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Epigenetics and DNA repair. Is a chromatin remodeling process involved in the higher UV sensitivity of nucleotide excision repair defective cells? (EPINER2007)
Start date: Jun 1, 2010, End date: May 31, 2011 PROJECT  FINISHED 

"The knowledge on regulatory roles of epigenetic mechanisms (heritable changes in the genome function without a change in the DNA sequence) has grown very fast during the last decade since they can be the target for treating several pathologies related to cancer and neurodegeneration. In the base of these diseases deficiencies in DNA repair mechanisms have also been found. In this respect, two human syndromes (Xeroderma Pigmentosum and Cockayne’s Syndrome) affecting one of the major DNA repair systems in human cells called nucleotide excision repair (NER) characterized by sensitivity to UV irradiation, are interesting models to unravel the link between chromatin remodeling processes and DNA repair. Expected results on the possible influence of chromatin remodeling processes on the higher sensitivity to UV radiation of Cockayne’s Syndrome cells will allow further investigations in order to understand how these mechanisms are involved in the development of cancer and/or neurodegeneration found in these patients. Since the proposed investigation requires a multidisciplinary study (cytogenetics, molecular biology and immunocytochemistry), it is of the utmost importance not only for the planned research activity at the Laboratory of Prof. Palitti (since this line of research fits very well with the purposes already established by the Network of Excellence - NoE – Epigenetic Network created by several laboratories from Europe and supported by the FP6 Program from the European Community) but also for having the possibility to incorporate new methodologies and strategies to continue with the study of possible links between epigenetic and DNA repair in our laboratory in Uruguay with the aim to initiate studies on epigenetic therapy mainly applied to facilitate chemotherapy treatment of cancer diseases."
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