STAT3 in arsenic lung carcinogenicity

Gang Chen

doi:10.1080/2162402X.2014.995566

STAT3 in arsenic lung carcinogenicity

Gang Chen

Pharmacology and Nutritional Sciences

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

5 Scopus citations

Abstract

We recently found that the chronic sterile inflammation contributes to arsenic lung tumorigenesis which is inhibited by autophagy. STAT3 regulates the interaction between inflammation and autophagy. STAT3 may also play a critical role in mediating the crosstalk between lung epithelial cells and their microenvironment, including immune cells, during arsenic lung carcinogenesis.

Original language	English
Journal	OncoImmunology
Volume	4
Issue number	4
DOIs	https://doi.org/10.1080/2162402X.2014.995566
State	Published - 2015

Bibliographical note

Publisher Copyright:
© 2015 Taylor & Francis Group, LLC.

Keywords

Arsenic
Autophagy
Immunosurveillance
Lung tumorigenesis
Microenvironment
STAT3

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Oncology

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10.1080/2162402X.2014.995566

Cite this

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title = "STAT3 in arsenic lung carcinogenicity",

abstract = "We recently found that the chronic sterile inflammation contributes to arsenic lung tumorigenesis which is inhibited by autophagy. STAT3 regulates the interaction between inflammation and autophagy. STAT3 may also play a critical role in mediating the crosstalk between lung epithelial cells and their microenvironment, including immune cells, during arsenic lung carcinogenesis.",

keywords = "Arsenic, Autophagy, Immunosurveillance, Lung tumorigenesis, Microenvironment, STAT3",

author = "Gang Chen",

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year = "2015",

doi = "10.1080/2162402X.2014.995566",

language = "English",

volume = "4",

number = "4",

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AU - Chen, Gang

PY - 2015

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N2 - We recently found that the chronic sterile inflammation contributes to arsenic lung tumorigenesis which is inhibited by autophagy. STAT3 regulates the interaction between inflammation and autophagy. STAT3 may also play a critical role in mediating the crosstalk between lung epithelial cells and their microenvironment, including immune cells, during arsenic lung carcinogenesis.

AB - We recently found that the chronic sterile inflammation contributes to arsenic lung tumorigenesis which is inhibited by autophagy. STAT3 regulates the interaction between inflammation and autophagy. STAT3 may also play a critical role in mediating the crosstalk between lung epithelial cells and their microenvironment, including immune cells, during arsenic lung carcinogenesis.

KW - Arsenic

KW - Autophagy

KW - Immunosurveillance

KW - Lung tumorigenesis

KW - Microenvironment

KW - STAT3

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UR - http://www.scopus.com/inward/citedby.url?scp=84954349778&partnerID=8YFLogxK

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DO - 10.1080/2162402X.2014.995566

M3 - Article

AN - SCOPUS:84954349778

SN - 2162-4011

VL - 4

JO - OncoImmunology

JF - OncoImmunology

IS - 4

ER -

STAT3 in arsenic lung carcinogenicity

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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