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Clinicopathologic significance of GLUT1 expression and its correlation with Apaf-1 in colorectal adenocarcinomas

Authors
Jun, Young JinJang, Se MinHan, Hu LinLee, Kang HongJang, Ki-SeokPaik, Seung Sam
Issue Date
Apr-2011
Publisher
BAISHIDENG PUBLISHING GROUP INC
Keywords
Adenocarcinoma; Colorectum; Glucose transporter-1; Apoptosis-activating factor-1; Prognosis; Survival
Citation
WORLD JOURNAL OF GASTROENTEROLOGY, v.17, no.14, pp.1866 - 1873
Indexed
SCIE
SCOPUS
Journal Title
WORLD JOURNAL OF GASTROENTEROLOGY
Volume
17
Number
14
Start Page
1866
End Page
1873
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/168755
DOI
10.3748/wjg.v17.i14.1866
ISSN
1007-9327
Abstract
AIM: To investigate the role of glucose transporter 1 (GLUT1) expression in colorectal carcinogenesis and evaluate the correlation with clinicopathological parameters and apoptosis-activating factor-1 (Apaf-1) expression in colorectal adenocarcinomas. METHODS: We used tissue microarrays consisting of 26 normal mucosa, 50 adenomas, 515 adenocarcinomas, and 127 metastatic lesions. Medical records were reviewed and clinicopathological analysis was performed. RESULTS: GLUT1 expression was absent in normal mucosa and low or moderately apparent in 19 cases (38.0%) of 50 adenomas. However, GLUT1 expression was detected in 423 (82.1%) of 515 adenocarcinomas and in 96 (75.6%) of 127 metastatic lesions. GLUT1 expression was significantly correlated with female gender (P = 0.009), non-mucinous tumor type (P = 0.045), poorer differentiation (P = 0.001), lymph node metastasis (P < 0.001), higher AJCC and Dukes stage (P < 0.001 and P < 0.001, respectively). There was a significant inverse correlation between GLUT1 expression and Apaf-1 expression (P = 0.001). In univariate survival analysis, patients with GLUT1 expression demonstrated poor overall survival and disease-free survival (P = 0.047 and P = 0.021, respectively, log-rank test). CONCLUSION: GLUT1 expression was frequently increased in adenocarcinomas and metastatic lesions. GLUT1 expression was significantly correlated with poorer clinicopathologic phenotypes and survival of patients with colorectal adenocarcinomas.
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