4.4 Article

MCM4 and MCM7, potential novel proliferation markers, significantly correlated with Ki-67, Bmil, and cyclin E expression in esophageal adenocarcinoma, squamous cell carcinoma, and precancerous lesions

Journal

HUMAN PATHOLOGY
Volume 57, Issue -, Pages 126-135

Publisher

W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.humpath.2016.07.013

Keywords

MCM4; MCM7; Ki-67; Esophageal adenocarcinoma; Esophageal squamous cell carcinoma; Barrett's esophagus

Categories

Funding

  1. NIH [NM R01-DK100342]

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Minichromosomal maintenance (MCM) proteins are participants of DNA replication and may represent more accurate markers in determining the proliferative fraction within a tumor than proliferative marker Ki-67. Our study investigated the correlation between MCM4 and MCM7 expression and Ki-67, Bmil, and cyan E expression in esophageal adenocarcinoma, squamous cell carcinoma, and precancerous lesions. MCM4 and MCM7 expression had similar distribution as Ki-67 and Emil expression in esophageal carcinoma and pre cancerous lesions. The mean percentage of MCM4, MCM7, and Ki-67 expression increased from squamous epithelium (5.5%, 7.3%, and 5.9%, respectively), to columnar cell metaplasia (11.2, 13.5%, and 3,.4%), Barrett's esophagus (27.7%, 35.3%, and 8.3%), low-grade dysplasia (42.6%, 52.2%, and 12.9%), high-grade dysplasia (63.2%, 77.7%, and 29.6%), adenocarcinoma (61.3%, 75.5%, and 24.5%), and squamous cell 'carcinoma (74.1, 85.4%, and 36.3%). The percentages of MCM4 and MCM7 expression were significantly higher than Ki-67 expression. Using univariate analysis we found a high percentage of MCM4 expression (>70%) to be significantly associated with lymph node metastasis and shorter survival in the adenocarcinoma group. We also demonstrated the percentage of MCM4 and MCM7 expression to be significantly correlated with Ki-67, Bmil, and cyclin E expression in esophageal carcinoma and precancerous lesions. MCM4 and MCM7 may serve as more sensitive proliferative markers for the evaluation of esophageal lesions. (C) 2016 The Authors. Published by Elsevier Inc.

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