Molecular pathways: Myeloid complicity in cancer

Ingunn M. Stromnes, Philip D. Greenberg, Sunil R. Hingorani

Research output: Contribution to journalReview articlepeer-review

31 Scopus citations

Abstract

Cancer-induced inflammation results in accumulation of myeloid cells. These myeloid cells include progenitors and progeny of monocytes, granulocytes, macrophages, and dendritic cells. It has become increasingly evident that tumor-dependent factors can condition myeloid cells toward an immunosuppressive and protumorigenic phenotype. Thus, myeloid cells are not simply bystanders in malignancy or barometers of disease burden. Reflecting their dynamic and plastic nature, myeloid cells manifest a continuum of cellular differentiation and are intimately involved at all stages of neoplastic progression. They can promote tumorigenesis through both immune-dependent and -independent mechanisms and can dictate response to therapies. A greater understanding of the inherent plasticity and relationships among myeloid subsets is needed to inform therapeutic targeting. New clinical trials are being designed to modulate the activities of myeloid cells in cancer, which may be essential to maximize the efficacy of both conventional cytotoxic and immune-based therapies for solid tumors.

Original languageEnglish (US)
Pages (from-to)5157-5170
Number of pages14
JournalClinical Cancer Research
Volume20
Issue number20
DOIs
StatePublished - Oct 15 2014

Bibliographical note

Publisher Copyright:
© 2014 AACR.

Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.

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