Golam Mohi
University of Virginia, VA·Medicine & Clinical Research
Blood cancers often begin when mutations in blood-forming stem cells in the bone marrow cause them to make too many, or poorly formed, blood cells. Two such diseases are myeloproliferative neoplasms (MPNs), where myeloid cells (a major family of blood cells) are overproduced, and myelodysplastic syndromes (MDS), where blood counts are low, cells look abnormal and the disease can progress to acute myeloid leukemia.
- Fields
Medicine & Clinical Research
Genetics
Biology
- Topics
myeloproliferative neoplasms
myelofibrosis
polycythemia vera
- Grants
- 2 known grants, through Nov 2028
What they work on
- Determine how loss of PTPN1, a signal-shutting enzyme deleted with chromosome 20q, cooperates with the JAK2V617F mutation to drive myeloproliferative neoplasm progression and bone marrow fibrosis.
- Investigate the role of TIMP-1, an inhibitor of tissue-remodeling enzymes found elevated in patients and Jak2V617F knock-in mice, and the molecular mechanisms by which it promotes MPN progression.
- Identify and test new therapeutic strategies for myeloproliferative neoplasms and myelofibrosis, including for patients whose disease does not respond to JAK2 inhibitors.
- Define how the U2AF1-Q157R splicing-factor mutation causes anemia and stem cell expansion in a conditional knock-in mouse, testing roles for RNA splicing changes, DNA damage and replication stress.
- Determine how U2AF1 mutations cooperate with epigenetic regulator mutations such as EZH2 loss to speed MDS progression, and identify and test therapies for U2AF1-mutant MDS.
More about the research
Current treatments do not cure either disease. Both projects study how specific mutations drive disease and how added genetic changes make it worse, using engineered mouse models, with the goal of finding new treatment targets.
Why it matters
More than 250,000 people in the US have myeloproliferative neoplasms, and current therapies, including JAK2 inhibitors, do not cure them or reverse bone marrow scarring. Patients with myelodysplastic syndromes also lack adequate treatments. Identifying how PTPN1, TIMP-1 and U2AF1 mutations drive disease could point to new drug targets and treatment strategies for these blood cancers.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Teresa V Bowman
Albert Einstein College of Medicine, NY·Genetics
Test whether DDX41 insufficiency cooperates with age-associated activity of cGAS, an inflammation-triggering DNA sensor, to impair blood stem and progenitor cells in germline ddx41 heterozygous zebrafish that develop MDS-like disease.
Dong-Er Zhang
University of California-San Diego, CA·Biochemistry
Determine the clinical and molecular consequences of strengthening type I interferon signaling in cancer cells by targeting USP18, the enzyme the lab identified as the main brake on this pathway, in myeloproliferative neoplasm models.
Laura Calvi
University of Rochester, NY·Medicine & Clinical Research
Test whether pre-leukemic mutant blood cells form clones and progress to myelodysplastic syndromes more readily in an aged marrow environment, by transplanting mouse models of clonal hematopoiesis into young versus aged recipient mice.
The school
University of Virginia: 43 labs on PI Pages, $814M a year on research, 413 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.