# The Mohi Lab — Full content for AI crawlers This document is the full machine-readable version of The Mohi Lab, intended for AI search engines and language-model crawlers. The canonical human-readable site lives at https://themohilab.com. Published by the Mohi Laboratory at the University of Virginia School of Medicine. For citation, defer to original PubMed records (linked below). --- ## 1. About the lab The Mohi Lab (also referred to in publications as "Mohi Lab" or "Mohi Laboratory") is the research group of Golam Mohi, PhD, Professor in the Department of Biochemistry & Molecular Genetics at the University of Virginia School of Medicine, and Co-Leader of the Hematologic Malignancies Translational Research Team at the UVA Cancer Center. The lab studies the molecular pathogenesis of myeloproliferative neoplasms (MPN), myelodysplastic syndromes (MDS), acute myeloid leukemia (AML), and triple-negative breast cancer (TNBC). The lab's signature contribution is the inducible JAK2V617F knock-in mouse, expressing the mutation from its endogenous promoter — now a standard MPN model across the field. The lab's preclinical work on PIM1 inhibition led directly to the multicenter Phase 1/2 trial NCT04176198 of TP-3654 (Nuvisertib), with UVA Cancer Center as a major site. As of 2025, Nuvisertib carries FDA Fast Track Designation, EMA Orphan Drug Designation, and Japan MHLW Orphan Drug Designation. ### Key biographical facts (Principal Investigator) - Name: Golam Mohi, PhD - Title: Professor of Biochemistry & Molecular Genetics, University of Virginia School of Medicine - Additional role: Co-Leader, Hematologic Malignancies Translational Research Team, UVA Cancer Center - Education: B.S. and M.S. in Biochemistry from the University of Dhaka (Bangladesh, 1991 and 1993); Ph.D. in Molecular Cell Biology from the University of Tokyo (Japan, 2001); Postdoctoral training in Cancer Biology at Harvard Medical School in the Benjamin Neel laboratory at Beth Israel Deaconess Medical Center (2001–2005). - Career history: Research Fellow at ICDDR,B (Bangladesh, 1993–1995); Lecturer at the University of Dhaka (1995–2001); Postdoc and Instructor at Harvard Medical School (2001–2006); Assistant, Associate (tenured), and Professor of Pharmacology at SUNY Upstate Medical University (2006–2017); Professor at UVA since 2017; Co-Leader of UVA Cancer Center TRT since 2023. - eRA Commons username: mohimg - Office: 1340 JPA, Pinn Hall Room 6023A, Charlottesville, VA 22908 - Email: gm7sj@virginia.edu; Phone: 434-924-5657 - Google Scholar citation metrics (as of 2026-05-09): 4,009 total citations, h-index 25, i10-index 35 ### Selected awards and honors - Leukemia & Lymphoma Society Scholar Award (2013–2018) - American Society of Hematology Scholar Award (2005–2008) - Leukemia & Lymphoma Society Postdoctoral Fellowship (2001–2004) - SUNY Upstate Medical University President's Award for Excellence in Basic Research (2012) - Japanese Ministry of Education Scholarship for doctoral studies (1996–2001) - University Grants Commission Merit Scholarship for Excellence, Bangladesh (1992–1993) - Gold medals for first position in B.S. (1991) and M.S. (1993), University of Dhaka ### Active NIH funding - R01 (NIH): "Molecular Basis for Progression of Myeloproliferative Neoplasms Induced by JAK2V617F," $2.4M announced 2025-02. PI: Mohi. - R01 (NIH/NHLBI): "Molecular basis for myelodysplasia induced by U2AF1 mutations," awarded 2023. PI: Mohi. - R21 (NIH/NCI): "Pharmacologic inhibition of IL-1 signaling in pre-clinical models of myelofibrosis," awarded 2023. PI: Mohi. ### Society memberships - ASH Scientific Committee on Myeloid Neoplasia (2023–present) - American Association for Cancer Research, AACR (2009–present) - American Society of Hematology, ASH (2004–present) - American Association for the Advancement of Science, AAAS (2003–present) ### Translational milestone The lab's preclinical demonstration that genetic ablation of PIM1 or pharmacologic inhibition with TP-3654 ameliorates myelofibrosis in murine models (Dutta et al., Leukemia 2022, PMID 34741118) led directly to the multicenter Phase 1/2 trial NCT04176198 of TP-3654 (now Nuvisertib) in myelofibrosis patients. UVA Cancer Center is a major site for this trial. Regulatory milestones for Nuvisertib include FDA Orphan Drug Designation (2022), Japan MHLW Orphan Drug Designation (2024), FDA Fast Track Designation (June 2025), and EMA Orphan Drug Designation (July 2025). --- ## 2. Research themes (six fronts) ### JAK2V617F · MPN · How a single mutation drives three blood cancers. > Polycythemia vera, essential thrombocythemia, myelofibrosis. The same JAK2V617F mutation produces three distinct myeloproliferative neoplasms. We use inducible knock-in mouse models to ask why dose, cell-of-origin, and cooperating mutations decide the disease that emerges. #### Why this matters Most myeloproliferative neoplasm patients carry the JAK2V617F mutation, yet present with one of three diseases that range from a manageable chronic condition to a life-threatening bone marrow failure. Understanding why the same mutation produces such different outcomes is the difference between a uniform JAK-inhibitor strategy and personalized therapy. #### The biology JAK2V617F sits in the kinase's pseudokinase domain and disrupts an autoinhibitory loop, leaving JAK2 constitutively active and constitutively phosphorylating STAT5, STAT3, and other downstream effectors. The result is cytokine-independent proliferation of the affected hematopoietic lineages. The lab's foundational contribution is an inducible JAK2V617F knock-in mouse expressing the mutation from its endogenous promoter. Heterozygous expression alone is sufficient to drive a polycythemia vera-like disease; homozygous expression accelerates progression toward myelofibrosis. The model recapitulates the dose-dependent phenotypic divergence seen in patients and is now a standard tool across the MPN field. Genetic dissection in this background has identified the critical effectors. STAT5 deletion completely blocks JAK2V617F-induced PV, naming STAT5 as the pivotal downstream node. STAT3, despite being the canonical JAK partner, is dispensable. Tyrosine 201 of JAK2V617F is required for constitutive activation — a structural constraint relevant to inhibitor design. Cooperating mutations shape disease trajectory. Loss of the polycomb component EZH2 cooperates with JAK2V617F to accelerate myelofibrosis, partly by derepressing HMGA2; HMGA2 in turn drives MF through TGF-β1 and CXCL12 signaling. Loss of the wild-type Jak2 allele in V617F mice worsens disease, mirroring the clinical observation that homozygous patients fare worse. #### Open questions What determines whether a patient with JAK2V617F follows the PV, ET, or MF trajectory? The cooperating-mutation hypothesis is supported but incomplete; clonal architecture, cell-of-origin, and microenvironment all contribute, and the lab's current R01 is built around finding the molecular hand on the steering wheel. #### Our contribution 1. Heterozygous JAK2V617F drives PV; homozygous expression accelerates progression to myelofibrosis. 