Khashayarsha Khazaie Research Centers and Institutes, Lurie Cancer Center

Khashayarsha Khazaie

Research Interest Keywords

Autoimmunity, Breast Cancer, Cancer: Digestive System (esophagus, stomach, colon, and rectum), Cancer: Pancreas, Cancer: Prostate, Immunology, Inflammation, Inflammatory Bowel Disease

Office phone



Scopus Publication Detail

The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in Scopus. This abstract is what is used to create the fingerprint of the publication.

Tumor STAT1 transcription factor activity enhances breast tumor growth and immune suppression mediated by myeloid-derived suppressor cells

Laura M. Hix; John Karavitis; Mohammad W. Khan; Yihui H. Shi; Khashayarsha Khazaie; Ming Zhang

(Profiled Authors: Khashayarsha Khazaie; Ming Zhang)

Journal of Biological Chemistry. 2013;288(17):11676-11688.


Previous studies had implicated the IFN-γ transcription factor signal transducer and activator of transcription 1 (STAT1) as a tumor suppressor. However, accumulating evidence has correlated increased STAT1 activation with increased tumor progression in multiple types of cancer, including breast cancer. Indeed, we present evidence that tumor up-regulation of STAT1 activity in human and mouse mammary tumors correlates with increasing disease progression to invasive carcinoma. A microarray analysis comparing low aggressive TM40D and highly aggressive TM40D-MB mouse mammary carcinoma cells revealed significantly higher STAT1 activity in the TM40D-MB cells. Ectopic overexpression of constitutively active STAT1 in TM40D cells promoted mobilization of myeloid-derived suppressor cells (MDSCs) and inhibition of antitumor T cells, resulting in aggressive tumor growth in tumor-transplanted, immunocompetent mice. Conversely, gene knockdown of STAT1 in the metastatic TM40D-MB cells reversed these events and attenuated tumor progression. Importantly, we demonstrate that in human breast cancer, the presence of tumor STAT1 activity and tumor-recruited CD33+ myeloid cells correlates with increasing disease progression from ductal carcinoma in situ to invasive carcinoma. We conclude that STAT1 activity in breast cancer cells is responsible for shaping an immunosuppressive tumor microenvironment, and inhibiting STAT1 activity is a promising immune therapeutic approach. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.

PMID: 23486482     PMCID: PMC3636858    

Scientific Context

This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.

Related Publications

Related Topics

Appears in this Publication Appears in this Document

Related Experts

Author of this Publication Author of this Document