Teresa V Bowman
Albert Einstein College of Medicine, NY·Genetics
Every blood and immune cell traces back to a small pool of blood-forming (hematopoietic) stem and progenitor cells. Some arise in the embryo and must keep working for a lifetime.
- Fields
Genetics
Biology
Medicine & Clinical Research
- Topics
hematopoiesis
hematopoietic stem cells
myelodysplastic syndromes
- Grants
- 2 known grants, through Nov 2030
What they work on
- 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.
- Determine how co-mutation of DDX41 with CUX1, a gene governing cell development, produces aberrant blood cell differentiation and disrupted red blood cell production.
- Map unexpected connections and unrealized differentiation potential among hematopoietic stem cells, HSC-independent progenitors and their progeny, using whole-organism visualization and transcriptional profiling in zebrafish.
- Identify when, where and how embryos generate hematopoietic stem cells but not progenitors, using temporal and spatial lineage tracing, whole-mount in situ hybridization, in vivo genetic screening and native-environment functional assays.
More about the research
With age these cells can falter, causing bone marrow failure or blood cancer. Working mainly in zebrafish, whose transparent embryos allow blood cells to be watched as they form, the lab asks how distinct blood-forming cells are made during development and how inherited mutations and aging drive them toward disease.
Why it matters
MDS affects roughly 10,000 people in the United States each year, and inherited DDX41 mutations are common in adult-onset cases; mapping how they combine with inflammation and secondary mutations could reveal biomarkers and treatment strategies for inherited and sporadic disease alike. Understanding how distinct blood stem and progenitor cells form may also inform immune disorders and efforts to produce such cells from human pluripotent stem cells for therapy.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Golam Mohi
University of Virginia, VA·Medicine & Clinical Research
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.
Emery H. Bresnick
University of Wisconsin-Madison, WI·Genetics
Test whether GATA2 and C/EBPε, a factor that drives granulocyte formation, work together and separately to set up progenitor gene activity, using GATA2 activation of a Cebpe enhancer as the entry point.
Britta Will
Albert Einstein College of Medicine, NY·Biology
Map when chaperone-mediated autophagy (CMA), a selective protein-recycling pathway, is active in precancerous CHIP blood stem cells and leukemic stem cells, using a CMA reporter mouse and lentiviral CMA biosensors in patient cells.
The school
Albert Einstein College of Medicine: 21 labs on PI Pages, $361M a year on research, 36 research doctorates a year.
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