By Maren Oehlmann, Cathal Mahon, Heinz-Peter Nasheuer (auth.), Director Fabrizio d'Adda di Fagagna, Director Susanna Chiocca, Director Fraser McBlane, Director Ugo Cavallaro (eds.)
Proceedings of the 2d Annual IFOM-IEO assembly on melanoma. this can be a new assembly, it has approximately 2 hundred attendees from Australia, Austria, Belgium, Brazil, Canada, England, France, Germany, Greece, eire, Italy, Japan, Netherlands, Spain, Sweden, Switzerland, and the USA.
The second IFOM-IEO foreign assembly on melanoma will supply a discussion board within which the world’s best melanoma researchers and younger scientists will talk about the newest advances in molecular oncology. The impression of modern breakthroughs in simple study and of rising applied sciences on molecular medication in melanoma might be highlighted.
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Additional info for Advances in Molecular Oncology: Edited under the auspices of the European Institute of Oncology (IEO) and The FIRC Institute of Molecular Oncology Foundation (IFOM)
It has been speculated that these amino termini play a role mediating an interaction with scaffold proteins in macromolecular signalling complexes. Gel filtration analyses indicate that both ATM and ATR are constitutive residents of very high molecular weight protein complexes (>2 MDa) in mammalian cells (Wright et al. 1998). The identification of the composition of these complexes is an area of increasing interest. However, for the purposes of this report it is important to indicate the importance of the PIKK proteins in the regulation of the DNA damage response.
MiR-Vec-YFP was cloned similar to miR-Vec-Ctrl, only starting from pMSCV-YFP. , 2005). p53kd, p16kd, p14ARFkd, p21cip1kd shRNA constructs were described before (Voorhoeve and Agami, 2003; Duursma and Agami, 2005). pMSCV-Blast RASV12-ERTAM was made by subcloning RASV12ERTAM into pMSCV-Blast. p21-RFP was produced by cloning p21 to the N terminus of dsRFP. , 2003). The miRNA minigenes were PCR amplified from genomic human DNA, cloned downstream of the CMV promoter in miR-Vec, and sequence verified.
Our results indicate that due to enhanced tolerance to oncogenic mutations, deregulated expression of miR-372&3 predisposes cells for accumulation of carcinogenic events. Thus, the expression of these miRNAs must be carefully controlled during differentiation to prevent progression to cancer. Which factors control miR-371–3 expression during differentiation and whether their activity is causally related to development of TGCTs remain to be explored. Nevertheless, our experiments stress the importance of a strong downregulation of factors that maintain rapid cell proliferation, as in the absence of this downregulation safeguard mechanisms against oncogene emergence are functionally impaired.