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. it is 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 overseas assembly on melanoma will supply a discussion board during which the world’s best melanoma researchers and younger scientists will talk about the most recent advances in molecular oncology. The influence of modern breakthroughs in uncomplicated examine and of rising applied sciences on molecular drugs in melanoma can 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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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). Lats2, a putative tumor suppressor, inhibits G1/S transition. Oncogene 22, 4398–4405. M. (2005). Microarray analysis shows that some microRNAs downregulate large numbers of target mRNAs. Nature 433, 769–773. , et al. (2005). MicroRNA expression profiles classify human cancers.

2, 804–810. , and Koberle, B. (2003). Curing metastatic cancer: lessons from testicular germ-cell tumours. Nat. Rev. Cancer 3, 517–525. , and Bokemeyer, C. (2003). Molecular determinants of treatment response in human germ cell tumors. Clin. 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.

To shed more light on this aspect, we examined the effect of miR-372&3 expression on p53 activation in response to oncogenic stimulation. We used for this experiment A 100 bp cluster 372mut 371&2 373 Y ctrl P cluster 373 372mut 371&2 P Y ctrl clusler 371&2 372mut Y ctrl P ctrl miR-Vec 373mut miR-Vec cluster miR-Vec 372mut probe Cyclo Protected miR probe mature miRs Probes: 371 372 ϩRASV12 B 6 Cumulative growth advantage 373 4 12 miR-Vec ctrl miR-Vec 371&2 miA-Vec ctrl miR-Vec 371&2 miR-Vec 372 mutant miR-Vec 373 miR-Vec 373 mutant pRS 53kd pRS 14kd 10 miR-Vec 372 mutant miR-Vec 373 miR-Vec 373 mutant pRS 53kd pRS 14kd 8 6 2 4 2 0 days 0 0 5 10 0 5 10 FIGURE 3.

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