4.8 Editorial Material

Tumor-directed dysregulation of erythroid progenitors drives immunosuppressive myeloid cells

期刊

CANCER CELL
卷 40, 期 6, 页码 597-599

出版社

CELL PRESS
DOI: 10.1016/j.ccell.2022.04.017

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资金

  1. National Institutes of Health (NIH) [R01-CA184185, R01-CA233512, R01-CA262121, P01-CA250984, 4, P30-CA076292]
  2. Florida Department of Health [20B04]

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This study demonstrates how tumors can manipulate erythroid progenitors to promote immunosuppression. These reprogrammed cells, similar to myeloid-derived suppressor cells, are associated with poor response to immune-checkpoint inhibitors and tumor-related anemia.
In this issue of Cancer Cell, Long et al. demonstrate that tumors can reprogram erythroid progenitors into myeloid-erythroid cells that promote immunosuppression. Erythroid-differentiated myeloid cells (EDMCs) expand in cancer-bearing individuals, resemble the functionality of myeloid-derived suppressor cells (MDSCs), and correlate with poor response to immune-checkpoint inhibitors (ICIs) and tumor-related anemia.

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