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CRCL seminars
04 May 2012
The next CRCL seminar will take place on Friday the 14th of June at 11.30pm, in the ONCORA meeting room, at the Centre Léon Bérard. We are pleased to welcome Ulf Nehrbass, DR CNRS from Strasbourg. His talk will be on "From Genes to Drugs : imaging based approaches to cancer drug development".
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Other scientific seminars in Lyon
06 April 2012
• At the International Agency for Research on Cancer (IARC)
- meetings: click here - seminars: click here
• Seminars at the CGphiMC (Center of Genetic and Molecular and Cellular Physiology), Doua campus, Lyon: click here
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“Resistance to targeted therapies" Congress, Grenoble France, 3-4. October 2013
29 April 2013
This meeting, organized by the Grenoble Institute of Research on Cancer will address topics such as: cancer stem cell biology, resistance via novel mutations, application of innovative functional genomics tools to reveal mechanisms of resistance, cancer epigenetics, identification of biomarkers and personalized medicine. Information and registration: click here
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Congress and conference in oncology - EACR
11 March 2013
You can find on the EACR website various congresses, symposiums or workshops in the field of oncology research. More information: click here
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American Association for Cancer Research - Annual Meeting 2013
05 December 2012
From the 6th to the 10th of April 2013, Walter E. Washington Convention Center, Washington, D.C. (USA). Organized by the American Association for Cancer Research (AACR) More information here. Deadline for registration 21st of December 2012
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Results of the international iCOGS study - breast cancer
05 April 2013
The CRCL team of Sylvie Mazoyer and Olga Sinilnikova (“Genetics of breast cancer”) has taken part in the largest study to date aiming at identifying genes or genomic regions associated with an increased susceptibility to breast, ovarian and prostate cancers in the general population, and an increased breast cancer risk in BRCA1 and BRCA2 mutation carriers. Within this international iCOGS study (Collaborative Oncological Gene-environment Study), the frequency of 200,000 highly selected SNPs was compared between 100,000 patients and 100,000 controls, and allowed the identification of more than 70 new susceptibility loci for these 3 hormone-related cancers. These results are presented in 13 coordinated papers, with 5 appearing in Nature Genetics in an “iCOGS Focus”, as well as 3 in PLOS Genetics, 2 in Nature Communications, 2 in Human Molecular Genetics, and 1 in American Journal of Human Genetics. The CRLC team was involved more specifically in a study revealing the association of several distinct SNPs located in the TERT region with telomere length and risks of breast and ovarian cancer (Bojensen et al, Nat Genet 2013), and in two studies identifying new modifier loci in BRCA1 (Couch et al Plos Genetics 2013) and BRCA2 (Gaudet et al PLoS Genetics 2013) mutation carriers.
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p58IPK-Mediated Attenuation of the Proapoptotic PERK-CHOP Pathway Allows Malignant Progression
15 March 2013
Cellular transformation requires active reprogramming of energy metabolism and nutrient uptake to support anabolic growth and most cancer cells present a higher avidity for glucose than normal cells. However, as enhanced glucose uptake can outstrip microenvironment supplies, the growing tumour has to cope with a potentially lethal metabolic stress until it is partly relieved by angiogenesis How malignant cells cope with this potentially lethal metabolic stress remains poorly understood. The group of Serge Manié in Toufic Renno's team, recently published in Molecular cell results showing that glucose shortage associated with malignant progression triggers apoptosis through the endoplasmic reticulum (ER) unfolded protein response (UPR). Overcoming this barrier to malignancy requires the selective attenuation of the pro-apoptotic PERK-CHOP arm of the UPR by the molecular chaperone p58IPK. Furthermore, p58IPK-mediated adaptive response enables cells to benefit from the protective features of chronic UPR. Thus, ER stress activation and p58IPK expression control the fate of malignant cells facing glucose shortage. Mol Cell paper: click here
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