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Omics · dataset · 2022

Tumors hijack erythropoiesis for myelopoiesis and immunosuppression

Listed in Teesside University Research Data Repository

Despite the unprecedented success of immune checkpoint inhibitors (ICIs) as anti-cancer therapy, it remains a prevailing clinical need to identify additional mechanisms underlying ICIs therapeutic efficacy and potential drug resistance.

Description

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, the EDMCs content within tumor tissues is negatively associated with T cell inflammation for the majority of solid cancers; moreover, EDMCs enrichment, in accordance with anemia manifestation, is predictive of poor prognosis in various cohorts of patients undergoing ICIs therapy.

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Together, our findings reveal a feed-forward mechanism by which tumors exploit anemia-triggered erythropoiesis for myeloid transdifferentiation and immunosuppression.

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Inferred from text
Cancer 75%
Provenance · 1 source records, 8 field assertions
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Teesside University Research Data Repositoryoai:data.mendeley.com/5ttrnmvjjx.417 h agoJSON v1
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concepts[disease].local:disease:cancerenrichment · researchdata tees ac ukkeyword-concept-rules@1.0.0title+description (75%)
concepts[field].local:field:earth-environmentalmapping · researchdata tees ac ukconnector:researchdata_tees_ac_uk@1.0.0
concepts[modality].local:modality:rna-seqmapping · researchdata tees ac ukvocabulary-mapper@1.0.0keywords['RNA Sequencing']
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