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Morphological and molecular characterization of colorectal sessile serrated lesions with dysplasia

发育不良 克拉斯 PDGFRA公司 病理 PTEN公司 增生性息肉 神经母细胞瘤RAS病毒癌基因同源物 结直肠癌 医学 生物 癌症研究 癌症 内科学 遗传学 结肠镜检查 PI3K/AKT/mTOR通路 细胞凋亡 主旨 间质细胞
作者
Filippo Cappello,Valentina Angerilli,Luca Dal Santo,Giada Munari,Marianna Sabbadin,Marcello Mele,Gianmaria Pennelli,Claudio Luchini,Paola Parente,Stefano Lazzi,Matteo Fassan
出处
期刊:Pathology Research and Practice [Elsevier BV]
卷期号:240: 154214-154214
标识
DOI:10.1016/j.prp.2022.154214
摘要

In sessile serrated lesions (SSLs) with adenomatous dysplasia, the dysplastic component and the serrated component without dysplasia should be considered as part of the same lesion, classified as SSL with dysplasia. However, some of these lesions may actually represent collisions between a serrated polyp and a conventional adenoma. Further supporting the "collision theory", conventional adenomatous dysplasia may be found in association with hyperplastic polyps (HPs). In order to determine the molecular and biological landscape of conventional type dysplasia in serrated lesions, we collected 17 cases of colorectal serrated lesions with adenomatous dysplasia, classifying them as SSL with dysplasia (n = 10) or as mixed lesions comprising a HP component and a conventional adenomatous component (n = 7). We characterized the dysplastic and the non-dysplastic component of each lesion, after microdissection, through the targeted mutational analysis of 11 commonly altered genes in colorectal cancer (AKT1, APC, BRAF, CTNNB1, KIT, KRAS, NRAS, PDGFRA, PIK3CA, PTEN and TP53). We also characterized MMR and p53 status by immunohistochemistry. Overall, 14/17 (82.4 %) cases harbored a mutation in at least one of the two components. The most altered genes were BRAF in 10/17 (58.8 %) cases, APC in 2/17 (11.8 %) and TP53 in 4/17 (23.5 %). Among the SSL with dysplasia, the mutational profile was concordant between the two components in 7/10 (70 %) cases, while among the mixed lesions, the mutational profile was concordant in 1/7 (14.3 %). In all but two cases of SSL with dysplasia, MMR status was concordant between the two components of the serrated lesions. Our findings suggest that adenomatous dysplasia may develop in SSL as part of the serrated lesion, even if some SSL with dysplasia may actually be collision lesions. On the other hand, the polyps that are morphologically classifiable as mixed lesions composed of a HP and a conventional adenomatous component are more likely to be collision lesions.
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