The landscape of somatic copy-number alteration across human cancers

available in PMC 2010 August 18.A powerful way to discover key genes with causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. Here we present high-resolution analyses of somatic copy-number alterations (SCNAs) from 3,131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across several cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several gene families are enriched among these regions of focal SCNA, including the BCL2 family of apoptosis regulators and the NF-κΒ pathway. We show that cancer cells containing amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend on the expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in several cancer types.National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P50CA90578)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, R01CA109038))National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, R01CA109467)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P01CA085859)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P01CA 098101)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, K08CA122833

Vascular endothelial growth factor in gingival tissues and crevicular fluids of diabetic and healthy periodontal patients

WOS: 000189110800011PubMed ID: 15025220Background: Periodontal disease is one of the major oral problems encountered in patients with diabetes mellitus (DM). Vascular changes, neutrophil dysfunction, altered collagen synthesis, and genetic predisposition observed in DM may contribute to periodontitis; and the vascular alterations observed in such patients may depend on vascular endothelial growth factor (VEGF) actions. Few reports are available about the mechanism of neovascularization and the angiogenic factors that contribute to the periodontal pathology and the role of VEGF in periodontal diseases. The aim of this study is to compare VEGF expression in healthy and periodontally diseased tissues with gingival crevice fluid (GCF) of healthy persons and diabetic patients. Methods: Gingival tissue and GCF samples were collected from sites of periodontitis in 10 healthy subjects and in 10 type 2 diabetic patients, and from the sites of healthy gingiva within the same groups. Therefore, each patient became his/her own control. Additionally, 10 people without any systemic or periodontal diseases were enrolled, forming a negative control group. Thus, a total of 50 tissue and 50 GCF samples were provided. Results: No VEGF staining was observed in the negative control group or in the systemically healthy people's healthy tissue samples, whereas four samples of diabetic patients showed positive staining (P 0.05). In all test groups, GCF VEGF levels were higher in periodontal sites (P <0.05) than in healthy sites. Conclusion: The results of this study showed that VEGF is increased in all periodontal tissues of both groups and in the healthy sites of diabetic patients. Additionally, GCF VEGF values increased in periodontal sites of all test groups