January 2014

Researchers discover an epigenetic mark that could be useful for classifying leukemic origin and disease relapse

An international study between the Imprinting and Cancer Group within the Cancer Epigenetics and Biology Program (PEBC) and the Institute of Human Genetics, at Christian-Albrechts University, Kiel, Germany, describe a methylation signature that is a promising marker for classifying myeloid-derived leukemias. Gene Wilms tumor 1 (WT1) is over-expressed in numerous cancers with respect to normal […]

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Manel Esteller,Vanguardia Science Award

The researcher Manel Esteller, Director of Epigenetics and Cancer Biology program at the Institute of Biomedical Research of Bellvitge (IDIBELL ), ICREA researcher and professor of Genetics at the University of Barcelona has won the Vanguardia Award for Science 2013. The selected job has been published in 2013 in the journal Genome Research and shows

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Gonzalo Arévalo: ”10% of H2020 funding goes directly to Health but there are other areas that can provide opportunities for researchers”

The first calls of the European Horizon 2020 program have begun. On 17 January, the National Contact Point for Legal and Financial Affairs also part of the team of the Office of European Institute of Health Carlos III Project, Gonzalo Arévalo told investigators IDIBELL funding opportunities that may represent Horizon 2020 (H2020). “Between 25 and

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An international study allows a better prediction of the risk of hereditary cancer

The paper analyzes the role of different genetic variants involved in Lynch syndrome , an inherited disease that increases the risk of various tumors The study is published in the journal Nature Genetics and has had the participation of Gabriel Capellá and Marta Pineda, form the Hereditary Cancer Program at the Catalan Institute of Oncology

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Researchers discover a tumor suppressor gene in a very aggressive lung cancer

The Genes and Cancer Group at the Cancer Epigenetics and Biology Program of the IDIBELL has found that the MAX gene, which encodes a partner of the MYC oncogene, is genetically inactivated in small cell lung cancer. Reconstitution of MAX significantly reduced cell growth in the MAX-deficient cancer cell lines. These findings show that MAX

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