Supriya Joshi
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View article: 204 Exposure to hyperphysiologic glucose during therapeutic T cell manufacturing impairs antitumor efficacy
204 Exposure to hyperphysiologic glucose during therapeutic T cell manufacturing impairs antitumor efficacy Open
View article: Figure S6 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing
Figure S6 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing Open
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View article: Table S1 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing
Table S1 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing Open
Suplementary Table 1
View article: Figure S3 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing
Figure S3 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing Open
Suplementary Figure 3
View article: Figure S2 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing
Figure S2 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing Open
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View article: Figure S5 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing
Figure S5 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing Open
Suplementary Figure 5
View article: Figure S1 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing
Figure S1 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing Open
Suplementary Figure 1
View article: Figure S4 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing
Figure S4 from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing Open
Suplementary Figure 4
View article: Data from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing
Data from Reprogramming CD8<sup>+</sup> T-cell Branched <i>N-</i>Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing Open
T-cell therapies have transformed cancer treatment. Although surface glycans have been shown to play critical roles in regulating T-cell development and function, whether and how the glycome influences T cell–mediated tumor immunity remain…
View article: Dysfunction of exhausted T cells is enforced by MCT11-mediated lactate metabolism
Dysfunction of exhausted T cells is enforced by MCT11-mediated lactate metabolism Open
CD8 + T cells are critical mediators of antitumor immunity but differentiate into a dysfunctional state, known as T cell exhaustion, after persistent T cell receptor stimulation in the tumor microenvironment (TME). Exhausted T (T ex ) cell…
View article: 243 Hyperglycemic culture conditions during therapeutic T cell expansion impair tumor immunity and repress T cell signaling linked to altered intracellular glycosylation states
243 Hyperglycemic culture conditions during therapeutic T cell expansion impair tumor immunity and repress T cell signaling linked to altered intracellular glycosylation states Open
View article: 273 Hypermetabolic expansion conditions imprint lasting dysfunction on adoptive cell therapies
273 Hypermetabolic expansion conditions imprint lasting dysfunction on adoptive cell therapies Open
Background Adoptive cell therapies, like chimeric antigen receptor (CAR) T cell therapy act by redirecting and enhancing a patient's immune response to tumor cells, with success in hematologic malignancies. However, many patients relapse d…
View article: Metabolic reprogramming via an engineered PGC-1α improves human chimeric antigen receptor T-cell therapy against solid tumors
Metabolic reprogramming via an engineered PGC-1α improves human chimeric antigen receptor T-cell therapy against solid tumors Open
Background Cellular immunotherapies for cancer represent a means by which a patient’s immune system can be augmented with high numbers of tumor-specific T cells. Chimeric antigen receptor (CAR) therapy involves genetic engineering to ‘redi…
View article: Fully murine CD105-targeted CAR-T cells provide an immunocompetent model for CAR-T cell biology
Fully murine CD105-targeted CAR-T cells provide an immunocompetent model for CAR-T cell biology Open
The modeling of chimeric antigen receptor (CAR) T cell therapies has been mostly focused on immunodeficient models. However, there are many advantages in studying CAR-T cell biology in an immunocompetent setting. We generated a fully murin…
View article: The RAPID risk model: A novel risk score to predict significant prostate cancer in men with an mpMRI lesion
The RAPID risk model: A novel risk score to predict significant prostate cancer in men with an mpMRI lesion Open
View article: A membrane fusion protein, Ykt6, regulates epithelial cell migration via microRNA-mediated suppression of Junctional Adhesion Molecule A
A membrane fusion protein, Ykt6, regulates epithelial cell migration via microRNA-mediated suppression of Junctional Adhesion Molecule A Open
Vesicle trafficking regulates epithelial cell migration by remodeling matrix adhesions and delivering signaling molecules to the migrating leading edge. Membrane fusion, which is driven by soluble N-ethylmaleimide-sensitive factor associat…
View article: Autophagy-deficient breast cancer shows early tumor recurrence and escape from dormancy
Autophagy-deficient breast cancer shows early tumor recurrence and escape from dormancy Open
Breast cancer patients who initially respond to cancer therapies often succumb to distant recurrence of the disease. It is not clear why people with the same type of breast cancer respond to treatments differently; some escape from dormanc…