Experiences From the Cisplatin-Analysts Who Have Become Successful

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Версія від 05:24, 5 квітня 2017, створена Animal13neck (обговореннявнесок) (Створена сторінка: The results demonstrated that 51% of oesophageal adenocarcinomas overexpressed at least one of the RTK panel, with 21% of these overexpressing multiple receptor...)

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The results demonstrated that 51% of oesophageal adenocarcinomas overexpressed at least one of the RTK panel, with 21% of these overexpressing multiple receptors. Up-regulation of RTK expression was an early event corresponding with low-grade dysplasia development (25% in areas without dysplasia versus 63% in low-grade dysplasia, ). There was a trend for an increase in the prevalence of concomitant overexpression of multiple receptors as intestinal metaplasia progressed to low-grade dysplasia, 7% versus 10%; and from low-grade dysplasia to high-grade dysplasia, 10% versus 19% ( and 0.24, respectively). The timing of receptor up-regulation varied; FGFR, ErbB2, and Met overexpression occurred as dysplasia first developed, Cisplatin clinical trial whilst EGFR overexpression was predominately seen in invasive disease and ErbB3 overexpression was uniformly rare. We provide evidence for INPP5D a frequent and early role for multiple different RTKs in oesophageal carcinogenesis. Given the early timing of receptor deregulation, inhibiting RTKs in pre-invasive disease may also represent a novel and effective chemopreventive strategy. Copyright ? 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. ""Gastric cancer (GC) is the fourth most common cancer worldwide. In spite of the mortality incidence associated with GC, no reliable prognostic biomarkers are currently available for this malignancy. The sulfatases (or SULFs), SULF1 and SULF2, play a critical role in the pathogenesis check details of a variety of human cancers. We sought to evaluate the potential of SULFs as biomarkers for GC. Thirty pairs of GC and corresponding normal tissues were analysed for the expression and methylation status of SULFs. Furthermore, the functional role of SULF overexpression was investigated in GC cell lines and tumour xenograft animal models. Lastly, we validated the expression of SULF1 protein in a large cohort of 450 GC patients. GC tissues showed conspicuously higher expression of SULF1 (p = 0.0002) and SULF2 (p = 0.001) compared to normal mucosa, which was correlated with its promoter hypomethylation. Furthermore, high expression of SULFs caused marked acceleration in the growth of xenograft tumours in nude mice. The expression of SULF1 protein significantly correlated with higher recurrence rates (p = 0.0002) and worse overall survival (p