Restoring inflammatory balance as a potential preventive strategy for inflammation induced cancer

Simona Hefetz-Sela; Ilan Stein; Eli Pikarsky

doi:10.1080/2162402X.2015.1039764

Restoring inflammatory balance as a potential preventive strategy for inflammation induced cancer

Simona Hefetz-Sela
, Ilan Stein
, Eli Pikarsky

Department of Immunology and Cancer Research

The Hebrew University of Jerusalem

Research output: Contribution to journal › Article › peer-review

Abstract

In contrast to the accepted notion that tumor-derived signals polarize macrophages toward a protumorigenic M2 phenotype during tumor progression, we recently discovered that the inflammatory microenvironment is capable of driving macrophages toward an M2 phenotype. Moreover, our data suggests that inflammatory education is prominent during the early phases of hepatocellular carcinoma (HCC) suggesting that inflammatory modulation might effectively prevent HCC.

Original language	English
Journal	OncoImmunology
Volume	4
Issue number	11
DOIs	https://doi.org/10.1080/2162402X.2015.1039764
State	Published - 2 Nov 2015

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

c-Jun phosphorylation
hepatocellular carcinoma
immune check point drugs
inflammation-induced cancer
macrophage polarization

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Oncology

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10.1080/2162402X.2015.1039764

Cite this

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title = "Restoring inflammatory balance as a potential preventive strategy for inflammation induced cancer",

abstract = "In contrast to the accepted notion that tumor-derived signals polarize macrophages toward a protumorigenic M2 phenotype during tumor progression, we recently discovered that the inflammatory microenvironment is capable of driving macrophages toward an M2 phenotype. Moreover, our data suggests that inflammatory education is prominent during the early phases of hepatocellular carcinoma (HCC) suggesting that inflammatory modulation might effectively prevent HCC.",

keywords = "c-Jun phosphorylation, hepatocellular carcinoma, immune check point drugs, inflammation-induced cancer, macrophage polarization",

author = "Simona Hefetz-Sela and Ilan Stein and Eli Pikarsky",

note = "Funding Information: Research leading to these results received funding from the European Research Council Grant Agreements 281738 to E.P; the Dr. Miriam and Shel- don G. Adelson Medical Research Foun dation (AMRF); the Israel Science Foundation (ISF) Centers of Excellence (1779/11) to E.P; and ISF individual grant to I.S. Publisher Copyright: {\textcopyright} 2015 Taylor \& Francis Group, LLC.",

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doi = "10.1080/2162402X.2015.1039764",

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AU - Hefetz-Sela, Simona

AU - Stein, Ilan

AU - Pikarsky, Eli

N1 - Funding Information: Research leading to these results received funding from the European Research Council Grant Agreements 281738 to E.P; the Dr. Miriam and Shel- don G. Adelson Medical Research Foun dation (AMRF); the Israel Science Foundation (ISF) Centers of Excellence (1779/11) to E.P; and ISF individual grant to I.S. Publisher Copyright: © 2015 Taylor & Francis Group, LLC.

PY - 2015/11/2

Y1 - 2015/11/2

N2 - In contrast to the accepted notion that tumor-derived signals polarize macrophages toward a protumorigenic M2 phenotype during tumor progression, we recently discovered that the inflammatory microenvironment is capable of driving macrophages toward an M2 phenotype. Moreover, our data suggests that inflammatory education is prominent during the early phases of hepatocellular carcinoma (HCC) suggesting that inflammatory modulation might effectively prevent HCC.

AB - In contrast to the accepted notion that tumor-derived signals polarize macrophages toward a protumorigenic M2 phenotype during tumor progression, we recently discovered that the inflammatory microenvironment is capable of driving macrophages toward an M2 phenotype. Moreover, our data suggests that inflammatory education is prominent during the early phases of hepatocellular carcinoma (HCC) suggesting that inflammatory modulation might effectively prevent HCC.

KW - c-Jun phosphorylation

KW - hepatocellular carcinoma

KW - immune check point drugs

KW - inflammation-induced cancer

KW - macrophage polarization

UR - https://www.scopus.com/pages/publications/84941792498

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DO - 10.1080/2162402X.2015.1039764

M3 - Article

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VL - 4

JO - OncoImmunology

JF - OncoImmunology

IS - 11

ER -

Restoring inflammatory balance as a potential preventive strategy for inflammation induced cancer

Abstract

UN SDGs

Keywords

ASJC Scopus subject areas

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