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10.3390/ijms18091854

http://scihub22266oqcxt.onion/10.3390/ijms18091854
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suck abstract from ncbi


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pmid28841148
      Int+J+Mol+Sci 2017 ; 18 (9 ): ä
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  • Targeting Tumor Adaption to Chronic Hypoxia: Implications for Drug Resistance, and How It Can Be Overcome #MMPMID28841148
  • Kim JY ; Lee JY
  • Int J Mol Sci 2017[Aug]; 18 (9 ): ä PMID28841148 show ga
  • The rapid and uncontrolled proliferation of tumors limits the availability of oxygen and nutrients supplied from the tumor vasculature, thus exposing them to low oxygen environments. Thus, diminished oxygen availability, or hypoxia, is the most common microenvironment feature of nearly all solid tumors. All living cells have the ability to sense changes in oxygen tension and adapt to this stress to preserve survival. Likewise, cancer cells adapt to chronic hypoxic stress via several mechanisms, including promotion of angiogenic factor production, metabolic shift to consume less oxygen, and reduction of apoptotic potential. Adaptation of tumor cells to hypoxia is believed to be the main driver for selection of more invasive and therapy-resistant cancer phenotypes. In this review, we discuss molecular mechanisms by which tumor cells adapt to hypoxia, with a specific focus on hypoxia-inducible factor (HIF) transcription factor. We further discuss the current understandings on hypoxia-mediated drug resistance and strategies to overcome it.
  • |Adaptation, Biological/*drug effects [MESH]
  • |Animals [MESH]
  • |Antineoplastic Agents/pharmacology/therapeutic use [MESH]
  • |Drug Resistance, Neoplasm/drug effects/genetics [MESH]
  • |Gene Expression Regulation, Neoplastic/drug effects [MESH]
  • |Humans [MESH]
  • |Hypoxia-Inducible Factor 1, alpha Subunit/genetics/metabolism [MESH]
  • |Hypoxia/*genetics/*metabolism [MESH]
  • |Molecular Targeted Therapy [MESH]
  • |Neoplasms/*genetics/*metabolism/therapy [MESH]


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