2. STAT5 deletion completely blocks JAK2V617F-induced PV; STAT3 is dispensable. 3. Loss of EZH2 cooperates with JAK2V617F to promote myelofibrosis. 4. HMGA2 sits downstream of EZH2 and drives MF through TGF-β1 and CXCL12. 5. Tyrosine 201 of JAK2V617F is required for constitutive activation. #### Targets, drugs, models - Targets: JAK2, STAT5, STAT3, EZH2, HMGA2, TGF-β1, CXCL12 - Drugs: Ruxolitinib - Models: JAK2V617F knock-in mouse, MPLW515L #### Anchor papers (PMIDs) - https://pubmed.ncbi.nlm.nih.gov/20197548/ - https://pubmed.ncbi.nlm.nih.gov/22144185/ - https://pubmed.ncbi.nlm.nih.gov/27081096/ - https://pubmed.ncbi.nlm.nih.gov/28637665/ - https://pubmed.ncbi.nlm.nih.gov/22837531/ - https://pubmed.ncbi.nlm.nih.gov/26044284/ #### Theme URL https://themohilab.com/research/mpn --- ### IL-1 · Inflammation · Chronic inflammation as a driver of clonal expansion. > Targeting the IL-1 axis in MPN. JAK inhibitors manage MPN symptoms but don't reverse fibrosis or eliminate the mutant clone. We identified IL-1 signaling as a key driver of clonal expansion and bone marrow fibrosis, and showed that IL-1R1 antibody blockade reduces disease burden in murine MPN. #### Why this matters Patients with myeloproliferative neoplasms live with chronic systemic inflammation: bone pain, fatigue, fevers, splenomegaly. Current JAK inhibitors blunt the symptoms but leave the underlying clone and the marrow scarring largely intact. If inflammation isn't a side effect but a driver, then targeting it could be the missing half of treatment. #### The biology Patients with MPN show elevated circulating inflammatory cytokines, and the JAK2V617F-mutant clone exists inside a bone marrow niche that becomes progressively more inflammatory as disease advances. The lab's hypothesis was that this isn't only a consequence of the disease but part of what sustains it. Using the inducible JAK2V617F knock-in model, the lab showed that IL-1 signaling is markedly elevated and that genetic loss of IL-1 in the JAK2V617F context reduces clonal expansion and slows bone marrow fibrosis. Antibody blockade of IL-1R1 reproduces the genetic phenotype: less competitive advantage for the mutant clone, less fibrotic remodeling, less disease burden. Mechanistically, IL-1 functions as a microenvironmental amplifier. The mutant clone produces IL-1; supporting stromal and immune cells respond to IL-1; the response feeds back to support the mutant clone's expansion and the deposition of marrow scar. Cutting that loop is the therapeutic premise. #### Open questions Will IL-1 inhibitors combine well with JAK inhibitors in patients? What's the exact cellular source of IL-1 in the MPN bone marrow — and does targeting that source give the clone fewer escape routes than blocking the cytokine itself? An active R21 NCI award funds the preclinical answer. #### Our contribution 1. IL-1 signaling drives clonal expansion of JAK2V617F-mutant cells. 2. IL-1R1 antibody blockade reduces bone marrow fibrosis in murine MPN. 3. IL-1 inhibition complements JAK2 inhibition mechanistically. #### Targets, drugs, models - Targets: IL-1, IL-1R1, JAK2 - Models: JAK2V617F knock-in mouse #### Anchor papers (PMIDs) - https://pubmed.ncbi.nlm.nih.gov/36100596/ #### Theme URL https://themohilab.com/research/il1 --- ### PIM kinases · Bench to clinic · PIM1 inhibition: from a mouse model to a Phase 1/2 trial. > TP-3654, now Nuvisertib. PIM1 expression is markedly elevated in MPN progenitors. Genetic ablation blocks myelofibrosis; the small-molecule PIM1 inhibitor TP-3654 ameliorates disease in mice. The work led directly to a multicenter clinical trial, with UVA Cancer Center as a major site. #### Why this matters Most preclinical drug candidates die between the mouse and the patient. The lab's PIM1 work is one of the rare cases where a hypothesis tested in a knockout mouse moved through industry partnership into a multicenter trial — and recently into FDA Fast Track and EMA Orphan Drug designations. The compound now has a name (Nuvisertib) and patients on it. #### The biology PIM1 is a serine/threonine kinase that sits downstream of cytokine signaling and supports proliferation, survival, and metabolic adaptation in hematopoietic cells. The lab found PIM1 expression markedly elevated in MPN progenitors and asked whether it's a passenger of the disease state or a driver of it. Genetic Pim1 ablation in JAK2V617F mice answered the question: the mutant clone proliferates less, splenomegaly recedes, and bone marrow fibrosis fails to develop. The PIM1 axis is causal, not correlative. Pharmacologically, the small-molecule PIM1 inhibitor TP-3654 reproduces the genetic phenotype in mice — reducing leukocytosis, splenomegaly, and fibrotic markers, with concurrent inhibition of mTORC1, MYC, and TGF-β signaling and lower collagen output. Combination with Ruxolitinib delivers more than additive benefit: blood counts normalize and marrow fibrosis is abrogated, suggesting non-overlapping mechanisms. The compound is now Nuvisertib, in a Sumitomo Pharma-sponsored Phase 1/2 trial (NCT04176198) at UVA Cancer Center and other sites. As of mid-2025 it carries FDA Fast Track, EMA Orphan Drug, and Japan MHLW Orphan Drug designations. CDK6, independently elevated in MPN progenitors, is a parallel target: Palbociclib + Ruxolitinib synergize in mouse models, suggesting a portfolio of combination strategies. #### Open questions Which patients benefit most — by mutation status, by treatment history, by marrow fibrosis grade? Will combination strategies (PIM + JAK, PIM + CDK4/6) translate? The lab is positioned to answer mechanistic questions that the trial alone cannot. #### Our contribution 1. PIM1 expression elevated in MPN progenitors; genetic ablation prevents myelofibrosis. 2. TP-3654 reduces leukocytosis, splenomegaly, and bone marrow fibrosis in murine MPN. 3. TP-3654 inhibits mTORC1, MYC, and TGF-β signaling and reduces collagen output. 4. Combined TP-3654 + Ruxolitinib normalizes blood counts and abrogates marrow fibrosis. 