Untitled - Red TemÃ¡tica de investigaciÃ³n cooperativa en cÃ¡ncer

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Sesión de Tarde Moderadores: Dr. Joan Gil / Instituto de Investigación Biomédica de Bellvitge (IDIBELL) Dra. Mireia Olivan / Institut de Recerca-Hospital Universitari Vall d’Hebron 16:50 h O-07. “A DOMINANT-NEGATIVE N-TERMINAL FRAGMENT OF HER2 FREQUENTLY EXPRESSED IN BREAST CANCERS” Beatriz Morancho Armisen / Vall D’Hebrón Institut D’Oncologia (VHIO), Barcelona Grupo RTICC: RD06/0020/0022 17:10 h O-08. “MITOTIC ARREST DOWN-REGULATES FLIP EXPRESSION AND SENSITIZES TUMOR CELLS TO THE EXTRINSIC PATHWAY OF APOPTOSIS” Tania Sánchez Pérez / Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER), Sevilla Grupo RTICC: RD06/0020/0068 17:30 h O-09. “microRNA-BASED THERAPY FOR HIGH-RISK NEUROBLASTOMA” Aroa Soriano Fernández / Institut de Recerca Hospital Universitari Vall d’Hebron, Barcelona Grupo RTICC: RD06/0020/1021 17:50 h O-10. “INFLUENCE OF LKB1/STK11 IN GENE EXPRESSION PATTERNS INDUCED BY ENERGY STRESS IN LUNG CANCER CELL LINES” Rossana Gonçalves Restani / Instituto de Investigación Biomédica de Bellvitge (IDIBELL), Barcelona Grupo RTICC: RD06/0020/0062 18:10 h O-11. “IDENTIFICATION OF DIFFERENTIAL GENOMIC AND PROTEOMIC PROFILES ASSOCIATED WITH BONE METASTASES IN PROSTATE CANCER” Marta Garcia López / Institut de Recerca-Hospital Universitari Vall d’Hebron, Barcelona Grupo RTICC: RD06/0020/0058 18:30 h O-12. “DIOXIN RECEPTOR CONTROLS CSK-BINDING PROTEIN SIGNALING TO CAVEOLIN 1 AND Β1 INTEGRIN TO MODULATE CELL ADHESION AND MIGRATION” Martes 20 de Noviembre Sesión de Mañana Moderadores: Dr. Francesc Sole Ristol / Institut de Recerca Contra la Leucèmia Josep Carreras (IJC) Dra. Marina Rigau / Institut de Recerca-Hospital Universitari Vall d’Hebron 09:10 h O-13. “CD44 POSITIVITY CONFERS RESISTANCE TO SORAFENIB-INDUCED CELL DEATH IN HEPATOCELLULAR CARCINOMA (HCC) CELLS” Joan Fernando Peidró / Instituto de Investigación Biomédica de Bellvitge (IDIBELL), Barcelona Grupo RTICC: RD06/0020/0097 09:30 h O-14. “ANALYSIS OF NEW GENES DIRECTLY REGULATED BY FOXE1 IN THYROID CELLS” Lara Paula Fernández Álvarez / Instituto de Investigaciones Biomédicas “Alberto Sols” IIB, Madrid Grupo RTICC: RD06/0020/0060 09:50 h O-15. “MOLECULAR SUBSETS OF MANTLE CELL LYMPHOMA DEFINED BY THE IGHV MUTA- TIONAL STATUS AND SOX11 EXPRESSION HAVE DISTINCT BIOLOGICAL AND CLINICAL FEATURES” Alba Navarro Lopez / Instituto de Investigación Biomédica de Bellvitge (IDIBELL), Barcelona Grupo RTICC: RD06/0020/0039 10:10 h O-16. “ETV5 AND FOXM1 TRANSCRIPTION FACTORS ARE OVEREXPRESSED IN OVARIAN CANCER AND REGULATE CELLULAR ADHESION AND PROLIFERATION CONTRIBUTING TO TUMOR DISSEMINATION” Marta Llauradó Fernández / Institut de Recerca-Hospital Universitari Vall d’Hebron, Barcelona Grupo RTICC: RD06/0020/0058 10:30 h O-17. “COUNTERACTING AUTOPHAGY OVERCOMES RESISTANCE TO EVEROLIMUS IN MANTLE CELL LYMPHOMA” Laia Rosich Moya / Hospital Clínic-IDIBAPS, Barcelona Grupo RTICC: RD06/0020/0014 Javier Rey Barroso / Universidad de Extremadura, Badajoz Grupo RTICC: RD06/0020/1016 18:50 h Fin de las Sesiones 10:50 h O-18. “PIK3CA ALTERATIONS IN BLADDER CANCER RECURRENCE” Mónica Martínez Fernández / Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), Madrid Grupo RTICC: RD06/0020/0029 10 11
