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PMID: 26079100 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Review

The hypoxic tumor microenvironment: A driving force for breast cancer progression.

Biochimica et biophysica acta ·Vol. 1863 ·No. 3 ·2016-03-00 ·Pages 382-391

Semenza GL

Abstract

Intratumoral hypoxia is a common finding in breast cancer and is associated with a significantly increased risk of metastasis and patient mortality. Hypoxia-inducible factors activate the transcription of a large battery of genes encoding proteins that promote primary tumor vascularization and growth, stromal cell recruitment, extracellular matrix remodeling, premetastatic niche formation, cell motility, local tissue invasion, extravasation at sites of metastasis, and maintenance of the cancer stem cell phenotype that is required to generate secondary tumors. Recent preclinical studies suggest that the combination of cytotoxic chemotherapy with drugs that inhibit hypoxia-inducible factors may improve outcome for women with triple-negative breast cancer. This article is part of a Special Issue entitled: Tumor Microenvironment Regulation of Cancer Cell Survival, Metastasis, Inflammation, and Immune Surveillance edited by Peter Ruvolo and Gregg L. Semenza.

Keywords
Bone metastasis Lung metastasis Lymph node metastasis Mesenchymal stem cells Microvesicles Myeloid-derived suppressor cells Tumor-associated macrophages
MeSH Terms
Breast Neoplasms/metabolism,pathology,therapy Cell Hypoxia Cell Movement Disease Progression Female Humans Hypoxia-Inducible Factor 1/metabolism Models, Biological Tumor Microenvironment
Chemicals
Hypoxia-Inducible Factor 1
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Semenza Gregg L
Vascular Program, Institute for Cell Engineering Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Radiation Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address: gsemenza@jhmi.edu.
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Article Info
Journal
Biochimica et biophysica acta
Abbr.
Biochim Biophys Acta
ISSN
0006-3002
Published
2016-03-00
Epub
2015-00-14
Pages
382-391
Language
English
Region
Netherlands
NLM ID
0217513
PMCID
PMC4678039
Subset
IM
Grants
NCI NIH HHS · U54 CA143868 · United States
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