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Proceedings of the second Annual IFOM-IEO assembly on melanoma. it is 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 offer a discussion board during which the world’s top melanoma researchers and younger scientists will speak about the most recent advances in molecular oncology. The influence of modern breakthroughs in simple learn and of rising applied sciences on molecular drugs in melanoma should be highlighted.
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Extra 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)
A system for stable expression of short interfering RNAs in mammalian cells. Science 296, 550–553. , and Stoter, G. (1998). Expression of p53, Bcl-2 and Bax in cisplatin-induced apoptosis in testicular germ cell tumour cell lines. Br. J. Cancer 77, 1562–1567. P. (2004). MicroRNAs modulate hematopoietic lineage differentiation. Science 303, 83–86. , et al. (2005). Crucial role of p53-dependent cellular senescence in suppression of Ptendeficient tumorigenesis. Nature 436, 725–730. , et al. (2005).
Growth B Primary cells C 4 ctr + miRLib Micro-array analysis of miRNA inserts Extract DNA +PCR culture for three weeks Transduce and select +RASV/2 Extract DNA +PCR 1st experiment 2nd experiment 3 Log2 ratio (RAS ctrl) 3rd experiment 2 1 0 −1 −2 −3 −4 6 7 8 9 10 11 12 # miR-Vec 371&2 @ miR-Vec 373 13 14 15 16 Log2 signal FIGURE 2. Identification of miR-Vecs that inhibit oncogene-induced senescence. (A) The effects of oncogenic RASV12 on cellular growth. (B) A flow chart of the screen. Cells transduced with the miR-Lib were grown for 2 to 3 weeks in the presence or absence of RASV12.
Indeed, TGCTs conform to this profile (Masters and Koberle, 2003). This could for instance be a result of high mdm2 levels, as was previously suggested for mouse teratocarcinomas (Lutzker and Levine, 1996). However, by several criteria mouse teratocarcinomas are counterparts of human germ cell tumors of neonates and infants rather than TGCT (Oosterhuis and Looijenga, 2005). , 2000). Therefore, it is highly significant that we found that miR372&3-expressing TGCTs did not contain mutated p53 alleles, whereas a subset of miR-371–3 negative primary TGCTs and cell lines did.