Enrique A. Mesri

TL;DR: It is concluded that the KSHV G-protein-coupled receptor is a viral oncogene that can exploit cell signalling pathways to induce transformation and angiogenesis in K SHV-mediated oncogenesis.

TL;DR: The epidemiology of KS and KSHV is described, and the insights into the remarkable mechanisms through which K SHV can induce KS that have been gained in the past 16 years are described.

TL;DR: The Hallmarks of Cancer framework of Hanahan and Weinberg (2000 and 2011) is used to dissect the viral, host, and environmental cofactors that contribute to the biology of multistep oncogenesis mediated by established human oncoviruses.

TL;DR: These findings suggest that the KSHV GPCR oncogene subverts convergent physiological pathways leading to angiogenesis and provide the first insight into a mechanism whereby growth factors and oncogenes acting upstream from MAPK, as well as inflammatory cytokines and cellular stresses that activate p38, can interact with the hypoxia-dependent machinery of angiynthesis.

TL;DR: A glycosylation-dependent pathway is identified that compensates for the absence of cognate ligand and preserves angiogenesis in response to VEGF blockade and may increase the efficacy of anti-VEGF treatment.