Wei Du
University of Pittsburgh, PA·Medicine & Clinical Research
Cancer cells do not grow alone. They are surrounded by normal cells that can help them survive and spread.
- Fields
Medicine & Clinical Research
Microbiology & Immunology
Genetics
- Topics
leukemia
myelodysplastic syndrome
Fanconi anemia
- Grants
- 1 known grant, through Jul 2029
What they work on
- Examine how TREM1, a stress-induced immune receptor, acts within leukemia-associated macrophages during leukemia development, using inducible macrophage-specific Trem1 knockout mice in Fanca-deficient and MLL-AF9 leukemia models.
- Determine how deleting Trem1 shifts macrophages toward the inflammatory M1-like state and lowers PD-L1, a protein that lets tumors evade immune attack, in leukemia-bearing mice.
- Investigate how TREM1-positive macrophages stimulate the migration and expansion of leukemic stem cells, the cells that sustain the cancer, in both mouse leukemia models.
- Test whether TREM1-positive macrophages from acute myeloid leukemia patients promote engraftment of leukemia cells in a patient-derived xenograft mouse model.
More about the research
In leukemia, a blood cancer that starts in the bone marrow, one such helper is the macrophage, an immune cell that normally clears debris and fights infection. Macrophages that move into leukemia tissue are called leukemia-associated macrophages, or LAMs. Scientists have long linked these cells to blood cancers, but how they push leukemia forward is poorly understood.
Why it matters
Acute myeloid leukemia and pre-leukemic disorders, including those arising in Fanconi anemia patients, remain hard to prevent and treat. By clarifying how TREM1 on supporting macrophages helps leukemic stem cells grow, this work could show whether blocking TREM1 or its signaling partners is a useful strategy for preventing or treating leukemia.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Xunlei Kang
University of Missouri-Columbia, MO·Medicine & Clinical Research
Determine how DPP4, a cell-surface enzyme, controls the location, survival and self-renewal of human AML stem cells, using colony-forming assays and mice carrying human AML cells.
Corynn Kasap
University of California-San Francisco, CA·Medicine & Clinical Research·Early-career
Use computational protein engineering to build a CAR-T cell based on the natural ligand of CD70, a protein found on AML cells but largely absent from normal tissue, and test whether it clears CD70-low leukemia blasts.
The school
University of Pittsburgh: 83 labs on PI Pages, $1.5B a year on research, 403 research doctorates a year.
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