Format

Send to

Choose Destination
Oncogene. 2009 Jan 15;28(2):306-12. doi: 10.1038/onc.2008.384. Epub 2008 Oct 13.

PI(3) kinase is associated with a mechanism of immunoresistance in breast and prostate cancer.

Author information

1
Department of Neurological Surgery, University of California San Francisco, San Francisco, CA 94143, USA.

Abstract

Immune escape describes a critical event whereby tumor cells adopt an immunoresistant phenotype to escape adaptive surveillance. We show that expression of a pivotal negative regulator of T-cell function, B7-H1, correlates with PI(3) kinase activation in breast and prostate cancer patients. B7-H1-mediated immunoresistance can be attenuated by inhibitors of the PI(3) kinase pathway, and is dependent on S6K1-mediated translational regulation of B7-H1 protein. Breast and prostate carcinoma cells with activated PI(3) kinase lose the immunoresistant phenotype after treatment with B7-H1 siRNA. Conversely, breast and prostate carcinoma cells with minimal PI(3) kinase activation adopt an immunoresistant phenotype when engineered to overexpress B7-H1 protein. These observations describe a mechanism for immune escape from tumor dormancy in humans that relates to oncogenesis.

PMID:
18850006
PMCID:
PMC3786571
DOI:
10.1038/onc.2008.384
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center