title: Molecular pathways: myeloid complicity in cancer.
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. Clin Cancer Res; 20(20); 5157-70. ©2014 AACR.
authors.affiliation: Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Department of Immunology, University of Washington, Seattle, Washington.
authors.forename: Ingunn M
authors.initials: IM
authors.lastname: Stromnes
authors.affiliation: Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Department of Immunology, University of Washington, Seattle, Washington. Division of Medical Oncology, Department of Medicine, University of Washington School of Medicine, Seattle, Washington.
authors.forename: Philip D
authors.initials: PD
authors.lastname: Greenberg
authors.affiliation: Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Division of Medical Oncology, Department of Medicine, University of Washington School of Medicine, Seattle, Washington. Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. srh@fhcrc.org.
authors.forename: Sunil R
authors.initials: SR
authors.lastname: Hingorani
mesh_terms: D000818:Animals; D006801:Humans; D007167:Immunotherapy; D022423:Myeloid Cells / Q000276:immunology* / Q000378:metabolism*; D009369:Neoplasms / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D015398:Signal Transduction; D057170:Translational Research, Biomedical