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Maryalice Stetler-Stevenson

Researcher at National Institutes of Health

Publications -  281
Citations -  24373

Maryalice Stetler-Stevenson is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Minimal residual disease & Immunophenotyping. The author has an hindex of 67, co-authored 277 publications receiving 21068 citations. Previous affiliations of Maryalice Stetler-Stevenson include Science Applications International Corporation.

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B-cell depletion and remissions of malignancy along with cytokine-associated toxicity in a clinical trial of anti-CD19 chimeric-antigen-receptor–transduced T cells

TL;DR: Pro adoptive transfer of T cells genetically modified to express an anti-CD19 chimeric Ag receptor (CAR) has great promise to improve the treatment of B-cell malignancies because of a potent ability to eradicate CD19(+) cells in vivo; however, reversible cytokine-associated toxicities occurred after CAR-transduced T-cell infusions.
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Eradication of B-lineage cells and regression of lymphoma in a patient treated with autologous T cells genetically engineered to recognize CD19

TL;DR: A patient with advanced follicular lymphoma was treated by administering a preparative chemotherapy regimen followed by autologous T cells genetically engineered to express a chimeric antigen receptor (CAR) that recognized the B- cell antigen CD19, and B-cell precursors were selectively eliminated from the patient's bone marrow after infusion of anti-CD19-CAR-transduced T cells.
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ZAP-70 expression identifies a chronic lymphocytic leukemia subtype with unmutated immunoglobulin genes, inferior clinical outcome, and distinct gene expression profile

TL;DR: ZAP-70 expression and IgVH mutation status were comparable in their ability to predict time to treatment requirement following diagnosis, and reverse transcriptase-polymerase chain reaction and immunohistochemical assays for ZAP- 70 expression can be applied clinically and would yield important prognostic information for patients with CLL.