Multivariate modeling has demonstrated that the proliferation index （PI） of tumor cells is one of the strongest prognostic factors related to the survival of patients with astrocytic tumors. Studies have indicated that the glioma regenerative cells derived from nestin-positive （N^＋） cells after chemotherapy. Early removal of N^＋cells can block the malignant progress of tumor.2 However, few studies compared the PI between N^＋cells and glial fibrillary acidic protein （GFAP）-positive （GFAP^＋） cells in human astrocytic tumors. In the present study, we investigated the distribution and proliferation ofN^＋cells and GFAP^＋ cells in human astrocytic tumors to clarify the role these cells play in the cytopathology of these tumors.
Yang LijuanWang XingfuChen YupengZhang ShengZhen ShimingLin Zhixiong
Although we have made great progress in understanding tumor pathogenesis through studies on gene mutation and cancer stem cells, the clinical outcome continues to be unfavorable for many cancers. The biological characteristics of cancers including autonomous proliferation, invasion, metastasis, and post-treatment recurrence result from interactions between cancers and their microenvironment, which involves complex molecular interactions.
Background Previous researches have indicated that glioma invasion may occur within a tumor-host microecology, and that fibronectin may be involved in glioma invasion as an important component of the extracellular matrix. However, how the interaction between tumor cells and vascular endothelial cells affects glioma invasion is poorly understood. The aim of this study was to investigate the effects of the interaction between tumor cells and vascular endothelial cells on glioma invasion, and the relationship of this interaction to fibronectin. Methods The localization of fibronectin in different brain astrocytoma tissues was determined by immunohistochemistry Then, vascular endothelial cells and glioma cells were co-cultured in a Transwell co-culturing system. Fibronectin expression was detected by reverse transcriptase-polymerase chain reaction, immunocytochemistry, and enzyme-linked immunosorbent assay. Additionally, the influence of the interaction between tumor cells and vascular endothelial cells on glioma cell invasion was determined by an in vitro rapid invasion test. Results In brain astrocytoma tissues, fibronectin was present on the endothelial cells, in the extracellular matrix. Fibronectin expression was greater in higher grade tumors than in lower grade tumors. The interaction of glioma cells and vascular endothelial cells in vitro induced fibronectin release from vascular endothelial cells, which in turn stimulated glioma cell migration. This effect was inhibited by fibronectin blocking antibody. Conclusion Glioma cells may induce vascular epithelial cells to express fibronectin, and in turn fibronectin could promote glioma cell invasion.
Glioma-related edema(GRE) is a significant contributor to morbidity and mortality from glioma.GRE is a complicated process involving not only peritumoral edema but also the water content of the tumor body.In terms of etiology,this condition derives from both GRE in the untreated state and GRE secondary to clinical intervention,and different cell types contribute to distinct components of GRE.Peritumoral edema was previously believed to loosen glioma tissue,facilitating tumor-cell invasion;however,the nutrition hypothesis of the tumor microecosystem suggests that tumor cells invade for the sake of nutrition.Edema is the pathologic consequence of the reconstructed trophic linkage within the tumor microecosystem.Glioma cells induce peritumoral brain edema via an active process that supplies a suitable niche for peritumoral invasive cells,suggesting that glioma-related peritumoral brain edema is determined by the invasive property of tumor cells.There are differences between pivotal molecular events and reactive molecular events in the development of GRE.Molecular therapy should target the former,as targeting reactive molecular events will produce undesired or even adverse results.At present,brain glioma angiogenesis models have not been translated into a new understanding of the features of brain images.The effect of these models on peritumoral brain edema is unclear.Clinical approaches should be transformed on the basis of new knowledge of the molecular mechanism underlying GRE.Exploring clinical assessment methods,optimizing the existing control strategy of GRE,and simultaneously developing new treatments are essential.
