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要旨●内視鏡後発生大腸癌(PCCRC)は,従来は内視鏡の見逃しによる発生と考えられてきたが,近年のゲノム解析により,その発生機序が多様であることが明らかになってきた.本稿では,MSI-high・CIMP-high・BRAFV600E変異を特徴とするserrated pathway由来腫瘍や,PIK3CA変異に伴う急速進行型腫瘍など,生物学的特徴に基づくPCCRCの多様性を整理した.また,flat adenoma由来の従来型腺腫の見逃しも依然として重要な要因である.これら分子特性の理解は,PCCRCの早期発見やサーベイランス戦略の最適化に寄与すると考えられる.
Traditionally, post-colonoscopy colorectal cancer(PCCRC)has been recognized as a consequence of lesions missed during colonoscopy. However, according to recent genomic analyses, its underlying mechanisms are heterogeneous. In this review, we summarize the biological diversity of PCCRC, including tumors with MSI-high status, CIMP-high phenotype, and BRAF mutations arising from the serrated pathway, as well as rapidly progressive tumors associated with PIK3CA mutations. Overlooked conventional adenomas, particularly flat ones, also remain an important etiological factor. Improving our knowledge of these molecular features may help improve early detection and optimized surveillance strategies for PCCRC.

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