5. CDK6 is independently elevated in MPN progenitors; Palbociclib + Ruxolitinib synergize. #### Targets, drugs, models - Targets: PIM1, CDK6, mTORC1, MYC, TGF-β - Drugs: TP-3654 (Nuvisertib), Palbociclib, Ruxolitinib - Models: JAK2V617F, MPLW515L - Trial: NCT04176198 — Phase 1/2 of TP-3654 (Nuvisertib) in primary or secondary myelofibrosis. Recruiting. Sponsor: Sumitomo Pharma America. #### Anchor papers (PMIDs) - https://pubmed.ncbi.nlm.nih.gov/34741118/ - https://pubmed.ncbi.nlm.nih.gov/34145036/ #### Theme URL https://themohilab.com/research/pim --- ### U2AF1 · MDS · When splicing fails, hematopoiesis collapses. > Splicing-factor mutations as MDS drivers. U2AF1 mutations are found in ~11% of MDS cases. We use conditional knockout and knock-in alleles to dissect how this single splicing-factor lesion produces stem-cell failure, replication stress, and the dysplastic phenotype. #### Why this matters Myelodysplastic syndromes are clonal disorders of the bone marrow that leave patients unable to produce healthy blood cells. A surprisingly large fraction carry mutations in RNA splicing factors — proteins not historically thought of as cancer drivers. Understanding how a splicing defect produces hematopoietic failure rewrites part of how we think about leukemic disease. #### The biology Pre-mRNA splicing is a foundational step in gene expression. U2AF1 is a small subunit of the U2 auxiliary factor that recognizes the 3' splice site of introns; without correct recognition, splice junctions fail and aberrant transcripts result. Mutations in U2AF1 (most commonly S34F and Q157R) are recurrent in MDS, secondary AML, and some MPN. The lab's conditional U2af1 knockout shows that the gene is essential for hematopoiesis. Loss produces pancytopenia, hematopoietic stem and progenitor cell ablation, bone marrow failure, and early lethality. The phenotype establishes U2AF1 as a non-redundant requirement for blood-cell production. To model the disease itself, the lab built a conditional U2AF1-Q157R knock-in mouse — expressing the most common patient mutation at endogenous levels. The animals develop macrocytic anemia and erythroid dysplasia (the morphological hallmarks of MDS) along with stem-cell expansion, recapitulating key clinical features. Mechanistically, the leading model is that mutant U2AF1 mis-recognizes 3' splice sites, producing aberrant transcripts of genes involved in cell cycle, DNA repair, and stem-cell maintenance. The downstream consequences — replication stress, DNA damage response activation, progenitor attrition — converge on the dysplastic phenotype. SRSF2, another splicing factor mutated in MDS, modifies JAK2V617F MPN by reducing erythrocytosis and impairing progenitor function, suggesting the splicing axis intersects with the MPN program too. #### Open questions Which spliceforms drive the disease, and which are bystanders? Can the splicing defect be drugged — by stabilizing wild-type-like splicing, by exploiting the mutant clone's vulnerability, or by hitting downstream synthetic-lethal partners? The lab's active R01 NHLBI award is built around answering these. #### Our contribution 1. U2AF1 deletion produces pancytopenia, HSPC loss, bone marrow failure, and early lethality. 2. U2AF1 is required for HSC maintenance, repopulation, and progenitor survival. 3. U2AF1-Q157R knock-in mice develop macrocytic anemia, erythroid dysplasia, and HSC expansion. 4. Likely mechanism: aberrant splicing → gene expression changes + DNA damage + replication stress. #### Targets, drugs, models - Targets: U2AF1, SRSF2, SF3B1 - Models: Conditional U2AF1 knockout, U2AF1-Q157R knock-in #### Anchor papers (PMIDs) - https://pubmed.ncbi.nlm.nih.gov/33414485/ - https://pubmed.ncbi.nlm.nih.gov/38012156/ #### Theme URL https://themohilab.com/research/mds --- ### AML · Progression · Mechanisms of AML evolution and therapy resistance. > What pushes MPN and MDS toward acute leukemia. JAK inhibitors reduce symptoms but don't cure; some patients progress to acute myeloid leukemia. We study the cooperating mutations and signaling rewires that license MPN/MDS to transform into AML, and what therapeutic windows exist before that transition. #### Why this matters Transformation from a chronic blood cancer to acute myeloid leukemia is one of the worst clinical events in this disease space — survival drops sharply once it occurs. Knowing what makes one patient transform and another stay stable is the difference between watchful waiting and aggressive intervention. #### The biology AML is a genetically heterogeneous acute leukemia driven by various combinations of signaling, epigenetic, and splicing-factor mutations. Many cases evolve from preceding myeloid disorders (MPN, MDS) through stepwise acquisition of cooperating events. The lab's earlier work in BCR/ABL- and PTPN11-driven leukemia models established a framework: a single signaling driver is rarely sufficient. Postdoctoral work demonstrated GAB2 is essential for hematopoietic transformation by BCR/ABL through both PI3K/Akt and Erk/MAPK arms, and that combining mTOR inhibitors with TKIs synergizes against BCR/ABL- and FLT3-driven leukemias, including imatinib-resistant variants. Leukemia-associated PTPN11 (Shp2) mutants were shown to be more activating than the developmental Noonan-syndrome variants and to drive a JMML-like MPN — establishing Shp2 as the first oncogenic protein tyrosine phosphatase. More recent lab work in this theme: STAT3 activating mutations alone are insufficient to drive LGL leukemia in mice, suggesting cooperating events are required. Genetic ablation of PTPN1 (PTP1B) produces an MPN-like phenotype, suggesting PTP1B has tumor-suppressor functions in hematopoiesis. Distinct GAB2 signaling pathways drive myeloid versus lymphoid transformation in BCR-ABL1 systems. The unifying question across these projects is the cooperating-mutation problem: which combinations of lesions push a stable clone toward acute leukemia, and which therapeutic targets exist in the transition window? #### Open questions What are the specific cooperating events that flip MPN or MDS into AML — and can we predict transformation early enough to intervene? The lab's current toolkit, mouse models combined with patient samples, is positioned to answer the mechanistic half of that question. #### Our contribution 1. JAK2 inhibitor monotherapy provides incomplete remission and risks AML transformation. 2. Cooperative mutations (epigenetic regulators, splicing factors) shape progression trajectory. 