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 second Annual IFOM-IEO assembly on melanoma. this can be a new assembly, it has approximately two 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 speak about the newest advances in molecular oncology. The influence of contemporary breakthroughs in simple study and of rising applied sciences on molecular drugs in melanoma might be highlighted.

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Additional resources 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)

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2006). It is also becoming clearer how these proteins are becoming activated. Recent evidence suggests, that ATM, in the absence of DNA damage, is present in the nucleus as a homodimer. Upon DSB formation, the two ATM proteins phosphorylate each other at Ser1981 and this event results in disruption of oligomerization and hence activation of ATM kinase activity (Bakkenist and Kastan 2003). Autophosphorylation of ATM has been shown in vitro, requiring only addition of ATP. Other nucleotides and DNA are not required, however, under the same conditions ATP failed to activate both ATR and DNA-PK, once again emphasising the different possible responses these proteins have to DNA damage (Kozlov et al.

Cancer Res. 9, 767–773. , et al. (2004). Lats2/Kpm is required for embryonic development, proliferation control and genomic integrity. EMBO J. 23, 3677–3688. S. (2005). BRAFE600-associated senescence-like cell cycle arrest of human naevi. Nature 436, 720–724. , and Looijenga, L. (2000). Comparative genomic and in situ hybridization of germ cell tumors of the infantile testis. Lab. Invest. 80, 1055–1064. T. (2005). c-Myc-regulated microRNAs modulate E2F1 expression. Nature 435, 839–843. H. (2005).

2002). Role of P53 and MDM2 in treatment response of human germ cell tumors. J. Clin. Oncol. 20, 1551–1561. 1180 Cell 124, 1169–1181. , and Agami, R. (2005). A genetic screen identifies PITX1 as a suppressor of RAS activity and tumorigenicity. Cell 121, 849–858. B. (2003). Prediction of mammalian microRNA targets. Cell 115, 787–798. P. (2005). Conserved seed pairing, often flanked by adenosines, indicates that thousands of human genes are microRNA targets. Cell 120, 15–20. , and Tao, W. (2003).

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