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Glucose Transporter-1 (GLUT-1) Expression is Associated with Tumor Size and Poor Prognosis in Locally Advanced Gastric Cancer.

Chenqing YinBin GaoJu YangJingbo Wu
Published in: Medical science monitor basic research (2020)
BACKGROUND The clinicopathological parameters associated with glucose transporter-1 (GLUT-1) expression in advanced gastric cancer are still controversial. This study aimed to determine the clinicopathological parameters and prognosis associated with GLUT-1 expression in advanced gastric cancer. MATERIAL AND METHODS The GLUT-1 expression level of 234 consecutive gastric cancer samples was detected by immunohistochemical staining and evaluated by semiquantitative analysis. The clinicopathological data and expression level of GLUT-1 of enrolled patients were retrospectively analyzed with univariate and multivariate analyses. RESULTS Tumor size, depth of invasion, and Lauren classification were independent factors related to GLUT-1 expression (P<0.05). Within advanced gastric cancer, tumor size and Lauren type were independent factors associated with GLUT-1 (P=0.011, P<0.001, respectively). The mean survival time of GLUT-1-positive patients with stage M0 advanced gastric cancer who had undergone radical gastrectomy was shorter than that of GLUT-1-negative patients (61.26±6.12 versus 80.88±7.38, P=0.044). GLUT-1 was an independent prognosis factor in locally advanced gastric cancer patients who had undergone radical gastrectomy (hazard ratio [HR] 1.769, P=0.046). The mean survival time of adjuvant chemotherapy was significantly better than no adjuvant chemotherapy in the GLUT-1-positive group (71.10±6.88 versus 24.65±8.69, P<0.001) and in the GLUT-1 negative group (87.48±7.99 versus 49.39±11.71, P<0.001). CONCLUSIONS Tumor size and Lauren type independently affected GLUT-1 expression in advanced gastric cancer. GLUT-1 was not only related to poor prognosis but also predicted to be a metabolic biomarker for intestinal type in locally advanced gastric cancer. The relationship among GLUT-1, hepatic metastasis and chemotherapy regimens, and mechanism of chemotherapy responses related to GLUT-1 should be further investigated.
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