Journal
ONCOGENE
Volume 29, Issue 5, Pages 625-634Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2009.441
Keywords
angiogenesis; chemotherapy; metabolism; oxygen; radiation therapy; transcription
Funding
- NCI NIH HHS [U54 CA143868-02, U54 CA143868-01, T32 CA130840, U54 CA143868-03, U54 CA143868, T32 CA153952] Funding Source: Medline
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Adaptation of cancer cells to their microenvironment is an important driving force in the clonal selection that leads to invasive and metastatic disease. O-2 concentrations are markedly reduced in many human cancers compared with normal tissue, and a major mechanism mediating adaptive responses to reduced O-2 availability (hypoxia) is the regulation of transcription by hypoxia-inducible factor 1 (HIF-1). This review summarizes the current state of knowledge regarding the molecular mechanisms by which HIF-1 contributes to cancer progression, focusing on (1) clinical data associating increased HIF-1 levels with patient mortality; (2) preclinical data linking HIF-1 activity with tumor growth; (3) molecular data linking specific HIF-1 target gene products to critical aspects of cancer biology and (4) pharmacological data showing anticancer effects of HIF-1 inhibitors in mouse models of human cancer. Oncogene (2010) 29, 625-634; doi: 10.1038/onc.2009.441; published online 30 November 2009
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