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KRAS wild-type pancreatic ductal adenocarcinoma: molecular pathology and therapeutic opportunities

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dc.contributor.author신재일-
dc.date.accessioned2020-12-01T17:44:50Z-
dc.date.available2020-12-01T17:44:50Z-
dc.date.issued2020-10-
dc.identifier.issn0392-9078-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/180426-
dc.description.abstractPancreatic ductal adenocarcinoma (PDAC) is a deadly disease, whose main molecular trait is the MAPK pathway activation due to KRAS mutation, which is present in 90% of cases.The genetic landscape of KRAS wild type PDAC can be divided into three categories. The first is represented by tumors with an activated MAPK pathway due to BRAF mutation that occur in up to 4% of cases. The second includes tumors with microsatellite instability (MSI) due to defective DNA mismatch repair (dMMR), which occurs in about 2% of cases, also featuring a high tumor mutational burden. The third category is represented by tumors with kinase fusion genes, which marks about 4% of cases. While therapeutic molecular targeting of KRAS is an unresolved challenge, KRAS-wild type PDACs have potential options for tailored treatments, including BRAF antagonists and MAPK inhibitors for the first group, immunotherapy with anti-PD-1/PD-L1 agents for the MSI/dMMR group, and kinase inhibitors for the third group.This calls for a complementation of the histological diagnosis of PDAC with a routine determination of KRAS followed by a comprehensive molecular profiling of KRAS-negative cases.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherBioMed Central-
dc.relation.isPartOfJOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleKRAS wild-type pancreatic ductal adenocarcinoma: molecular pathology and therapeutic opportunities-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pediatrics (소아청소년과학교실)-
dc.contributor.googleauthorClaudio Luchini-
dc.contributor.googleauthorGaetano Paolino-
dc.contributor.googleauthorPaola Mattiolo-
dc.contributor.googleauthorMaria L Piredda-
dc.contributor.googleauthorAlessandro Cavaliere-
dc.contributor.googleauthorMarina Gaule-
dc.contributor.googleauthorDavide Melisi-
dc.contributor.googleauthorRoberto Salvia-
dc.contributor.googleauthorGiuseppe Malleo-
dc.contributor.googleauthorJae Il Shin-
dc.contributor.googleauthorSarah Cargnin-
dc.contributor.googleauthorSalvatore Terrazzino-
dc.contributor.googleauthorRita T Lawlor-
dc.contributor.googleauthorMichele Milella-
dc.contributor.googleauthorAldo Scarpa-
dc.identifier.doi10.1186/s13046-020-01732-6-
dc.contributor.localIdA02142-
dc.relation.journalcodeJ03807-
dc.identifier.eissn1756-9966-
dc.identifier.pmid33115526-
dc.subject.keywordBRAF-
dc.subject.keywordKRAS-
dc.subject.keywordMSI-
dc.subject.keyworddMMR-
dc.subject.keywordfusion genes-
dc.subject.keywordpancreatic cancer-
dc.contributor.alternativeNameShin, Jae Il-
dc.contributor.affiliatedAuthor신재일-
dc.citation.volume39-
dc.citation.number1-
dc.citation.startPage227-
dc.identifier.bibliographicCitationJOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH, Vol.39(1) : 227, 2020-10-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pediatrics (소아과학교실) > 1. Journal Papers

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