Proliferation kinetics and apoptosis of serrated adenoma of the colorectum

Authors

  • Koji Komori,

    1. Division of Molecular and Diagnostic Pathology, Department of Molecular Genetics and
    2. Department of Surgery, Graduate School of Medicine, Division of Surgical Oncology, Nagoya University, Nagoya, Japan
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    • *

      The first two authors (K. Komori and Y. Ajioka) have contributed equally to this work.

  • Yoichi Ajioka,

    1. Division of Molecular and Functional Pathology, Department of Cellular Function, Graduate School of Medical and Dental Sciences, Course for Molecular and Cellular Medicine, Niigata University and
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    • *

      The first two authors (K. Komori and Y. Ajioka) have contributed equally to this work.

  • Hidenobu Watanabe,

    1. Division of Molecular and Functional Pathology, Department of Cellular Function, Graduate School of Medical and Dental Sciences, Course for Molecular and Cellular Medicine, Niigata University and
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  • Koji Oda,

    1. Department of Surgery, Graduate School of Medicine, Division of Surgical Oncology, Nagoya University, Nagoya, Japan
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  • Yuji Nimura

    1. Department of Surgery, Graduate School of Medicine, Division of Surgical Oncology, Nagoya University, Nagoya, Japan
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Yoichi Ajioka, MD, Division of Molecular and Functional Pathology, Department of Cellular Function, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, Niigata 951-8510, Japan. Email: ajioka@med.niigata-u.ac.jp

Abstract

To elucidate the proliferation kinetics and cell loss by apoptosis of serrated adenoma (SA) of the colorectum, we performed Ki-67 immunohistochemistry and the terminal deoxynucleotidyl transferase (TdT)-mediated biotinylated deoxyuridine-triphosphate nick-end labeling (TUNEL) method for 24 SA, and compared the results to those of normal colonic mucosa (n = 15), hyperplastic polyp (HP) (n = 18) and traditional tubular adenoma (TA) (n = 55). The growth fraction (Ki-67 labeling index) of SA was 18.8%, which was significantly lower than those of TA (40.1%) and HP (23.8%), while the apoptotic index of SA (0.14%) was significantly lower than that of TA (1.17%). The proliferative compartment in SA was distributed either basally (47%, 60/117 crypts), or in the intermediate portion (51.3%, 55/117 crypts), and there was no superficial translocation of the proliferative compartment, which was seen in 81.2% (361/445 crypts) of TA crypts. These results indicate that SA is a tumor with low proliferative activity and its growth would be maintained by a low extent of cell loss by apoptosis. The results also indicate the neoplastic process in SA is characterized by the disorder of cell migration, maturation and exfoliation similar to HP, and its epithelial cell maturation and migration occasionally occur bidirectionally, toward the surface and to the bottom of the crypt.

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