Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Gynecol Oncol. 2011 Apr;121(1):181-6. doi: 10.1016/j.ygyno.2010.11.019. Epub 2010 Dec 16.
GLUT-1 is involved at various steps in the processes of tumor progression. The objective of this study was to examine the relationship between GLUT-1 expression and tumor proliferation and angiogenesis in epithelial ovarian carcinoma.
Specimens from 213 patients with epithelial ovarian carcinoma were evaluated by immunohistochemistry for GLUT-1, Ki-67, and vascular endothelial growth factor. Tumor microvessel density was assessed with CD34 immunostaining. We investigated the relationships between GLUT-1 expression and clinicopathologic characteristics, tumor angiogenesis (tumor MVD and vascular endothelial growth factor expression), and tumor proliferation (Ki-67). The effect of GLUT-1 expression on patient survival and on the volume of residual disease after cytoreduction was determined.
There was a significant positive correlation between expression of GLUT-1, Ki-67, and microvessel density. In univariate survival analysis, high GLUT-1 expression, high Ki-67 expression and high tumor microvessel density showed a significant impact on patient survival (p=0.0001). In multivariate analysis including patients with all tumor stages, after controlling for age, race, stage, grade, MVD, and the 3 markers (GLUT-1, Ki-67 and VEGF), only age (HR 1.5; 95% CI 1-2.3), stage (HR 3.6; 95% CI 1.8-7.5) and grade (HR 2.3; 95% CI 1.2-4.5) retained their significance as independent poor prognostic factors. Tumors simultaneously overexpressing GLUT-1 and Ki-67 were less likely to be optimally cytoreduced as compared to tumors overexpressing only one or neither of those two markers (OR: 3.8, p=0.01).
Expression of GLUT-1 correlates with tumor proliferation and microvessel density in epithelial ovarian carcinoma. In addition, patients with rapidly proliferating advanced stage tumors overexpressing GLUT-1 have a lesser chance for optimal cytoreduction.
GLUT-1 参与肿瘤进展的多个步骤。本研究的目的是研究 GLUT-1 表达与上皮性卵巢癌中肿瘤增殖和血管生成的关系。
通过免疫组织化学法检测 213 例上皮性卵巢癌患者标本中的 GLUT-1、Ki-67 和血管内皮生长因子。用 CD34 免疫染色评估肿瘤微血管密度。我们研究了 GLUT-1 表达与临床病理特征、肿瘤血管生成（肿瘤 MVD 和血管内皮生长因子表达）和肿瘤增殖（Ki-67）之间的关系。还确定了 GLUT-1 表达对患者生存和细胞减灭术后残留疾病体积的影响。
GLUT-1 表达、Ki-67 表达和微血管密度之间存在显著正相关。在单因素生存分析中，GLUT-1 高表达、Ki-67 高表达和肿瘤微血管密度高均对患者生存有显著影响（p=0.0001）。在包括所有肿瘤分期的多因素分析中，在控制年龄、种族、分期、分级、MVD 和 3 种标志物（GLUT-1、Ki-67 和 VEGF）后，只有年龄（HR 1.5；95%CI 1-2.3）、分期（HR 3.6；95%CI 1.8-7.5）和分级（HR 2.3；95%CI 1.2-4.5）仍然是独立的不良预后因素。与仅表达一种或两种标志物之一的肿瘤相比，同时过度表达 GLUT-1 和 Ki-67 的肿瘤更不可能进行最佳细胞减灭（OR：3.8，p=0.01）。
GLUT-1 在卵巢上皮性癌中与肿瘤增殖和微血管密度相关。此外，表达 GLUT-1 的快速增殖晚期肿瘤患者进行最佳细胞减灭的机会较少。
