Purpose: This study aimed to investigate whether metabolic tumor volume (MTV) measured from [18 F]-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT) predicts short-term outcome to radiotherapy with or without chemotherapy and disease-free survival (DFS) in patients with pharyngeal cancers. Experimental Design: The MTVs of primary sites with or without neck nodes were measured in 82 patients. Short-term outcome was assessed using the treatment response evaluation by the Response Evaluation Criteria in Solid Tumors and recurrence events during follow-up (complete response/no recurrence or residual disease/recurrence). Results: A total of 64 patients had complete response/no recurrence as of the last follow-up. A cutoff of 40 mL for the MTV was the best discriminative value for predicting treatment response. By univariate analyses, patients with MTV >40 mL showed a significantly lower number of complete response/no recurrence than did patients with MTV ≤40 mL [68.2% versus 87.8%; hazard ratio (HR), 3.34; 95% confidence interval (95% CI), 1.09-10.08; P = 0.03], as is the same in tumor-node-metastasis stage (87.5% for I-II versus 90% for III versus 63.8% for IV; P = 0.02). However, MTV was only a significant predictor of short-term outcome by multivariate analyses (HR, 4.09; 95% CI, 1.02-16.43; P = 0.04). MTV >40 mL indicated a significantly worse DFS than MTV ≤40 mL (HR, 3.42; 95% CI, 1.04-11.26;P = 0.04). The standardized uptake value for the primary tumor did not show any correlation with treatment outcome or DFS. Conclusion: MTV has a potential value in predicting short-term outcome and DFS in patients with pharyngeal cancers. (Clin Cancer Res 2009;15(18):5861-8)
Retinopathy of prematurity (ROP) and proliferative diabetic retinopathy (PDR) are ischemic retinal diseases caused by insufficient vascular network formation and vascular regression in addition to aberrant angiogenesis. We examined the role of angiopoietin-1 (Ang1) in retinal vascular network formation during postnatal development using Ang1 gain- and loss-of-function mouse models, and tested the effects of intraocular administration of Ang1 in an oxygen-induced retinopathy (OIR) mouse model that mimics cardinal features of ROP and PDR. We observed that Ang1 plays a substantial role in the formation of the retinal vascular network during postnatal development and that Ang1 supplementation can rescue vascular retinopathies by simultaneously promoting healthy vascular network formation and inhibiting subsequent abnormal angiogenesis, vascular leakage, and neuronal dysfunction in the retinas of the OIR model. We attribute these Ang1-induced effects to a dual signaling pathway-Tie2 signaling in the vascular region and integrin αvβ5 signaling in the astrocytes. The activation of integrin αvβ5 signaling promoted fibronectin accumulation and radial distribution along the sprouting endothelial cells, which consequently stimulated guided angiogenesis in the retina. These findings shed light on the role of Ang1 in the recovery of ischemic retinopathies such as ROP, PDR, and retinal vascular occlusive disease.
The features and regulation of uterine angiogenesis and vascular remodelling during pregnancy are poorly defined. Here we show that dynamic and variable decidual angiogenesis (sprouting, intussusception and networking), and active vigorous vascular remodelling such as enlargement and elongation of ‘vascular sinus folding’ (VSF) and mural cell drop-out occur distinctly in a spatiotemporal manner in the rapidly growing mouse uterus during early pregnancy — just after implantation but before placentation. Decidual angiogenesis is mainly regulated through VEGF-A secreted from the progesterone receptor (PR)-expressing decidual stromal cells which are largely distributed in the anti-mesometrial region (AMR). In comparison, P4-PR-regulated VEGF-A-VEGFR2 signalling, ligand-independent VEGFR3 signalling and uterine natural killer (uNK) cells positively and coordinately regulate enlargement and elongation of VSF. During the postpartum period, Tie2 signalling could be involved in vascular maturation at the endometrium in a ligand-independent manner, with marked reduction of VEGF-A, VEGFR2 and PR expressions. Overall, we show that two key vascular growth factor receptors — VEGFR2 and Tie2 — strikingly but differentially regulate decidual angiogenesis and vascular remodelling in rapidly growing and regressing uteri in an organotypic manner.
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