Isabelle Lemasson
East Carolina University, NC·Microbiology & Immunology
Some viruses cause cancer by rewiring the cells they infect. Human T-cell leukemia virus type 1, a retrovirus, infects immune cells called CD4+ T cells and in a small fraction of carriers leads to adult T-cell leukemia, a fatal blood cancer that resists chemotherapy.
- Fields
Microbiology & Immunology
Genetics
Medicine & Clinical Research
- Topics
human T-cell leukemia virus
adult T-cell leukemia
annexin A1
- Grants
- 1 known grant, through Jul 2027
What they work on
- Characterize how abnormally high vascular cell adhesion molecule 1, a surface protein that grips neighboring cells, combined with suppressed annexin A1 on HTLV-1-infected T cells, affects transmission of the virus to target CD4+ T cells.
- Determine whether the viral proteins Tax and HBZ act together to repress ANXA1, the gene for annexin A1, in infected T-cell lines, and whether this repression promotes cell-to-cell contact needed for infection.
- Analyze early immunogenic cell death events after anthracycline chemotherapy kills HTLV-1-transformed T cells, comparing dendritic cell recruitment and engulfment signals between cells with repressed and with restored annexin A1 expression.
More about the research
Leukemia arises when a single infected T cell accumulates changes that make it immortal and then malignant, so the more efficiently the virus spreads from cell to cell, the greater the lifetime risk. Two viral proteins, Tax and HBZ, drive both the spread of infection and the cancer, and they usually control different sets of genes. Unusually, both switch off the same gene, ANXA1, and that gene is quiet in infected T-cell lines. The protein it encodes, annexin A1, binds to cell membranes and, once released or moved to the cell surface, damps down inflammation; it also helps launch the immune cleanup of dying cancer cells. This project asks whether silencing annexin A1 is a strategy that helps the virus spread and helps the tumor survive chemotherapy.
Why it matters
Adult T-cell leukemia is fatal and responds poorly to chemotherapy, and people carrying human T-cell leukemia virus type 1 live with a lifelong risk of developing it. If loss of annexin A1 helps infected cells pass the virus to new cells, blocking that step could lower the risk of disease; if restoring annexin A1 lets dying leukemia cells recruit the immune system, it could make existing chemotherapy more effective and potentially less toxic for patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Eric Ubil
University of Kentucky, KY·Microbiology & Immunology
Determine how tumor cells regulate secretion of proteins that activate the macrophage Mer receptor, and test whether their levels in human tumors predict response to chemotherapy.
Hideki Aihara
University of Minnesota, MN·Biochemistry
Investigate how host cell factors take part in integration of Human T-cell Leukemia virus and Rous sarcoma virus, building on structural studies of their intasomes, the protein–DNA complexes that insert viral DNA into chromosomes.
Harry Kim
University of Texas Southwestern Medical Center, TX·Medicine & Clinical Research
Determine whether washing damage-associated molecular patterns (DAMPs) and dead-cell debris out of necrotic bone reduces harmful inflammatory macrophage responses, using a piglet model of femoral head osteonecrosis and lab-dish experiments.
The school
East Carolina University: 5 labs on PI Pages, $73M a year on research, 102 research doctorates a year.
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