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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE132297 | GEO | 2021/05/03

REPOSITORIES: GEO

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [mouse]

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [human]

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [human]

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Anti-PD-L1 Lead-in Before MAPKi Combination Maximizes Anti-Tumor Efficacy and Immunity.

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-08-19 | GSE177902 | GEO

Tumor-Induced Erythroid Precursor-Differentiated Myeloid Cells Mediate Immunosuppression and Curtail Anti-PD-1/PD-L1 Treatment Efficacy

Project description:Despite the unprecedented success of immune checkpoint inhibitors (ICIs) as anti-cancer therapy, it remains a prevailing clinical need to identify additional mechanisms underlying ICI therapeutic efficacy and potential drug resistance. Here, using lineage tracking in cancer patients and tumor-bearing mice, we demonstrate that erythroid progenitor cells lose their developmental potential and switch to the myeloid lineage. Single-cell transcriptome analyses reveal that, notwithstanding quantitative differences in erythroid gene expression, erythroid differentiated myeloid cells (EDMCs) are transcriptionally indistinguishable from their myeloid-originated counterparts. EDMCs possess multifaceted machinery to curtail T cell-mediated anti-tumor responses. Consequently, EDMC content within tumor tissues is negatively associated with T cell inflammation for the majority of solid cancers; moreover, EDMC enrichment, in accordance with anemia manifestation, is predictive of poor prognosis in various cohorts of patients undergoing ICI therapy. Together, our findings reveal a feed-forward mechanism by which tumors exploit anemia-triggered erythropoiesis for myeloid transdifferentiation and immunosuppression.

2022-04-30 | GSE201715 | GEO

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