作者: Yoshiaki Kumon , Saburo Sakaki , Katsuyuki Hamada , Kohji Sato , Kou Nakagawa
DOI:
关键词: Cancer research 、 Neovascularization 、 Vascular endothelial growth factor 、 Angiogenesis 、 Biology 、 Gene product 、 Genetic transfer 、 Genetic enhancement 、 Tumor suppressor gene 、 Glioma
摘要: Recent studies have indicated that the loss of p16 is a frequent event in progression malignant gliomas. The promotes acquisition characteristics gliomas, which are among most angiogenic all human tumors. High-grade gliomas distinguished from low-grade by intense angiogenesis addition to their p16. New therapeutic strategies aimed at inhibiting tumor on basis molecular mechanisms theoretically attractive. Here we evaluate effect gene replacement Infection with recombinant replication-defective adenovirus vector containing cDNA wild-type significantly reduced expression vascular endothelial growth factor, thought be pivotal mediator angiogenesis, p16-deleted glioma cells. Restoring into cells markedly inhibited induced vivo. Furthermore, neovascularization more potently than did p53 transfer. These findings indicate plays an important role regulation suggesting novel function gene.