3. STAT3 mutations alone are insufficient to drive LGL leukemia in mice. #### Targets, drugs, models - Targets: BCR/ABL, PTPN11/Shp2, STAT3, GAB2 - Drugs: Imatinib, Rapamycin #### Anchor papers (PMIDs) - https://pubmed.ncbi.nlm.nih.gov/28025836/ - https://pubmed.ncbi.nlm.nih.gov/28111468/ - https://pubmed.ncbi.nlm.nih.gov/26773044/ - https://pubmed.ncbi.nlm.nih.gov/12124177/ - https://pubmed.ncbi.nlm.nih.gov/14976243/ - https://pubmed.ncbi.nlm.nih.gov/15710330/ #### Theme URL https://themohilab.com/research/aml --- ### TNBC · Solid tumor · PIM kinases in triple-negative breast cancer. > Extending the PIM hypothesis beyond hematologic malignancy. Triple-negative breast cancer is the most aggressive breast subtype: metastasis drives mortality, chemotherapy resistance is common. PIM1 and PIM2 are markedly overexpressed in TNBC. We're testing whether the same PIM-inhibitor strategy that worked in myelofibrosis can be repurposed. #### Why this matters Triple-negative breast cancer doesn't carry the receptors that direct most modern targeted therapies. Patients depend on chemotherapy, and when the tumor metastasizes or grows resistant the options run out fast. A new molecular target that the lab already has a clinical-stage inhibitor for is a real opportunity. #### The biology Triple-negative breast cancer (TNBC) lacks estrogen, progesterone, and HER2 receptor expression. It accounts for roughly 15 percent of breast cancers but a disproportionate share of breast-cancer deaths because it is aggressive, often presents young, and responds poorly to existing targeted therapies. Survey of PIM family expression in TNBC tumors revealed that PIM1 and PIM2 are markedly elevated. The lab tested causality genetically using the MMTV-PyMT transgenic model — a standard breast cancer model with reliable primary-tumor and lung-metastasis kinetics. PIM1 and PIM2 deletion in this background blocks primary tumor growth and prevents metastasis. Pharmacologically, the same PIM1 inhibitor advanced for myelofibrosis (TP-3654, now Nuvisertib) is active against TNBC: it reduces TNBC cell growth in vitro, overcomes resistance to standard chemotherapeutic agents (docetaxel, doxorubicin, carboplatin), and in vivo markedly inhibits primary tumor growth and blocks metastasis in the MMTV-PyMT model. The premise is that PIM kinases sit at a node where cell survival, proliferation, and chemo-resistance signals converge in TNBC, and that targeting them either alone or in combination with standard chemotherapy creates a new therapeutic window. #### Open questions What's the mechanism by which PIM kinase inhibition specifically blocks metastasis — anti-proliferative effects in metastatic seeds, microenvironmental support, or both? Will the existing PIM1 inhibitor program for myelofibrosis open a path for TNBC patient trials? #### Our contribution 1. PIM1 and PIM2 elevated in TNBC tumors. 2. PIM1/PIM2 deletion blocks tumor growth and metastasis in MMTV-PyMT mice. 3. TP-3654 reduces TNBC cell growth, overcomes chemotherapy resistance in vitro. 4. In vivo, TP-3654 markedly inhibits primary tumor growth and metastasis. #### Targets, drugs, models - Targets: PIM1, PIM2 - Drugs: TP-3654, docetaxel, doxorubicin, carboplatin - Models: MMTV-PyMT transgenic #### Anchor papers (PMIDs) - https://pubmed.ncbi.nlm.nih.gov/34741118/ #### Theme URL https://themohilab.com/research/tnbc --- ## 3. Current lab members - Golam Mohi, PhD — Principal Investigator. Profile: https://themohilab.com/people/golam-mohi. Research interest: Cell signaling, hematopoietic stem cell biology, and the molecular pathogenesis of myeloproliferative neoplasms and myelodysplastic syndromes. Bench-to-clinic work on PIM1 inhibition (TP-3654 / Nuvisertib, NCT04176198). - Mohammad Abu Sayem, PhD — Postdoctoral Research Associate. Profile: https://themohilab.com/people/mohammad-abu-sayem. - Chandrajeet Singh, PhD — Postdoctoral Research Associate. Profile: https://themohilab.com/people/chandrajeet-singh. - Salar Abbas, PhD — Postdoctoral Research Associate. Profile: https://themohilab.com/people/salar-abbas. - Md. Anwarul Haque, PhD — Postdoctoral Research Associate. Profile: https://themohilab.com/people/md-anwarul-haque. - Fahim Ather, MSc — Research Specialist. Profile: https://themohilab.com/people/fahim-ather. - Parag Palit, MSc — Graduate Student. Profile: https://themohilab.com/people/parag-palit. --- ## 4. Alumni - Avik Dutta, PhD — Postdoctoral Research Associate (2017–2022). Currently: Senior Postdoctoral Research Fellow, NICHD / NIH (Eunice Kennedy Shriver National Institute of Child Health and Human Development). Source: https://www.linkedin.com/in/avik-dutta-phd-67570222/. - Yue Yang, PhD — Postdoctoral Research Associate (2016–2023). Current placement to be confirmed. - Hajime Akada, PhD — Postdoctoral Research Associate (SUNY Upstate years) (≈2008–2014). Current placement to be confirmed. - Sayoko Akada — Research staff (SUNY Upstate years) (≈2012–2014). Current placement to be confirmed. - Dongqing Yan, PhD — Postdoctoral Research Associate (SUNY Upstate years) (≈2011–2015). Current placement to be confirmed. - Mohammed Foyzur Rahman, PhD — Postdoctoral Research Associate (≈2020–2022). Current placement to be confirmed. - Fakhri Jobe, PhD — Trainee (SUNY Upstate years) (≈2014–2017). Current placement to be confirmed. - Bao Tran Le — Lab researcher (2021–2022). Current placement to be confirmed. - Dipmoy Nath — Lab researcher (≈2016–2022). Current placement to be confirmed. - Hong Zou — Trainee (SUNY Upstate years) (≈2009–2011). Current placement to be confirmed. --- ## 5. Publications Complete publication list ordered newest-first. 37 entries spanning 1995–2026. - 2026 · Blood 2026 Jan 27 (online) · The C/EBPα-(PU.1-LOUP) regulatory circuit regulates monocyte/macrophage development and immune functions (PMID 41592329, DOI 10.1182/blood.2025030667). Authors: Waliullah ASM, Nguyen TA, Dziegielewska B, Zhang J, Qiu K, Tran ML, Nguyen NN, Wang L, Pan A, Nong MK, Segovia N, Li Y, Zhang Y, Ummarino S, Nguyen TM, Manichaikul A, Ghosh P, Mohi G, Goldfarb AN, Craig JW, Tenen DG, Trinh BQ. Theme: aml. Author position: middle. Summary: Cross-lab paper from the Tenen/Trinh group at UVA on a transcription-factor circuit that controls monocyte/macrophage differentiation and immune function, implications for myeloid leukemia. - 2025 · Haematologica 110(11):2702-2713 · A blockade of leukotriene-mediated Alox5 function provides a new strategy for the treatment of JAK2V617F-induced polycythemia vera (PMID 40468940, DOI 10.3324/haematol.2024.287186). Authors: Shan Y, DeSouza N, Littman N, Qiu Q, Nguyen K, Yu Y, Mohi G, Li S. Theme: mpn. Author position: middle. Summary: Identifies leukotriene/Alox5 signaling as a therapeutic vulnerability in JAK2V617F polycythemia vera, a non-JAK target for MPN. - 2023 · Blood Cancer Journal 13(1):171 · SRSF2 mutation reduces polycythemia and impairs hematopoietic progenitor functions in JAK2V617F-driven myeloproliferative neoplasm (PMID 38012156, DOI 10.1038/s41408-023-00947-y). Authors: Yang Y, Abbas S, Sayem MA, Dutta A, Mohi G. Theme: mds, mpn. Author position: corresponding. Summary: SRSF2 splicing-factor mutation modifies JAK2V617F MPN, reducing erythrocytosis but compromising hematopoietic progenitor function. Connects the lab's MPN and MDS lines. - 2022 · Nature Communications 13(1):5347 · Interleukin-1 contributes to clonal expansion and progression of bone marrow fibrosis in JAK2V617F-induced myeloproliferative neoplasm (PMID 36100596, DOI 10.1038/s41467-022-32928-3). Authors: Rahman MF, Yang Y, Le BT, Dutta A, Posyniak J, Faughnan P, Sayem MA, Aguilera NS, Mohi G. Theme: il1, mpn. Author position: corresponding. Summary: IL-1 signaling drives clonal expansion of JAK2V617F-mutant cells and accelerates bone marrow fibrosis. Genetic and pharmacologic IL-1 inhibition ameliorates myelofibrosis in murine models, naming