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要旨 目的:大腸低分化腺癌の臨床病理学的,分子病理学的検討を行った.対象と方法:低分化腺癌42例,分化型腺癌57例を用いた.低分化腺癌は,大胞巣型,小胞巣型,索状型,に分類した.低分化腺癌は分化型成分と低分化成分に分けて解析を行った(32/42例).腫瘍細胞の粘液形質,p53,Ki-67,β- catenin,MLH1およびMSH2の発現は免疫組織化学的に行った.Ki-rasおよびBRAF変異解析はパイロシークエンス法で解析した.MSIはPCR-microsatellite法を用いて行った.結果:各低分化腺癌はリンパ管侵襲像の頻度が高く,小胞巣型は静脈侵襲像の頻度が高かった.p53過剰発現は分化型腺癌と比較して差がなかった.大胞巣型ではKi-ras変異の頻度が低かったが,BRAF変異は高い傾向があった.MSIは大胞巣型で頻度が高かったが,索状型にはみられなかった.結語:低分化腺癌は分化型腺癌を経由して発生することが多いが,臨床病理学的,分子病理学的にも異なっていた.
We studied 42 sporadic PDAs(poorly differentiated adenocarcinomas)and compared them with 57 DTAs(differentiated-type adenocarcinomas). In the present study, PDAs were classified into three types of LSSN(large-sized solid nest), SSN(small-sized solid nest)and trabecular types. Potential clinicopathologic and molecular differences between the study groups were assessed. Differentiated area was often found in PDAs. Lymphatic invasion was significantly more common in the PDAs than in DTAs. p53 overespression of PDAs was similar to DTA groups. Although frequency of Ki-ras mutation in PDAs was lower than that of DTAs, BRAF mutation was frequently detected in PDAs. LSSN had high frequency MSI phenotype, compared with DTAs. Colorectal poorly differentiated adenocarcinoma seems to be a distinct clinicopathologic variant of CRC.
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