Myeloid Cells as Targets for Therapy in Solid Tumors

Tiziana Cotechini, Terry R. Medler, Lisa Coussens

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

It is well established that cancer development ensues based on reciprocal interactions between genomically altered neoplastic cells and diverse populations of recruited "host" cells co-opted to support malignant progression. Among the host cells recruited into tumor microenvironments, several subtypes of myeloid cells, including macrophages, monocytes, dendritic cells, and granulocytes contribute to tumor development by providing tumor-promoting factors as well as a spectrum of molecules that suppress cytotoxic activities of T lymphocytes. Based on compelling preclinical data revealing that inhibition of critical myeloid-based programs leads to tumor suppression, novel immune-based therapies and approaches are now entering the clinic for evaluation. This review discusses mechanisms underlying protumorigenic programming of myeloid cells and discusses how targeting of these has potential to attenuate solid tumor progression via the induction and of mobilization CD8 + cytotoxic T cell immunity. ©

Original languageEnglish (US)
Pages (from-to)343-350
Number of pages8
JournalCancer Journal (United States)
Volume21
Issue number4
DOIs
StatePublished - Jul 5 2015

Fingerprint

Myeloid Cells
Neoplasms
Therapeutics
Tumor Microenvironment
Cytotoxic T-Lymphocytes
Granulocytes
Dendritic Cells
Monocytes
Immunity
Macrophages
T-Lymphocytes
Population

Keywords

  • B cell
  • CD8 + T cell
  • chemotherapy
  • dendritic cell
  • eosinophil
  • immunotherapy
  • lymphocyte
  • macrophage
  • myeloid
  • neutrophil
  • tumor microenvironment

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Myeloid Cells as Targets for Therapy in Solid Tumors. / Cotechini, Tiziana; Medler, Terry R.; Coussens, Lisa.

In: Cancer Journal (United States), Vol. 21, No. 4, 05.07.2015, p. 343-350.

Research output: Contribution to journalArticle

Cotechini, Tiziana ; Medler, Terry R. ; Coussens, Lisa. / Myeloid Cells as Targets for Therapy in Solid Tumors. In: Cancer Journal (United States). 2015 ; Vol. 21, No. 4. pp. 343-350.
@article{bdd727104c9e42b0850d67d0665759c0,
title = "Myeloid Cells as Targets for Therapy in Solid Tumors",
abstract = "It is well established that cancer development ensues based on reciprocal interactions between genomically altered neoplastic cells and diverse populations of recruited {"}host{"} cells co-opted to support malignant progression. Among the host cells recruited into tumor microenvironments, several subtypes of myeloid cells, including macrophages, monocytes, dendritic cells, and granulocytes contribute to tumor development by providing tumor-promoting factors as well as a spectrum of molecules that suppress cytotoxic activities of T lymphocytes. Based on compelling preclinical data revealing that inhibition of critical myeloid-based programs leads to tumor suppression, novel immune-based therapies and approaches are now entering the clinic for evaluation. This review discusses mechanisms underlying protumorigenic programming of myeloid cells and discusses how targeting of these has potential to attenuate solid tumor progression via the induction and of mobilization CD8 + cytotoxic T cell immunity. {\circledC}",
keywords = "B cell, CD8 + T cell, chemotherapy, dendritic cell, eosinophil, immunotherapy, lymphocyte, macrophage, myeloid, neutrophil, tumor microenvironment",
author = "Tiziana Cotechini and Medler, {Terry R.} and Lisa Coussens",
year = "2015",
month = "7",
day = "5",
doi = "10.1097/PPO.0000000000000132",
language = "English (US)",
volume = "21",
pages = "343--350",
journal = "Cancer journal (Sudbury, Mass.)",
issn = "1528-9117",
publisher = "Lippincott Williams and Wilkins Ltd.",
number = "4",

}

TY - JOUR

T1 - Myeloid Cells as Targets for Therapy in Solid Tumors

AU - Cotechini, Tiziana

AU - Medler, Terry R.

AU - Coussens, Lisa

PY - 2015/7/5

Y1 - 2015/7/5

N2 - It is well established that cancer development ensues based on reciprocal interactions between genomically altered neoplastic cells and diverse populations of recruited "host" cells co-opted to support malignant progression. Among the host cells recruited into tumor microenvironments, several subtypes of myeloid cells, including macrophages, monocytes, dendritic cells, and granulocytes contribute to tumor development by providing tumor-promoting factors as well as a spectrum of molecules that suppress cytotoxic activities of T lymphocytes. Based on compelling preclinical data revealing that inhibition of critical myeloid-based programs leads to tumor suppression, novel immune-based therapies and approaches are now entering the clinic for evaluation. This review discusses mechanisms underlying protumorigenic programming of myeloid cells and discusses how targeting of these has potential to attenuate solid tumor progression via the induction and of mobilization CD8 + cytotoxic T cell immunity. ©

AB - It is well established that cancer development ensues based on reciprocal interactions between genomically altered neoplastic cells and diverse populations of recruited "host" cells co-opted to support malignant progression. Among the host cells recruited into tumor microenvironments, several subtypes of myeloid cells, including macrophages, monocytes, dendritic cells, and granulocytes contribute to tumor development by providing tumor-promoting factors as well as a spectrum of molecules that suppress cytotoxic activities of T lymphocytes. Based on compelling preclinical data revealing that inhibition of critical myeloid-based programs leads to tumor suppression, novel immune-based therapies and approaches are now entering the clinic for evaluation. This review discusses mechanisms underlying protumorigenic programming of myeloid cells and discusses how targeting of these has potential to attenuate solid tumor progression via the induction and of mobilization CD8 + cytotoxic T cell immunity. ©

KW - B cell

KW - CD8 + T cell

KW - chemotherapy

KW - dendritic cell

KW - eosinophil

KW - immunotherapy

KW - lymphocyte

KW - macrophage

KW - myeloid

KW - neutrophil

KW - tumor microenvironment

UR - http://www.scopus.com/inward/record.url?scp=84938597972&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84938597972&partnerID=8YFLogxK

U2 - 10.1097/PPO.0000000000000132

DO - 10.1097/PPO.0000000000000132

M3 - Article

VL - 21

SP - 343

EP - 350

JO - Cancer journal (Sudbury, Mass.)

JF - Cancer journal (Sudbury, Mass.)

SN - 1528-9117

IS - 4

ER -