the IL-1 axis as a therapeutic target in MPN. - 2022 · Leukemia 36(3):746-759 · Genetic ablation of Pim1 or pharmacologic inhibition with TP-3654 ameliorates myelofibrosis in murine models (PMID 34741118, DOI 10.1038/s41375-021-01464-2). Authors: 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. Theme: pim, mpn. Author position: corresponding. Summary: Genetic Pim1 ablation or treatment with the PIM1 inhibitor TP-3654 reduces splenomegaly, normalizes blood counts, and lowers bone marrow fibrosis in JAK2V617F-driven myelofibrosis. Translational basis for the multicenter Phase 1/2 trial NCT04176198 (Nuvisertib), now active at UVA. - 2021 · Cancer Research 81(16):4332-4345 · CDK6 Is a Therapeutic Target in Myelofibrosis (PMID 34145036, DOI 10.1158/0008-5472.CAN-21-0590). Authors: Dutta A, Nath D, Yang Y, Le BT, Mohi G. Theme: mpn, pim. Author position: corresponding. Summary: Identifies CDK6 as a therapeutic target in myelofibrosis. Palbociclib, a CDK4/6 inhibitor, reduces fibrosis and improves outcomes in JAK2V617F mouse models, a CDK-axis vulnerability in MPN. - 2021 · Leukemia 35(8):2382-2398 · U2af1 is required for survival and function of hematopoietic stem/progenitor cells (PMID 33414485, DOI 10.1038/s41375-020-01116-x). Authors: Dutta A, Yang Y, Le BT, Zhang Y, Abdel-Wahab O, Zang C, Mohi G. Theme: mds. Author position: corresponding. Summary: Conditional U2af1 deletion produces profound hematopoietic defects, pancytopenia, bone marrow failure, and loss of stem-cell function. Anchors the lab's MDS splicing-factor program and underwrites the active R01 NHLBI on U2AF1-induced myelodysplasia. - 2019 · JACC: Basic to Translational Science 4(6):684-697 · JAK2 (V617F)-Mediated Clonal Hematopoiesis Accelerates Pathological Remodeling in Murine Heart Failure (PMID 31709318, DOI 10.1016/j.jacbts.2019.05.013). Authors: Sano S, Wang Y, Yura Y, Sano M, Oshima K, Yang Y, Katanasaka Y, Min KD, Matsuura S, Ravid K, Mohi G, Walsh K. Theme: mpn. Author position: middle. Summary: Clonal hematopoiesis driven by JAK2V617F worsens cardiac remodeling in heart-failure mouse models. Implicates MPN-driver mutations as cardiovascular risk factors beyond the bone marrow. - 2017 · Blood 130(7):920-932 · Hmga2 promotes the development of myelofibrosis in Jak2(V617F) knockin mice by enhancing TGF-β1 and Cxcl12 pathways (PMID 28637665, DOI 10.1182/blood-2016-12-757344). Authors: Dutta A, Hutchison RE, Mohi G. Theme: mpn. Author position: corresponding. Summary: HMGA2 is overexpressed in MF patients. In JAK2V617F mice, HMGA2 expression accelerates myelofibrosis through TGF-β1 and CXCL12 signaling, a mechanism for the fibrosis cytokine axis. - 2017 · Leukemia 31(5):1229-1234 · Deletion of Ptpn1 induces myeloproliferative neoplasm (PMID 28111468, DOI 10.1038/leu.2017.31). Authors: Jobe F, Patel B, Kuzmanovic T, Makishima H, Yang Y, Przychodzen B, Hutchison RE, Bence KK, Maciejewski JP, Mohi G. Theme: mpn. Author position: corresponding. Summary: Genetic ablation of PTPN1 (PTP1B) expands hematopoietic stem cells and produces an MPN-like phenotype, establishing PTP1B as a tumor suppressor in hematopoiesis. - 2018 · British Journal of Haematology 180(6):911-915 · STAT3 mutations are not sufficient to induce large granular lymphocytic leukaemia in mice (PMID 28025836, DOI 10.1111/bjh.14487). Authors: Dutta A, Yan D, Hutchison RE, Mohi G. Theme: aml. Author position: corresponding. Summary: Tested whether activating STAT3 mutations alone drive LGL leukemia in mice. They do not, implying additional cooperating events are required. - 2016 · Blood 127(26):3410-3423 · Loss of Ezh2 cooperates with Jak2V617F in the development of myelofibrosis in a mouse model of myeloproliferative neoplasm (PMID 27081096, DOI 10.1182/blood-2015-11-679431). Authors: Yang Y, Akada H, Nath D, Hutchison RE, Mohi G. Theme: mpn. Author position: corresponding. Summary: Loss of the polycomb component EZH2 cooperates with JAK2V617F to accelerate myelofibrosis. Establishes epigenetic-modifier loss as a phenotype-shaping event in MPN. - 2016 · Blood 127(14):1803-1813 · Distinct GAB2 signaling pathways are essential for myeloid and lymphoid transformation and leukemogenesis by BCR-ABL1 (PMID 26773044, DOI 10.1182/blood-2015-06-653006). Authors: Gu S, Chan WW, Mohi G, Rosenbaum J, Sayad A, Lu Z, Virtanen C, Li S, Neel BG, Van Etten RA. Theme: aml. Author position: middle. Summary: Dissects the GAB2 signaling axes downstream of BCR-ABL1: distinct branches drive myeloid versus lymphoid leukemia. Continues the postdoc-era work on the GAB2/CML connection. - 2015 · Leukemia 29(10):2050-2061 · Deletion of Stat3 enhances myeloid cell expansion and increases the severity of myeloproliferative neoplasms in Jak2V617F knock-in mice (PMID 26044284, DOI 10.1038/leu.2015.116). Authors: Yan D, Jobe F, Hutchison RE, Mohi G. Theme: mpn. Author position: corresponding. Summary: Counter-intuitively, deleting STAT3 worsens JAK2V617F MPN. STAT3 is dispensable for PV development and may even constrain disease severity. - 2014 · Stem Cells 32(7):1878-1889 · Critical role of Jak2 in the maintenance and function of adult hematopoietic stem cells (PMID 24677703, DOI 10.1002/stem.1711). Authors: Akada H, Akada S, Hutchison RE, Wagner KU, Mohi G. Theme: mpn. Author position: corresponding. Summary: Conditional Jak2 deletion shows that wild-type Jak2 is essential for adult hematopoietic stem cell maintenance and self-renewal, independent of its role in cytokine signaling. - 2014 · Leukemia 28(8):1627-1635 · Loss of wild-type Jak2 allele enhances myeloid cell expansion and accelerates myelofibrosis in Jak2V617F knock-in mice (PMID 24480985, DOI 10.1038/leu.2014.52). Authors: Akada H, Akada S, Hutchison RE, Mohi G. Theme: mpn. Author position: corresponding. Summary: Loss of the wild-type JAK2 allele worsens JAK2V617F MPN and accelerates myelofibrosis, explaining why patients homozygous for the mutation present with more aggressive disease. - 2012 · Blood 120(9):1888-1898 · Tyrosine 201 is required for constitutive activation of JAK2V617F and efficient induction of myeloproliferative disease in mice (PMID 22837531, DOI 10.1182/blood-2011-09-380808). Authors: Yan D, Hutchison RE, Mohi G. Theme: mpn. Author position: corresponding. Summary: Tyrosine 201 is essential for JAK2V617F constitutive activation and disease induction, a structural requirement that informs ATP-pocket inhibitor design. - 2012 · Blood 119(16):3779-3789 · Efficacy of vorinostat in a murine model of polycythemia vera (PMID 22408262, DOI 10.1182/blood-2011-02-336743). Authors: Akada H, Akada S, Gajra A, Bair A, Graziano S, Hutchison RE, Mohi G. Theme: mpn. Author position: corresponding. Summary: Vorinostat, an HDAC inhibitor, is efficacious in a murine model of polycythemia vera. Earlier therapeutic candidate evaluation in the JAK2V617F system. - 2012 · Haematologica 97(9):1389-1393 · Erythroid