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

Authors
 Claudio Luchini  ;  Gaetano Paolino  ;  Paola Mattiolo  ;  Maria L Piredda  ;  Alessandro Cavaliere  ;  Marina Gaule  ;  Davide Melisi  ;  Roberto Salvia  ;  Giuseppe Malleo  ;  Jae Il Shin  ;  Sarah Cargnin  ;  Salvatore Terrazzino  ;  Rita T Lawlor  ;  Michele Milella  ;  Aldo Scarpa 
Citation
 JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH, Vol.39(1) : 227, 2020-10 
Journal Title
 JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH 
ISSN
 0392-9078 
Issue Date
2020-10
Keywords
BRAF ; KRAS ; MSI ; dMMR ; fusion genes ; pancreatic cancer
Abstract
Pancreatic 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.
Files in This Item:
T202004749.pdf Download
DOI
10.1186/s13046-020-01732-6
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pediatrics (소아과학교실) > 1. Journal Papers
Yonsei Authors
Shin, Jae Il(신재일) ORCID logo https://orcid.org/0000-0003-2326-1820
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/180426
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