作者: Takuya Furuta , Mitsutoshi Nakada , Kouichi Misaki , Yasunori Sato , Yutaka Hayashi
DOI: 10.1007/S10014-013-0142-4
关键词: Pathology 、 Temozolomide 、 Bevacizumab 、 Protein kinase A 、 Autocrine signalling 、 Signal transduction 、 Phosphorylation 、 Angiogenesis 、 Protein kinase B 、 Medicine
摘要: We treated a case of recurrent glioblastoma (GBM) with bevacizumab and assessed its effect biologically. A 55-year-old man left frontal lobe GBM was experiencing recurrence 7 months postoperation. administered concomitant temozolomide (TMZ). Follow-up magnetic resonance imaging (MRI) showed dramatic but temporal tumor reduction; however, the patient died re-recurrent disease 6 months after beginning bevacizumab. obtained an autopsy analyzed detailed molecular change. In specimen, quantity microvessels significantly reduced. Vascular endothelial growth factor receptor (VEGFR) 1 VEGFR2 were downregulated, most likely due to negative feedback mechanism by blocking VEGF signaling. Matrix metalloproteinase (MMP)-2 membrane-type MMP upregulated, resulting in higher activation MMP-2 specimen. MIB-1 staining index phosphorylation levels p44/42-mitogen-activated protein kinase did not change, whereas phosphorylated B (Akt) decreased suggesting compensation and/or amplification other proliferative signaling pathways such as suppression apoptosis Consequently, might inhibit autocrine loop, which then causes change expression related only enhancement invasion also maintenance proliferation.