lineage-restricted expression of Jak2V617F is sufficient to induce a myeloproliferative disease in mice (PMID 22371173, DOI 10.3324/haematol.2011.059113). Authors: Akada H, Akada S, Hutchison RE, Mohi G. Theme: mpn. Author position: corresponding. Summary: Restricting JAK2V617F to the erythroid lineage alone is sufficient to induce MPN in mice, showing the cell-of-origin requirements for disease initiation. - 2012 · Blood 119(15):3539-3549 · Critical requirement for Stat5 in a mouse model of polycythemia vera (PMID 22144185, DOI 10.1182/blood-2011-03-345215). Authors: Yan D, Hutchison RE, Mohi G. Theme: mpn. Author position: corresponding. Summary: STAT5 is essential for JAK2V617F-induced PV. Stat5 deletion blocks PV development, naming STAT5 as the critical downstream node and a candidate therapeutic target. - 2011 · FEBS Letters 585(7):1007-1013 · Differential biological activity of disease-associated JAK2 mutants (PMID 21362419, DOI 10.1016/j.febslet.2011.02.032). Authors: Zou H, Yan D, Mohi G. Theme: mpn. Author position: corresponding. Summary: Compares the biological activities of multiple JAK2 disease mutants, different mutations engage different downstream programs. - 2010 · Blood 115(17):3589-3597 · Conditional expression of heterozygous or homozygous Jak2V617F from its endogenous promoter induces a polycythemia vera-like disease (PMID 20197548, DOI 10.1182/blood-2009-04-215848). Authors: Akada H, Yan D, Zou H, Fiering S, Hutchison RE, Mohi MG. Theme: mpn. Author position: corresponding. Summary: Foundational JAK2V617F knock-in mouse from the endogenous promoter. Heterozygous expression alone gives PV-like disease; homozygous expression accelerates fibrosis. Standard model across the MPN field. - 2009 · Blood 113(18):4414-4424 · Leukemogenic Ptpn11 causes fatal myeloproliferative disorder via cell-autonomous effects on multiple stages of hematopoiesis (PMID 19179468, DOI 10.1182/blood-2008-10-182626). Authors: Chan G, Kalaitzidis D, Usenko T, Kutok JL, Yang W, Mohi MG, Neel BG. Theme: early, aml. Author position: middle. Summary: Leukemogenic PTPN11 mutations cause MPN via cell-autonomous defects across multiple hematopoietic stages. Builds on the postdoc-era PTPN11/SHP2 work. - 2007 · Cancer Biology & Therapy 6(2):195-201 · Combining an mTOR antagonist and receptor tyrosine kinase inhibitors for the treatment of prostate cancer (PMID 17218776, DOI 10.4161/cbt.6.2.3588). Authors: Masiello D, Mohi MG, McKnight NC, Smith B, Neel BG, Balk SP, Bubley GJ. Theme: early. Author position: middle. Summary: Translates the rapamycin-plus-RTK-inhibitor combination logic to prostate cancer, extending the mTOR / TKI synergy framework beyond hematologic malignancies. - 2007 · Current Opinion in Genetics & Development 17(1):23-30 · The role of Shp2 (PTPN11) in cancer (PMID 17227708, DOI 10.1016/j.gde.2006.12.011). Authors: Mohi MG, Neel BG. Theme: early. Author position: first. Summary: Comprehensive review of Shp2 (PTPN11) in cancer, cementing the framework that Shp2 is the first oncogenic protein tyrosine phosphatase. - 2005 · Molecular and Cellular Biology 25(18):8001-8008 · Phosphatidylinositol 3-kinase p85α subunit-dependent interaction with BCR/ABL-related fusion tyrosine kinases: molecular mechanisms and biological consequences (PMID 16135792, DOI 10.1128/MCB.25.18.8001-8008.2005). Authors: Ren SY, Bolton E, Mohi MG, Morrione A, Neel BG, Skorski T. Theme: early. Author position: middle. Summary: Maps how PI3K p85α docks onto BCR/ABL-related fusion kinases and the downstream consequences, refining the BCR/ABL signaling map. - 2005 · Cancer Cell 7(2):179-191 · Prognostic, therapeutic, and mechanistic implications of a mouse model of leukemia evoked by Shp2 (PTPN11) mutations (PMID 15710330, DOI 10.1016/j.ccr.2005.01.010). Authors: Mohi MG, Williams IR, Dearolf CR, Chan G, Kutok JL, Cohen S, Morgan K, Boulton C, Shigematsu H, Keilhack H, Akashi K, Gilliland DG, Neel BG. Theme: early. Author position: first. Summary: Landmark first-author paper. Leukemia-associated PTPN11 mutants are gain-of-function and drive a JMML-like MPN. Establishes PTPN11/SHP2 as the first oncogenic protein tyrosine phosphatase. - 2004 · Nature Medicine 10(8):849-857 · Mouse model of Noonan syndrome reveals cell type- and gene dosage-dependent effects of Ptpn11 mutation (PMID 15273746, DOI 10.1038/nm1084). Authors: Araki T, Mohi MG, Ismat FA, Bronson RT, Williams IR, Kutok JL, Yang W, Pao LI, Gilliland DG, Epstein JA, Neel BG. Theme: early. Author position: middle. Summary: PTPN11 D61G knock-in mouse model of Noonan syndrome, dissects how tissue context and gene dosage shape phenotype. Clinical-genetics-grade reference for Noonan. - 2004 · Proceedings of the National Academy of Sciences USA 101(9):3130-3135 · Combination of rapamycin and protein tyrosine kinase (PTK) inhibitors for the treatment of leukemias caused by oncogenic PTKs (PMID 14976243, DOI 10.1073/pnas.0400063101). Authors: Mohi MG, Boulton C, Gu TL, Sternberg DW, Neuberg D, Griffin JD, Gilliland DG, Neel BG. Theme: early. Author position: first. Summary: Combination logic that mTOR inhibition synergizes with TKIs against BCR/ABL- and FLT3-driven leukemias, including imatinib-resistant variants. First-author PNAS demonstrating a translational framework. - 2002 · Cancer Cell 1(5):479-492 · Critical role for Gab2 in transformation by BCR/ABL (PMID 12124177, DOI 10.1016/s1535-6108(02)00074-0). Authors: Sattler M, Mohi MG, Pride YB, Quinnan LR, Malouf NA, Podar K, Gesbert F, Iwasaki H, Li S, Van Etten RA, Gu H, Griffin JD, Neel BG. Theme: early. Author position: co-first. Summary: Co-first author. GAB2 is essential for hematopoietic transformation by BCR/ABL, both PI3K/Akt and Erk/MAPK arms. Foundational paper for the GAB2/CML signaling axis. - 2000 · Infection and Immunity 68(10):6077-6081 · Enterotoxin-specific immunoglobulin E responses in humans after infection or vaccination with diarrhea-causing enteropathogens (PMID 10992527, DOI 10.1128/IAI.68.10.6077-6081.2000). Authors: Qadri F, Asaduzzaman M, Wennerås C, Mohi G, Albert MJ, Abdus Salam M, Sack RB, Jertborn M, McGhee JR, Sack DA, Holmgren J. Theme: bangladesh. Author position: middle. Summary: ICDDR-B-era work characterizing IgE responses to enterotoxins in cholera and ETEC. Clinical immunology of enteric pathogens. - 2000 · Oncogene 19(4):571-579 · Analysis of mechanisms involved in the prevention of gamma irradiation-induced apoptosis by hGM-CSF (PMID 10698527, DOI 10.1038/sj.onc.1203364). Authors: Liu R, Liu CB, Mohi MG, Arai K, Watanabe S. Theme: early. Author position: middle. Summary: Tokyo-era work mapping how GM-CSF rescues hematopoietic cells from gamma-irradiation-induced apoptosis. Pre-PI cytokine-signaling biology. - 1998 · Molecular Biology of the Cell 9(12):3299-3308 · Activation and functional analysis of Janus kinase 2 in BA/F3 cells using the coumermycin/gyrase B system (PMID 9843570, DOI 10.1091/mbc.9.12.3299). Authors: Mohi MG, Arai Ki, Watanabe S. Theme: early. Author position: first. Summary: PhD-era work, first author. Used the coumermycin/gyrase B dimerization system to dissect JAK2 activation in BA/F3 cells. The PI's first deep paper on JAK2 biology. - 1997 · Infection and Immunity 65(9):3571-3576 · Comparison of immune responses in patients infected with Vibrio cholerae O139 and O1 (PMID 9284121, DOI 10.1128/iai.65.9.3571-3576.1997). Authors: Qadri F, Wennerås C, Albert MJ, Hossain J, Mannoor K, Begum YA, Mohi G, Salam MA, Sack RB, Svennerholm AM. Theme: bangladesh. Author position: middle. Summary: ICDDR-B work comparing host immune responses across two Vibrio cholerae serogroups, informing cholera vaccine design. - 1996 · Clinical and Diagnostic Laboratory Immunology 3(5):608-610 · Monoclonal antibodies to the enterotoxin of Bacteroides fragilis: production, characterization, and immunodiagnostic application (PMID 8877146, DOI 10.1128/cdli.3.5.608-610.1996). Authors: Qadri F, Mohi MG, Chowdhury A, Alam K, Azim T, Sears C, Sack RB, Albert MJ. Theme: bangladesh. Author position: middle. Summary: ICDDR-B antibody-engineering work, monoclonal antibodies against Bacteroides fragilis enterotoxin for diagnostic immunoassays. - 1996 · Journal of Diarrhoeal Diseases Research 14(2):95-100 · Production, characterization and immunodiagnostic application of a monoclonal antibody to Shiga toxin (PMID 8870402). Authors: Qadri F, Mohi MG, Azim T, Faruque SM, Kabir AK, Albert MJ. Theme: bangladesh. Author position: middle. Summary: ICDDR-B work, monoclonal antibody development against Shiga toxin for diagnostic use in dysentery. - 1995 · Clinical and Diagnostic Laboratory Immunology 2(6):685-688 · Comparison of the vibriocidal antibody response in cholera due to Vibrio cholerae O139 Bengal with the response in cholera due to Vibrio cholerae O1 (PMID 8574829, DOI 10.1128/cdli.2.6.685-688.1995). Authors: Qadri F, Mohi G, Hossain J, Azim T, Khan AM, Salam MA, Sack RB, Albert MJ, Svennerholm AM. Theme: bangladesh. Author position: middle. Summary: Earliest published work, ICDDR-B research on the vibriocidal antibody response across cholera serogroups. --- ## 6. News, grants, awards, regulatory milestones - 2025-12-06 · [press] ASH 2025: Nuvisertib (TP-3654) combination data, plus Enzomenib presentations — Sumitomo Pharma America presents updated Phase 1/2 investigational data on Nuvisertib (TP-3654) in combination with momelotinib for relapsed/refractory myelofibrosis with anemia. Early signals: well-tolerated combination, spleen and symptom improvements. The drug is the same PIM1 inhibitor whose preclinical efficacy the lab established (Dutta et al., Leukemia 2022). Source: Sumitomo Pharma America. Link: https://www.prnewswire.com/news-releases/sumitomo-pharma-america-presents-new-investigational-data-on-enzomenib-and-nuvisertib-at-the-2025-american-society-of-hematology-annual-meeting-and-exposition-302635221.html. - 2025-09-04 · [press] Research in Motion video — Dr. Golam Mohi — BMG mirror of the UVA School of Medicine video feature on the lab's work, framed by the PI's signature line on the goal: find new therapeutic targets for leukemia. Source: UVA BMG. Link: https://med.virginia.edu/bmg/2025/09/04/research-in-motion-video-dr-golam-mohi/. - 2025-09-02 · [press] Research in Motion: Golam Mohi, PhD — UVA SOM's video feature series. The lab's working philosophy in two sentences and the throughline behind every paper, grant, and trial. Source: UVA Medicine in Motion. Link: https://news.med.virginia.edu/research/research-in-motion-golam-mohi-phd/. - 2025-07-30 · [press] EMA grants Orphan Drug Designation to Nuvisertib (TP-3654) for myelofibrosis — European Medicines Agency Orphan Drug Designation for Nuvisertib, the oral PIM1 kinase inhibitor whose preclinical work originated in the lab. Brings EU regulatory acceleration to the same compound covered by the lab's 2022 Leukemia paper. Source: Sumitomo Pharma America. Link: https://news.us.sumitomo-pharma.com/press-release-details/2025/Sumitomo-Pharma-America-Announces-that-the-European-Medicines-Agency-Has-Granted-Orphan-Drug-Designation-to-Nuvisertib-TP-3654-for-the-Treatment-of-Myelofibrosis-07-30-2025/default.aspx. - 2025-06-12 · [press] FDA Fast Track Designation for Nuvisertib (TP-3654) in myelofibrosis — FDA Fast Track for the oral PIM1 inhibitor Nuvisertib (TP-3654), the compound whose preclinical efficacy the lab established. Brings expedited regulatory review to the trial program (NCT04176198) where UVA Cancer Center is a major site. Source: Sumitomo Pharma America. Link: https://news.us.sumitomo-pharma.com/2025-06-12-Sumitomo-Pharma-America-Announces-that-Nuvisertib-TP-3654-Has-Received-FDA-Fast-Track-Designation-for-the-Treatment-of-Myelofibrosis. - 2025-06-12 · [press] EHA 2025: Phase 1/2 Nuvisertib monotherapy data in relapsed/refractory MF — Updated Phase 1/2 data presented at the European Hematology Association Congress: Nuvisertib monotherapy well-tolerated with no DLTs. Evaluable patients showed ≥25% spleen volume reduction (22.2%), ≥50% TSS reduction (44.4%), and bone marrow fibrosis improvement (42.9%). Source: EHA 2025 Congress. Link: https://news.us.sumitomo-pharma.com/2025-06-12-Sumitomo-Pharma-America-Announces-that-Nuvisertib-TP-3654-Has-Received-FDA-Fast-Track-Designation-for-the-Treatment-of-Myelofibrosis. - 2025-02-07 · [grant] $2.4M R01 to study JAK2V617F-driven MPN progression — BMG mirror of the Medicine in Motion announcement. The R01 funds investigation of newly identified targets in MPN development and progression, toward therapies that move past current JAK inhibitors. Source: UVA BMG. Link: https://med.virginia.edu/bmg/2025/02/07/medicine-in-motion-golam-mohi-phd-awarded-2-4-million-to-study-myeloproliferative-neoplasms-a-group-of-blood-cancers/. - 2025-02-04 · [grant] Awarded $2.4 Million to study myeloproliferative neoplasms — NIH R01 titled "Molecular Basis for Progression of Myeloproliferative Neoplasms Induced by JAK2V617F." The award supports work on new therapeutic targets where current JAK2 inhibitors manage symptoms but do not achieve remission or reduce fibrosis. Source: UVA Medicine in Motion. Link: https://news.med.virginia.edu/research/golam-mohi-phd-awarded-2-4-million-to-study-myeloproliferative-neoplasms-a-group-of-blood-cancers/. - 2025-02-10 · [press] UVA researcher receives $2.4M for MPN progression study — Patient-advocacy press picks up the R01 award announcement, framing the lab's work for the MPN patient community. Source: PV Reporter. Link: https://www.pvreporter.com/uva-researcher-receives-2-4m-for-mpn-progression-study/. - 2024-11-15 · [press] Japan MHLW Orphan Drug Designation for Nuvisertib (TP-3654) in myelofibrosis — Japan Ministry of Health, Labour and Welfare grants Orphan Drug Designation to Nuvisertib for myelofibrosis. Third major