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- W1993484190 abstract "Inducible nitric oxide synthase (NOS2) is an inflammation responsive enzyme (EC 1.14.13.39) that is induced during acute and chronic inflammation and tissue injury as part of the host defense and wound healing process. NOS2 up-regulation leads to increased nitric oxide (NO) production, the means by which this enzyme can initiate NO-dependent signal transduction, influence the redox state of cells and induce modifications of proteins, lipids, and DNA. Aberrant expression of NOS2 has been observed in many types of human tumors. In breast cancer, increased NOS2 is associated with markers of poor outcome and decreased survival. Growth factor and cytokine signaling, tissue remodeling, NF-kB activation, and hypoxia are candidate mechanisms that induce NOS2 in tumor epithelial and tumor-infiltrating cells. NOS2 induction will trigger the release of variable amounts of NO into the tumor microenvironment and can activate oncogenic pathways, including the Akt, epidermal growth factor receptor and c-Myc signaling pathways, and stimulate tumor microvascularization. Constitutively increased NO levels may also select for mutant p53 cells to overcome the tumor suppressor function of NO-activated wild-type p53. More recent findings suggest that NO induces stem cell-like tumor characteristics in breast cancer. In this review, we will discuss the effects of NO in tumor biology and disease progression with an emphasis on breast cancer, and will examine the mechanisms that link increased NO to a basal-like transcription pattern in human breast tumors and poor disease outcome." @default.
- W1993484190 created "2016-06-24" @default.
- W1993484190 creator A5017672961 @default.
- W1993484190 creator A5032870776 @default.
- W1993484190 date "2011-02-15" @default.
- W1993484190 modified "2023-10-03" @default.
- W1993484190 title "Candidate pathways linking inducible nitric oxide synthase to a basal-like transcription pattern and tumor progression in human breast cancer" @default.
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- W1993484190 doi "https://doi.org/10.4161/cc.10.4.14864" @default.
- W1993484190 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3043082" @default.
- W1993484190 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21293193" @default.
- W1993484190 hasPublicationYear "2011" @default.
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