Supplementary Figure S3 from GPR65 Inactivation in Tumor Cells Drives Antigen-Independent CAR T-cell Resistance via Macrophage Remodeling

Mavuluri, Jayadev; Dhungana, Yogesh; Jones, Lindsay L.; Bhatara, Sheetal; Shi, Hao; Yang, Xu; Lim, Song-Eun; Reyes, Noemi; Chi, Hongbo; Yu, Jiyang; Geiger, Terrence L.

doi:10.1158/2159-8290.28917712

Supplementary Figure S3 from GPR65 Inactivation in Tumor Cells Drives Antigen-Independent CAR T-cell Resistance via Macrophage Remodeling

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posted on 2025-05-02, 07:20 authored by Jayadev Mavuluri, Yogesh Dhungana, Lindsay L. Jones, Sheetal Bhatara, Hao Shi, Xu Yang, Song-Eun Lim, Noemi Reyes, Hongbo Chi, Jiyang Yu, Terrence L. Geiger

Figure S3 shows that GPR65 KO mediated CAR-T resistance is independent of antigen expression and CAR-T cell expansion.

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National Institute of General Medical Sciences (NIGMS)

United States Department of Health and Human Services

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National Cancer Institute (NCI)

United States Department of Health and Human Services

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ARTICLE ABSTRACT

The study identifies GPR65 as an important determinant of B-cell acute lymphoblastic leukemia response to CAR T-cell therapy. Notably, GPR65 absence signals CAR T resistance. By emphasizing the therapeutic potential of targeting VEGFA or host macrophages, our study identifies routes to optimize CAR T-cell therapy outcomes in hematologic malignancies via tumor microenvironment manipulation.

Supplementary Figure S3 from GPR65 Inactivation in Tumor Cells Drives Antigen-Independent CAR T-cell Resistance via Macrophage Remodeling

Funding

National Institute of General Medical Sciences (NIGMS)

National Cancer Institute (NCI)

History

ARTICLE ABSTRACT

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