STAT3 in arsenic lung carcinogenicity

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


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 languageEnglish
Issue number4
StatePublished - 2015

Bibliographical note

Funding Information:
This work was supported by fundingfrom the American Cancer Society (RSG-11-116-01-CNE).

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


  • Arsenic
  • Autophagy
  • Immunosurveillance
  • Lung tumorigenesis
  • Microenvironment
  • STAT3

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Oncology


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