PURPOSE: To investigate the role of stimulators and inhibitors of angiogenesis in the pathogenesis of diabetic retinopathy. METHODS: Undiluted vitreous samples and simultaneous paired plasma samples were obtained from 30 diabetic patients (35 eyes) undergoing vitreous surgery. The levels of vascular endothelial growth factor (VEGF), endostatin, and platelet factor-4 (PF-4) were measured simultaneously in each specimen by enzyme-linked immunosorbent assay. The severity of diabetic retinopathy was evaluated according to the modified Early Treatment Diabetic Retinopathy Study retinopathy severity scale. RESULTS: Vitreous levels of VEGF and endostatin were significantly correlated with the severity of diabetic retinopathy (rho = 0.52, rho = 0.48, respectively), but the vitreous level of PF-4 was not (rho = 0.12). Vitreous levels of VEGF, endostatin, and PF-4 were not significantly correlated with their plasma levels. The vitreous level of VEGF was significantly correlated with that of endostatin (rho = 0.42). The VEGF concentration was significantly higher in the vitreous than in the plasma, while the endostatin concentration was not. CONCLUSIONS: The present study showed that VEGF and endostatin were expressed in the vitreous of patients with diabetic retinopathy and may be involved in the pathogenesis of this condition.

Adult↗

PubMedDate not supplied

Frequent allelic loss/imbalance on the long arm of chromosome 21 in oral cancer: evidence for three discrete tumor suppressor gene loci.

Frequent allelic imbalances including loss of heterozygosity (LOH) and microsatellite instability (MI) on the long arm of chromosome 21 (21q) have been found in several types of human cancer. This study was designed to identify tumor suppressor locus (or loci) associated with oral squamous cell carcinoma (SCC) on 21q. Among 38 patients with oral SCC tested, 15 (44%) of 34 informative cases showed LOH at one or more loci. Deletion mapping of these 15 tumors revealed three discrete commonly deleted regions on the chromosome arm. A minimal region with frequent LOH was found at the marker D21S236 mapped on 21q11.1. Another region of frequent deletion was identified between markers D21S11 and D21S1436 on 21q21, and a further commonly deleted region was found at D21S1254 on 21q22.1. In addition, we have detected MI on the chromosome arm in our oral SCC samples with significant correlation with tumor stage. Thus, our results strongly suggest that allelic imbalances on 21q may be involved in the development of oral SCC; and that at least three different putative tumor suppressor genes contributing to the pathogenesis of this disease are present on 21q.

Chromosome Mapping↗