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Traditional serrated adenoma with BRAF mutation is associated with synchronous/metachronous BRAF ‐mutated serrated lesions
Author(s) -
Tsai JiaHuei,
Cheng ChienHsuan,
Chen ChienChuan,
Lin YuLin,
Lin LiangIn,
Chen MeiLing,
Liau JauYu
Publication year - 2016
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/his.12814
Subject(s) - kras , hyperplastic polyp , microsatellite instability , mutation , colorectal cancer , cancer research , adenoma , medicine , pathology , cancer , biology , colonoscopy , genetics , gene , microsatellite , allele
Aims To determine whether traditional serrated adenoma ( TSA ) results in an increased risk of developing subsequent serrated polyps or colorectal cancer ( CRC ). Methods and results We recruited 111 patients with an index TSA , and analysed the pathological and molecular features of their synchronous/metachronous serrated lesions. Fifty hyperplastic polyps, 14 sessile serrated adenomas, an additional 27 TSA s and 17 CRC s were identified from 46 patients. Twenty‐seven percent of TSA s showed a precursor serrated polyp in the periphery and were strongly correlated with BRAF mutation ( P < 0.001). Serrated polyps occurred more commonly in patients with BRAF ‐mutated index TSA s than in patients with KRAS ‐mutated index TSA s. BRAF ‐mutated index TSA s were strongly associated with a right‐sided location and BRAF mutation of synchronous/metachronous serrated polyps ( P = 0.013 and P = 0.005, respectively). The 17 CRC s occurred more frequently in women, and were characterized by a high BRAF mutation rate (59%), a positive CpG island methylator phenotype (59%), and stable or low levels of microsatellite instability (77%). Conclusions BRAF ‐mutated TSA is distinct from KRAS ‐mutated TSA in predisposing to the acquisition of subsequent serrated neoplasia. This indicates the presence of an intestinal field defect in the tumour microenvironment that results in tumour initiation and malignant progression.