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Jennifer S. Y. Ma

Researcher at Torrey Pines Institute for Molecular Studies

Publications -  14
Citations -  1136

Jennifer S. Y. Ma is an academic researcher from Torrey Pines Institute for Molecular Studies. The author has contributed to research in topics: Cytotoxic T cell & Chimeric antigen receptor. The author has an hindex of 12, co-authored 14 publications receiving 907 citations. Previous affiliations of Jennifer S. Y. Ma include Children's National Medical Center.

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Switch-mediated activation and retargeting of CAR-T cells for B-cell malignancies

TL;DR: It is shown that switches specific for CD19 govern the activity, tissue-homing, cytokine release, and phenotype of switchable CAR-T cells in a dose-titratable manner using xenograft mouse models of B-cell leukemia.
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Versatile strategy for controlling the specificity and activity of engineered T cells.

TL;DR: It is demonstrated that a switch-mediated CAR-T approach enables the titration of engineered T-cell antitumor activity, which was observed to be highly advantageous in reducing treatment-related toxicities in vivo.
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Redirection of genetically engineered CAR-T cells using bifunctional small molecules.

TL;DR: It is demonstrated that a bifunctional small molecule "switch" consisting of folate conjugated to fluorescein isothiocyanate (folate-FITC) can redirect and regulate FITC-specific CAR-T cell activity toward folate receptor (FR)-overexpressing tumor cells.
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Design of Switchable Chimeric Antigen Receptor T Cells Targeting Breast Cancer.

TL;DR: A switchable CAR-T cell platform in which the activity of the engineered cell is controlled by dosage of an antibody-based switch is developed, which may facilitate the application of immunotherapy to solid tumors by affording comparable efficacy with improved safety owing to switch-based control of theCAR-T response.
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Targeting Human C‐Type Lectin‐like Molecule‐1 (CLL1) with a Bispecific Antibody for Immunotherapy of Acute Myeloid Leukemia

TL;DR: The synthesis of a novel bispecific antibody, αCLL1-αCD3, is described, using the genetically encoded unnatural amino acid, p-acetylphenylalanine, which demonstrates potent and selective cytotoxicity against several human AML cell lines and primary AML patient derived cells in vitro.