O, Zang C, Mohi G

Conditional deletion of U2AF1 produces profound defects in hematopoiesis — pancytopenia, bone marrow failure, and loss of stem-cell function. The work anchors the lab's MDS splicing-factor program and grounds the active R01 NHLBI award on U2AF1-induced myelodysplasia.

DOI: 10.1038/s41375-020-01116-x ↗PMID: 33414485 ↗

The full archive

The lab’s complete bibliography — searchable, filterable by year, theme, and author position — lives on the publications page.

All publications
The people

Postdocs, students, staff —
the lab as a differentiation tree.

  • Golam Mohi, PhD

    Principal Investigator

  • Mohammad Abu Sayem, PhD

    Postdoctoral Research Associate

  • Chandrajeet Singh, PhD

    Postdoctoral Research Associate

  • Salar Abbas, PhD

    Postdoctoral Research Associate

  • Md. Anwarul Haque, PhD

    Postdoctoral Research Associate

  • Fahim Ather, MSc

    Research Specialist

  • Parag Palit, MSc

    Graduate Student

See everyone
In the news
Join us

We are seeking postdoctoral fellows and graduate students.

If you have hands in molecular biology, mouse genetics, or computational biology — and if you want your next paper to matter clinically — write to gm7sj@virginia.edu. Include a CV and a paragraph on what you want to build.

Open positionsVisit the lab →

The lab

Golam Mohi, PhD

Biochemistry & Molecular Genetics

University of Virginia School of Medicine

1340 JPA, Pinn Hall Room 6023A

Charlottesville, VA 22908

434-924-5657