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BRAF V600E immunohistochemistry demonstrates that some sessile serrated lesions with adenomatous dysplasia may represent collision lesions
Author(s) -
Bettington Mark,
Liu Cheng,
Gill Anthony,
Walker Neal,
Leggett Barbara,
Whitehall Vicki,
Rosty Christophe
Publication year - 2019
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.13851
Subject(s) - dysplasia , medicine , pathology , mlh1 , adenoma , immunohistochemistry , cancer , colorectal cancer , dna mismatch repair
Aims Sessile serrated lesions ( SSL ) with dysplasia are uncommon polyps with a high risk of rapid malignant transformation. Most of these lesions have a BRAF mutation and 75% show loss of MLH 1 expression in their dysplastic component. Different morphological patterns of dysplasia occurring in these polyps have recently been described. We hypothesised that a subset of SSL s with dysplasia mimicking the dysplasia seen in conventional adenoma (adenomatous dysplasia) may represent a collision lesion between an ordinary SSL and a conventional adenoma. Methods and results We selected 80 SSL s with dysplasia, including 19 with adenomatous dysplasia, 18 with serrated dysplasia and 43 with dysplasia not otherwise specified ( NOS ). BRAF mutation analysis was performed using molecular testing (allelic discrimination) and the mutation‐specific BRAF ‐V600E immunohistochemistry (clone VE 1). The overall BRAF ‐ V600E mutation rate was 84% in all lesions, 68% in SSL s with adenomatous dysplasia, 89% in SSL s with serrated dysplasia and 88% in SSL s with dysplasia NOS . From the 63 SSL s with dysplasia that were positive for the BRAF ‐ V600E mutation, a negative BRAF ‐V600E immunostaining was observed in the dysplastic component of 83% of SSL s with adenomatous dysplasia, 0% of SSL s with serrated dysplasia and 3% of SSL s with dysplasia NOS ( P < 0.001). Conclusions These findings suggest that SSL s with adenomatous dysplasia may not represent advanced SSL s, but instead may be a collision between a non‐dysplastic SSL and a conventional adenoma.