INTESTINE Vol.14 No.6(2-1)


「個人年間予約購読者用全文閲覧サービス」でこの号を見る
特集名 直腸（Rb）癌の謎
題名 ［各論］(1) 鋸歯状病変：直腸と結腸病変の違い -- 腫瘍占居部位別からみた鋸歯状腫瘍の臨床病理学的および分子生物学的特徴
発刊年月 2010年 11月
著者 小西 一男 昭和大学医学部内科学講座消化器内科学部門
著者 片桐 敦 昭和大学医学部内科学講座消化器内科学部門
著者 矢持 淑子 昭和大学医学部第二病理
著者 矢野 雄一郎 昭和大学医学部内科学講座消化器内科学部門
著者 久保田 祐太郎 昭和大学医学部内科学講座消化器内科学部門
著者 村元 喬 昭和大学医学部内科学講座消化器内科学部門
著者 吉川 望海 昭和大学病院内視鏡センター
著者 太田 秀一 昭和大学医学部第二病理
著者 井廻 道夫 昭和大学医学部内科学講座消化器内科学部門
【 要旨 】 近年，過形成性ポリープから鋸歯状腫瘍を経て大腸癌に至るserrated pathwayの存在が注目されている．われわれは，大腸鋸歯状腫瘍86病変〔traditional serrated adenoma（TSA）56病変，sessile serrated adenoma（SSA）15病変，mixed polyp（MP）15病変〕を対象とし，これら86病変を直腸群22例，左側結腸群30例，右側結腸群34例の3群に分類し，臨床病理学的および分子生物学的に比較検討を行った．直腸群・左側結腸群では，約80％がTSAであったのに対し，右側結腸群では約半数の病変がSSAあるいはMPであった．また，直腸群では，KRAS変異がほかの群に比べ有意に高率であったのに対し，CpG island methylator phenotype（CIMP）は，右側結腸群においてほかの群に比して有意に高率であった．左側大腸，とくに直腸では，過形成性ポリープからTSAを介し，KRAS変異を特徴とする発癌のpathway，右側大腸では，過形成性ポリープからSSAを介し，CIMPを特徴とする発癌のpathwayが存在する可能性が推定された．
Theme Mystery concerning the lower rectum
Title Clinicopathological and molecular differences between rectal and colonic serrated neoplasias
Author Kazuo Konishi Division of Gastroenterology, Department of Medicine, Showa University School of Medicine
Author Atsushi Katagiri Division of Gastroenterology, Department of Medicine, Showa University School of Medicine
Author Toshiko Yamochi Second Department of Pathology, Showa University School of Medicine
Author Yuichiro Yano Division of Gastroenterology, Department of Medicine, Showa University School of Medicine
Author Yutaro Kubota Division of Gastroenterology, Department of Medicine, Showa University School of Medicine
Author Takashi Muramoto Division of Gastroenterology, Department of Medicine, Showa University School of Medicine
Author Nozomi Yoshikawa Endoscopic Center, Showa University Hospital
Author Hidekazu Ota Second Department of Pathology, Showa University School of Medicine
Author Michio Imawari Division of Gastroenterology, Department of Medicine, Showa University School of Medicine
[ Summary ] Recently, it has been reported that some hyperplastic polyps may develop from serrated neoplasias into cancer. However, it remains unclear whether there are different mechanisms related to progression of cancer in the colon versus the rectum. We examined a total of 86 serrated neoplasias (SNs) (56 traditional serrated adenomas [TSAs], 15 sessile serrated adenomas [SSAs] and 15 mixed polyps [MPs]). Of these, 22 tumors were located in the rectum (R-group), 30 were in the distal colon (D-group) and 34 were in the proximal colon (P-group). We evaluated clinicopathological and molecular findings in the three groups. Approximately 80 % of R and D-group tumors were TSAs, whereas a half of P-group tumors were SSAs or MPs. The incidence of KRAS mutations was significantly higher in the R-group lesions than in other groups. However, we observed a significantly higher incidence of CpG island methylator phenotype (CIMP) in P-group tumors than other groups. These findings suggest that the development of proximal and distal SNs, especially rectal SNs, may occur through the sessile and traditional serrated pathways.
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