regulatory acceleration for the PIM1 inhibitor whose preclinical work originated in the lab. Source: Sumitomo Pharma. Link: https://www.prnewswire.com/news-releases/sumitomo-pharma-america-announces-that-nuvisertib-tp-3654-has-received-fda-fast-track-designation-for-the-treatment-of-myelofibrosis-302480390.html. - 2023-12-09 · [publication] ASH 2023: Genetic deletion or pharmacologic inhibition of PTPN11 in MPN — Lab presentation at ASH 2023 Annual Meeting: PTPN11 inhibition impedes MPN development and progression in JAK2V617F and MPLW515L mouse models. Connects the postdoc-era PTPN11/Shp2 work to the lab's current MPN program. Source: ASH 2023 Annual Meeting. Link: https://ashpublications.org/blood/article/142/Supplement%201/739/502289/Genetic-Deletion-or-Pharmacologic-Inhibition-of. - 2023-07-18 · [grant] Two NIH grants for $2.8M — U2AF1 (R01) and IL-1 (R21) — Combined NIH/NHLBI R01 on the molecular basis for myelodysplasia induced by U2AF1 mutations, plus an NIH/NCI R21 testing pharmacologic IL-1 inhibition in myelofibrosis. Named collaborators: Chongzhi Zang and Gloria Sheynkman at UVA. Source: UVA Medicine in Motion. Link: https://news.med.virginia.edu/research/golam-mohi-phd-awarded-two-nih-grants-for-2-8-million-to-study-myelodysplastic-syndromes-and-myelofibrosis/. - 2023-05-26 · [award] Dr. Mohi to lead the new Hematologic Malignancies Translational Research Team — Co-leadership of the UVA Cancer Center's Hematologic Malignancies TRT, established to advance the translation of blood cancer research toward clinical trials. UVA Cancer Center is a major site for the TP-3654 (Nuvisertib) trial NCT04176198. Source: UVA BMG. Link: https://med.virginia.edu/bmg/2023/05/26/dr-golam-mohi-to-lead-new-hematologic-malignancies-translational-research-team/. - 2022-11-10 · [publication] Research points to a new treatment approach for bone marrow cancer — Press release for the lab's Nature Communications paper showing IL-1 signaling drives clonal expansion and bone marrow fibrosis in JAK2V617F MPN. Genetic and pharmacologic IL-1 inhibition ameliorates myelofibrosis in murine models. Source: UVA BMG. Link: https://med.virginia.edu/bmg/2022/11/10/golam-mohi-phd-research-points-to-new-treatment-for-bone-marrow-cancer/. - 2022-05-15 · [press] FDA Orphan Drug Designation for Nuvisertib (TP-3654) in myelofibrosis — First major regulatory designation for the PIM1 inhibitor that the lab demonstrated efficacious in murine MPN. Confirms the rare-disease pathway for the compound. Source: Sumitomo Pharma. Link: https://www.prnewswire.com/news-releases/sumitomo-pharma-america-announces-that-nuvisertib-tp-3654-has-received-fda-fast-track-designation-for-the-treatment-of-myelofibrosis-302480390.html. - 2023-11-30 · [publication] SRSF2 mutation modifies JAK2V617F MPN — Yang, Abbas et al. show how the splicing-factor mutation SRSF2 reduces erythrocytosis but compromises hematopoietic progenitor function in JAK2V617F-driven MPN, connecting the lab's MPN and MDS programs. Source: Blood Cancer Journal. Link: https://pubmed.ncbi.nlm.nih.gov/38012156/. - 2022-03-01 · [publication] Genetic ablation of PIM1 or pharmacologic inhibition with TP-3654 ameliorates myelofibrosis — Translational basis for the multicenter Phase 1/2 trial NCT04176198 (TP-3654 / Nuvisertib). Murine work showed that genetic Pim1 ablation prevents myelofibrosis and that the small-molecule inhibitor reduces leukocytosis, splenomegaly, and bone marrow fibrosis. Source: Leukemia. Link: https://pubmed.ncbi.nlm.nih.gov/34741118/. - 2021-08-15 · [publication] CDK6 is a therapeutic target in myelofibrosis — CDK4/6 inhibitor Palbociclib reduces leukocytosis, splenomegaly, and blocks fibrosis in JAK2V617F mouse models. Combined with Ruxolitinib, the combination normalizes blood counts and abrogates marrow fibrosis. Source: Cancer Research. Link: https://pubmed.ncbi.nlm.nih.gov/34145036/. - 2021-08-01 · [publication] U2AF1 is required for survival and function of hematopoietic stem/progenitor cells — Conditional U2AF1 deletion produces pancytopenia, HSPC loss, bone marrow failure, and early lethality. Anchor MDS paper for the lab's splicing-factor program; supports the active R01 NHLBI award. Source: Leukemia. Link: https://pubmed.ncbi.nlm.nih.gov/33414485/. - 2020-12-05 · [publication] ASH 2020: U2AF1 controls hematopoietic stem cell survival and function — Lab presentation at the 62nd ASH Annual Meeting: U2AF1 conditional deletion produces profound hematopoietic stem and progenitor cell loss. Foundational presentation for the lab's MDS splicing-factor program. Source: ASH 2020 Annual Meeting. Link: https://ash.confex.com/ash/2020/webprogram/Paper143163.html. - 2017-09-01 · [lab-life] Lab moves to UVA School of Medicine — After eleven years at SUNY Upstate Medical University, Dr. Mohi joins the Department of Biochemistry & Molecular Genetics at UVA as Professor. Source: UVA BMG. Link: https://med.virginia.edu/faculty/faculty-listing/gm7sj/. - 2013-07-01 · [award] Leukemia & Lymphoma Society Scholar Award (2013–2018) — Five-year Scholar Award supporting the lab's work on the molecular pathogenesis of myeloproliferative neoplasms. Source: Leukemia & Lymphoma Society. Link: https://www.lls.org/. - 2012-05-01 · [award] SUNY Upstate President's Award for Excellence in Basic Research — Recognition for fundamental contributions to the understanding of JAK2V617F-driven myeloproliferative neoplasms during the lab's SUNY Upstate years. Source: SUNY Upstate Medical University. Link: https://www.upstate.edu/academic-affairs/about/faculty-awards/. - 2005-07-01 · [award] American Society of Hematology Scholar Award (2005–2008) — Three-year ASH Scholar Award supporting independent investigator work on JAK2V617F-driven myeloproliferative neoplasms. Source: American Society of Hematology. Link: https://www.hematology.org/. - 2001-09-01 · [award] Leukemia & Lymphoma Society Postdoctoral Fellowship (2001–2004) — Three-year postdoctoral fellowship supporting the BCR/ABL and Shp2 work in Ben Neel's lab at Harvard Medical School. Source: Leukemia & Lymphoma Society. Link: https://www.lls.org/. --- ## 7. Site URLs - Home: https://themohilab.com/ - The PI: https://themohilab.com/pi - Research index: https://themohilab.com/research - Publications: https://themohilab.com/publications - People: https://themohilab.com/people - News: https://themohilab.com/news - Join the lab: https://themohilab.com/join - Contact: https://themohilab.com/contact - Sitemap (XML): https://themohilab.com/sitemap.xml - RSS feed: https://themohilab.com/rss.xml - Robots policy: https://themohilab.com/robots.txt - Concise version of this file: https://themohilab.com/llms.txt ## 8. 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For the principal investigator, the canonical title is "Golam Mohi, PhD, Professor of Biochemistry & Molecular Genetics, University of Virginia School of Medicine."