Titlebook: Cancer Genome and Tumor Microenvironment; Andrei Thomas-Tikhonenko Book 2010 Springer-Verlag New York 2010 Chromosom.angiogenesis.cell.gen

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HGF/c-MET Signaling in Advanced Cancersease, which is caused by inactivation of the VHL gene –( see Chapter 6). RCCP genes map to several loci; one of each on 7q31.1-q34 encodes the c-Met oncoprotein (Schmidt et al. 1997). In the original publication, missense mutations in the tyrosine kinase domain of the MET gene were found both in the

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TGF-β Signaling Alterations in Neoplastic and Stromal Cellsse, a condition characterized by hyperostosis and sclerosis of the diaphyses of long bones (Janssens et al., 2000; Kinoshita et al., 2000). However, mutations in the TGFB genes do not appear to occur in cancer. In contrast, type I and II TGF-β receptors and their downstream effectors SMADs are often

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Bacterial Efflux Pump Inhibitors, could occur via aberrant Akt signaling, direct somatic mutations in . are frequent in epithelial tumors such as diffuse-type gastric and lobular breast cancers, where they can be found in up to 50% of primary neoplasms (Berx et al. 1998). . mutations were also observed in primary endometrial and ov

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Lin Wang,Minghu Jiang,Stefan Wölflk.a. ARHH). This gene has been found to be rearranged in non-Hodgkin’s lymphomas and multiple myeloma, along with mutations in the 5.UTR in diffuse large cell lymphomas (Preudhomme et al. 2000; Pasqualucci et al. 2001). The common rearrangement found in these hematopoietic cancers is caused by a t(3