Depressed Colorectal Cancer: A New Paradigm in Early Colorectal Cancer

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  • Shin-ei Kudo
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Yuta Kouyama
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Yushi Ogawa
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Katsuro Ichimasa
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Tsuyoshi Hamada
    Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan;
  • Kazuki Kato
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Koki Kudo
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Takaaki Masuda
    Kyushu University Beppu Hospital, Beppu, Japan;
  • Hajime Otsu
    Kyushu University Beppu Hospital, Beppu, Japan;
  • Masashi Misawa
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Yuichi Mori
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Toyoki Kudo
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Takemasa Hayashi
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Kunihiko Wakamura
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Hideyuki Miyachi
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Naruhiko Sawada
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Toshiro Sato
    Department of Gastroenterology, Keio University School of Medicine, Tokyo, Japan;
  • Tatsuhiro Shibata
    Division of Cancer Genomics, National Cancer Center Research Institute and Laboratory of Molecular Medicine, Tokyo, Japan;
  • Shigeharu Hamatani
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Tetsuo Nemoto
    Department of Pathology, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Fumio Ishida
    Digestive Disease Center, Showa University Northern Yokohama Hospital, Yokohama, Japan;
  • Atsushi Niida
    Department of Pathology, The Jilei University School of Medicine, Tokyo, Japan;
  • Satoru Miyano
    Division of Health Medical Computational Science, Health Intelligence Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan;
  • Masanobu Oshima
    Division of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan;
  • Shuji Ogino
    Program in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA;
  • Koshi Mimori
    Kyushu University Beppu Hospital, Beppu, Japan;

説明

<jats:sec> <jats:title>INTRODUCTION:</jats:title> <jats:p>In contrast to most colorectal carcinomas arising from pedunculated or sessile protruded adenomas, submucosal-invasive (pT1) colorectal carcinoma exhibiting a depressed surface (hereinafter, “depressed colorectal carcinoma,” identified by means of high-definition endoscopy) is considered to be derived from depressed precursors. We hypothesized that depressed colorectal neoplasms have unique clinicopathological features different that are different from those of protruded and flat colorectal neoplasms.</jats:p> </jats:sec> <jats:sec> <jats:title>METHODS:</jats:title> <jats:p>We classified 27,129 colorectal neoplasms (909 pT1 carcinomas and 26,220 adenomas) resected between 2001 and 2017 into depressed (211 carcinomas and 109 adenomas), flat (304 carcinomas and 11,246 adenomas), and protruded subtypes (394 carcinomas and 14,865 adenomas) and compared their clinicopathological features. As exploratory analyses of pT1 carcinomas, we conducted whole-exome sequencing for 19 depressed and 8 protruded subtypes and RNA sequencing for 8 depressed and 8 protruded subtypes.</jats:p> </jats:sec> <jats:sec> <jats:title>RESULTS:</jats:title> <jats:p>pT1 carcinomas were more common in depressed lesions (66%) than in protruded (2.6%) and flat lesions (2.6%) (<jats:italic toggle="yes">P</jats:italic> < 0.001). Compared with nondepressed pT1 carcinomas, depressed pT1 carcinomas were positively correlated with lymphovascular invasion, tumor budding, and massive submucosal invasion and inversely correlated with the presence of an adenoma component (all <jats:italic toggle="yes">P</jats:italic> < 0.001). Depressed adenomas were more likely to contain high-grade dysplasia than nondepressed adenomas (49% vs 11%, <jats:italic toggle="yes">P</jats:italic> < 0.001). A <jats:italic toggle="yes">KRAS</jats:italic> mutation was observed only in one of the 19 depressed pT1 carcinomas. Relative to protruded carcinomas, depressed carcinomas generally exhibited higher expression of genes related to angiogenesis and epithelial-mesenchymal transition.</jats:p> </jats:sec> <jats:sec> <jats:title>DISCUSSION:</jats:title> <jats:p>Depressed colorectal neoplasms may harbor a unique combination of malignant histopathological phenotypes and molecular features.</jats:p> </jats:sec>

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