Roles for Autophagy in Esophageal Carcinogenesis: Implications for Improving Patient Outcomes
Identifieur interne : 000451 ( Main/Curation ); précédent : 000450; suivant : 000452Roles for Autophagy in Esophageal Carcinogenesis: Implications for Improving Patient Outcomes
Auteurs : Reshu Saxena ; Alena Klochkova ; Mary Grace Murray ; Mohammad Faujul Kabir ; Safiyah Samad ; Tyler Beccari ; Julie Gang ; Kishan Patel ; Kathryn E. Hamilton ; Kelly A. Whelan [États-Unis]Source :
- Cancers [ 2072-6694 ] ; 2019.
Abstract
Esophageal cancer is among the most aggressive forms of human malignancy with five-year survival rates of <20%. Autophagy is an evolutionarily conserved catabolic process that degrades and recycles damaged organelles and misfolded proteins to maintain cellular homeostasis. While alterations in autophagy have been associated with carcinogenesis across tissues, cell type- and context-dependent roles for autophagy have been reported. Herein, we review the current knowledge related to autophagy in esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC), the two most common subtypes of esophageal malignancy. We explore roles for autophagy in the development and progression of ESCC and EAC. We then continue to discuss molecular markers of autophagy as they relate to esophageal patient outcomes. Finally, we summarize current literature examining roles for autophagy in ESCC and EAC response to therapy and discuss considerations for the potential use of autophagy inhibitors as experimental therapeutics that may improve patient outcomes in esophageal cancer.
Url:
DOI: 10.3390/cancers11111697
PubMed: 31683722
PubMed Central: 6895837
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PMC:6895837Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Roles for Autophagy in Esophageal Carcinogenesis: Implications for Improving Patient Outcomes</title>
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<author><name sortKey="Samad, Safiyah" sort="Samad, Safiyah" uniqKey="Samad S" first="Safiyah" last="Samad">Safiyah Samad</name>
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<author><name sortKey="Beccari, Tyler" sort="Beccari, Tyler" uniqKey="Beccari T" first="Tyler" last="Beccari">Tyler Beccari</name>
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<author><name sortKey="Hamilton, Kathryn E" sort="Hamilton, Kathryn E" uniqKey="Hamilton K" first="Kathryn E." last="Hamilton">Kathryn E. Hamilton</name>
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</nlm:aff>
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<series><title level="j">Cancers</title>
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<front><div type="abstract" xml:lang="en"><p>Esophageal cancer is among the most aggressive forms of human malignancy with five-year survival rates of <20%. Autophagy is an evolutionarily conserved catabolic process that degrades and recycles damaged organelles and misfolded proteins to maintain cellular homeostasis. While alterations in autophagy have been associated with carcinogenesis across tissues, cell type- and context-dependent roles for autophagy have been reported. Herein, we review the current knowledge related to autophagy in esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC), the two most common subtypes of esophageal malignancy. We explore roles for autophagy in the development and progression of ESCC and EAC. We then continue to discuss molecular markers of autophagy as they relate to esophageal patient outcomes. Finally, we summarize current literature examining roles for autophagy in ESCC and EAC response to therapy and discuss considerations for the potential use of autophagy inhibitors as experimental therapeutics that may improve patient outcomes in esophageal cancer.</p>
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