Totally, 1423 patients from nineteen studies were included to assess the relationships between GLUT1 and clinicopathological parameters, the pooled OR indicated that positive GLUT1 expression was significantly related with classification (adenocarcinomas vs. squamous carcinomas, OR = 0.276, 95% CIs: 0.117-0.651, P = 0.003), tumor differentiation (G3-4 vs. G2~1, OR = 1.944, 95% CIs: 1.384-2.730; P < 0.001), lymph node metastasis (positive vs. negative, OR = 3.65, 95% CIs: 1.82-7.32, P < 0.001),tumor size (large tumor size vs. small tumor size, OR = 2.03, 95% CI: 1.42-2.91, P < 0.001), and advanced tumor stages (OR = 2.527, 95% CIs: 1.325-4.820).
The value of the maximum standardized uptake value (SUV<sub>max</sub>) for [<sup>18</sup>F]FAMT was significantly correlated with PD-L1 (E1L3N) expression, Glut1, and the SUV<sub>max</sub> for [<sup>18</sup>F]FDG in patients with histological results of adenocarcinoma (AC) and advanced disease.
Consistent with an increased transcriptional response to hypoxia in pancreatic adenocarcinomas bearing KDM6A inactivation, we showed that mutation or reduced KDM6A expression in SPNs is associated with increased expression of the HIF1α-regulated protein GLUT1 at both primary and metastatic sites.
GLUT1-positive adenocarcinoma patients had a lower OS than GLUT1-negative patients (p<0.001), whereas CAIX-positive and CAIX-negative patients showed similar OS rates (p=0.226).
These findings combined with survival analysis of public datasets suggest that MCT1 and GLUT1 may be potential prognostic markers in adenocarcinoma and druggable targets in squamous cell carcinoma.
The GLUT1 overexpression status was significantly correlated with gender (women 31.9% vs. men 54.5%, P<0.0001), smoking status (never smoker 31.4% vs. smoker 59.4%, P<0.0001) and pathological subtypes (adenocarcinoma 36.4% vs. non‑adenocarcinoma 74.5%, P<0.0001).
In addition, localized AC in situ revealed a considerably higher positive expression rate and similar degrees of overexpression for both Glut-1 and Glut-3 compared with AC-mixed.
However, both markers were more strongly expressed in serous adenocarcinomas (HIF-1alpha, 3 + 100%; GLUT-1, 3+76%) than in mucinous adenocarcinomas (HIF-1alpha, 3 + 61%; GLUT-1, 3 + 28%).
The present study supports the hypothesis that tumor cell differentiation in combination with overexpression of GLUT-1 and GLUT-3 determine the extent of FDG accumulation and that squamous cell carcinomas accumulate more FDG than adenocarcinomas or large cell carcinomas.
We immunohistochemically examined 47 specimens of surgically resected adenocarcinomas to evaluate the expression of the biological markers p53, Ki-67, vascular endothelial growth factor (VEGF) and glucose transporter-1 (Glut-1).
Forty-four (83%) of 53 colorectal adenocarcinomas expressed Glut1, and, of these, tumors in which >50% of the cancer cells expressed Glut1 had a significantly higher incidence of metastasis to the lymph nodes (P = 0.0001).