For COVID-19 vaccine updates, please review our information guide. For patient eligibility and scheduling availability, please visit VaccineTogetherNY.org.

Gene expression analysis in Interleukin-12-induced suppression of mouse mammary carcinoma.

TitleGene expression analysis in Interleukin-12-induced suppression of mouse mammary carcinoma.
Publication TypeJournal Article
Year of Publication2004
AuthorsShi X, Liu J, Xiang Z, Mitsuhashi M, Wu RS, Ma X
JournalInt J Cancer
Volume110
Issue4
Pagination570-8
Date Published2004 Jul 01
ISSN0020-7136
KeywordsAnimals, Female, Gene Expression Profiling, Interleukin-12, Lymphocytes, Tumor-Infiltrating, Mammary Neoplasms, Experimental, Mice, Mice, Inbred BALB C, Neovascularization, Pathologic, Reverse Transcriptase Polymerase Chain Reaction
Abstract

Interleukin-12 (IL-12) has potent antitumor activities via natural killer cells and cytotoxic T lymphocytes. However, the molecular mechanisms whereby IL-12 induces tumoricidal activities are poorly understood. Here, we report the genome-wide analysis of gene expression in a primary murine mammary carcinoma model that resembles human breast cancer, following the therapeutic application of recombinant IL-12, which restricted tumor growth and metastasis. IL-12 was able to curtail neovascularization in the tumor as well as enhance the number of tumor-infiltrating lymphocytes. Comprehensive examination of global gene expression revealed IL-12-induced molecular changes associated with tumor regression and reduced lung metastasis, thus providing a high-resolution snapshot of a host response against a developing malignancy and a rich source of potential targets for therapeutic intervention of breast cancer.

DOI10.1002/ijc.20145
Alternate JournalInt J Cancer
PubMed ID15122590
PubMed Central IDPMC2957898
Grant ListR01 CA100223 / CA / NCI NIH HHS / United States
R01 CA100223-01A1 / CA / NCI NIH HHS / United States

Weill Cornell Medicine Microbiology and Immunology 1300 York Avenue, Box 62 New York, NY 10065 Phone: (212) 746-6505 Fax: (212) 746-8587