11:10 h O-19. “PAPEL DEL CORREPRESOR NcoR EN LA INHIBICIÓN DE LA INVASIVIDAD Y FOR- MACIÓN DE METÁSTASIS POR TR” Olaia Antia Martinez Iglesias / Instituto de Investigaciones Biomédicas “Alberto Sols” IIB, Madrid Grupo RTICC: RD06/0020/0036 11:30 h O-20. “DIFFERENTIAL FUNCTIONS OF EVI1 SPLICE ISOFORMS IN CELL VIABILITY AND TRANSCRIPTIONAL REGULATION. THE EVI1 HUMAN PROTEIN REGULATES ITS OWN TRANSCRIP- TION” Miren Maicas Irigaray / Centro de Investigación Médica Aplicada (CIMA), Pamplona Grupo RTICC: RD06/0020/0078 12:00 h Descanso / Coffee Break 12:00 h Retirada de Pósters 12.30 h. Conferencia Coordinador Nacional de la RTICC Dr. Eugenio Santos / Coordinador Nacional de la RTICC, Centro de Investigación del Cáncer de Salamanca 12:40 h / Entrega PREMIO DE INVESTIGACIÓN COOPERATIVA EN ONCOLOGÍA RTICC 2012 12:50 h / Exposición del galardonado con el PREMIO DE INVESTIGACIÓN COOPERATI- VA EN ONCOLOGÍA RTICC 2012 13:35 h / Clausura Dr. Eugenio Santos / Centro de Investigación del Cáncer de Salamanca Dr. Luis Montuenga / Centro de Investigación Médica Aplicada (CIMA), Universidad de Navarra Dr. Jaume Reventos / Unidad de Investigación Biomédica y Oncología Traslacional i Pediátrica del Vall d’Hebron Institut de Recerca (VHIR) CONFERENCIA MAGISTRAL IDENTIFICATION OF NOVEL DRIVER MUTATIONS IN CHRONIC LYMPHOCYTIC LEUKEMIA THROUGH WHOLE GENOME SEQUENCING XOSE S. PUENTE DEPARTMENT OF BIOCHEMISTRY, UNIVERSITY OF OVIEDO Chronic lymphocytic leukemia (CLL), the most frequent leukemia in adults in Western countries, is a B-cell neoplasm clinically and biologically very heterogeneous. The differences in the behavior of the disease have been associated with two major molecular subtypes characterized by high and no or low number of somatic mutations in the variable region of immunoglobulin genes (IGHV-mutated and IGHV-unmutated, respectively). However, the genetic and molecular alterations leading to the development and progression of the disease are still poorly understood. The aim of the CLL Cancer Genome Consortium is to generate a comprehensive catalogue of genetic alterations relevant to the pathogenesis and clinical evolution of the disease using next generation sequencing combined with other genomic technologies in a large series of well characterized tumors. We have completed the sequencing and analysis of 109 cases of CLL using either whole genome sequencing (4 cases) or whole exome sequencing (105 cases). This has led us to the identification of about 1,000 somatic mutations per tumor genome in non-repetitive regions, and a median of 45 somatic mutations per case when using exome sequencing. Interestingly, IGHV-mutated tumors had more protein-altering mutations than CLL tumors without mutations in the IGHV region, as well as an increased number of A>C/T>G transversions. In addition, global analysis of these data resulted in the identification of 78 genes which are recurrently mutated in CLL. They include NOTCH1 and SF3B1, which are mutated in more than 10% of cases, or POT1, CHD2 and LRP1B, mutated in about 5% of tumors. There is a clear difference in the frequency of these mutations between IGHV-mutated and IGHV–unmutated CLL tumors, extending at the genomic level the clinical differences observed in these two CLL subtypes. Together with SF3B1, which encodes a subunit of the spliceosomal U2 small nuclear ribonucleoprotein, at least 30 genes involved in RNA maturation have mutations in CLL, suggesting that RNA splicing and maturation might constitute an important mechanism driving this disease. Finally, further analysis of more than 250 CLL cases showed that patients with mutations in either NOTCH1 or SF3B1 had faster disease progression and shorter overall survival. Together, these data illustrate the heterogeneity of the disease and the utility of genome-wide studies to identify the molecular mechanisms driving the development of CLL. This project is funded by the Spanish Ministry of Science and Innovation through the Institute of Health Carlos III. 12 13
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