Yohei Hisada
University of North Carolina at Chapel Hill, NC·Medicine & Clinical Research
Blood clotting has to be balanced: too little and patients bleed, too much and they form dangerous clots. In acute promyelocytic leukemia (APL), a subtype of acute myeloid leukemia, both go wrong at once.
- Fields
Medicine & Clinical Research
Physiology
Biochemistry
- Topics
acute promyelocytic leukemia
acute myeloid leukemia
disseminated intravascular coagulation
- Grants
- 1 known grant, last ended Aug 2026
What they work on
- Test whether podoplanin on leukemia blast cells drives platelet loss in acute promyelocytic leukemia by activating platelets through their CLEC-2 receptor, using xenograft and allograft mouse models that reproduce patient clotting abnormalities.
- Determine whether the S100A10/annexin A2 and urokinase-type plasminogen activator/receptor complexes on leukemia cells cause excessive clot breakdown, measured by plasmin-antiplasmin complexes and D-dimer in the mouse models.
- Define how much tissue factor from leukemia cells versus host cells contributes to coagulation activation, by inhibiting each source and measuring thrombin-antithrombin complex levels in both mouse models.
- Test whether blocking these pathways reduces bleeding in the mouse models, and use omics approaches to search for biomarkers identifying patients at high risk of bleeding.
More about the research
Patients develop disseminated intravascular coagulation, in which clotting is switched on throughout the circulation and consumes the body's clotting resources, and many then bleed catastrophically. Even though chemotherapy and differentiation therapy work well against the leukemia itself, 4-26% of patients die early, usually within 30 days of diagnosis, and severe bleeding, especially into the brain, is the leading cause. Why this bleeding happens is not known. This project sets out to define the mechanisms.
Why it matters
Severe bleeding, particularly into the brain, is the main cause of early death in acute promyelocytic leukemia even though the leukemia itself responds well to treatment. Pinpointing the pathways responsible could identify drug targets to prevent that bleeding and may also suggest treatments for the leukemia. Biomarkers emerging from this work could help clinicians identify, at diagnosis, which patients are at highest risk of bleeding.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Rafal Pawlinski
University of North Carolina at Chapel Hill, NC·Medicine & Clinical Research
Identify the disease-specific triggers that activate Factor XII, a protein that starts blood clotting, in sickle cell disease, using blood samples from patients and a mouse model of the disease.
David Ginsburg
University of Michigan, MI·Genetics
Map endothelial cell gene expression across diverse vascular beds in live mice at single-cell resolution, in models of thrombotic thrombocytopenic purpura and other vascular disorders, to explain organ-specific disease.
Congqing Wu
University of Kentucky, KY·Medicine & Clinical Research
Determine how NINJ1 in myeloid immune cells such as macrophages contributes to thrombosis. NINJ1 is the protein that actively ruptures the cell membrane during pyroptosis, an inflammatory form of cell death.
The school
University of North Carolina at Chapel Hill: 72 labs on PI Pages, $1.6B a year on research, 523 research doctorates a year.
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