NSAIDs Modulate CDKN2A, TP53, and DNA Content Risk for Progression to Esophageal Adenocarcinoma 英文参考文献.docVIP

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NSAIDs Modulate CDKN2A, TP53, and DNA Content Risk for Progression to Esophageal Adenocarcinoma 英文参考文献.doc

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NSAIDs Modulate CDKN2A, TP53, and DNA Content Risk for Progression to Esophageal Adenocarcinoma 英文参考文献

o PL SMEDICINE NSAIDsModulateCDKN2A,TP53,andDNA ContentRiskforProgressiontoEsophageal Adenocarcinoma Patricia C.Galipeau1,2[*,Xiaohong Li2[,Patricia L.Blount1,2,3,Carlo C.Maley4,Carissa A.Sanchez1,2,Robert D.Odze5, Kamran Ayub6,Peter S.Rabinovitch1,2,7,Thomas L.Vaughan2,8,Brian J.Reid1,2,3,9 1 Human Biology Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America, 2 Public Health Sciences Division, Fred Hutchinson CancerResearchCenter,Seattle,Washington,UnitedStatesofAmerica,3DepartmentofMedicine,UniversityofWashington,Seattle,Washington,UnitedStatesofAmerica, 4CellularandMolecularOncogenesisProgram,WistarInstitute,Philadelphia,Pennsylvania,UnitedStatesofAmerica,5DepartmentofPathology,HarvardMedicalSchool and Brigham and Women’s Hospital, Boston, Massachusetts, United States of America, 6 Department of Gastroenterology, Virginia Mason Medical Center, Seattle, Washington,UnitedStatesofAmerica,7DepartmentofPathology,UniversityofWashington,Seattle,Washington,UnitedStatesofAmerica,8DepartmentofEpidemiology, UniversityofWashington,Seattle,Washington,UnitedStatesofAmerica,9GenomeSciences,UniversityofWashington,Seattle,Washington,UnitedStatesofAmerica Funding:Thisstudywasfundedby theUSNationalInstitutesofHealth (P01CA91955,R01CA61202,and R01CA78828)withinterimsupport fromtheFredHutchinsonCancer ResearchCenter.Thefundershadno roleinstudydesign,datacollection andanalysis,decisiontopublish,or preparationofthemanuscript. ABSTRACT Background SomaticgeneticCDKN2A,TP53,andDNAcontentabnormalitiesarecommoninmanyhuman cancers and their precursors, including esophageal adenocarcinoma (EA) and Barrett’s esophagus (BE), conditions for which aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) have been proposed as possible chemopreventive agents; however, little is known abouttheabilityofabiomarkerpaneltopredictprogressiontocancernorhowNSAIDusemay modulate progression. We aimed to evaluate somatic genetic abnormalities with NS