Abstract

Background:Previous studies examining the prognostic value of glucose transporter 1 in breast cancer have yielded inconsistent results. We, therefore, performed a meta-analysis to clarify this issue.Methods:The research was reported according to the preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines. Relevant studies were retrieved from PubMed, Web of Science, EMBASE, and Cochrane library.Results:A total of 7 reports with 1861 patients were finally chosen. GLUT1 overexpression was found to be associated with high histological grade (OR = 3.74, 95% CI = 2.45–5.69, P < .001), negative PR status (OR = 0.33, 95% CI = 0.22–0.49, P < .001), and negative estrogen receptor (ER) status (OR = 0.27, 95% CI = 0.17–0.42, P < .001). However, no significant correlation was seen between GLUT1 levels and presence of lymph node metastasis, tumor size or the status of human epidermal growth factor receptor 2 (HER2). Overexpression of GLUT1 also correlated with a poor overall survival (hazard ratio [HR] = 1.65, 95% confidence interval [CI] = 1.17–2.31, P = .004) and disease-free survival (HR = 2.35, 95% CI = 1.4–3.94, P < .001). No evidence of significant publication bias was found.Conclusion:This meta-analysis indicates that GLUT1 expression is associated with poor prognostic and a series of clinicopathological features in breast cancer. GLUT1 might be a potential biomarker and therapeutic target in breast cancer.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.