CtIP as a novel tumor suppressor and its relevance for initiation, prognosis and treatment of cancer

Abstract

Póster presentado al 22nd IUBMB & 37th FEBS Congress: From Single Molecules to Systems Biology, celebrado en Sevilla (España) del 4 al 9 de septiembre de 2012DNA damage and repair are closely linked to cancer, not only during tumor initiation and progression, but also as a potent antitumoral therapeutical opportunity. From the many types of damaged DNA, double strand breaks (DSBs) are specially relevant in oncology. DSBs are repaired by two major mechanisms that compete for the same substrate. Both ends of the DSB can be simple re-joined with little or no processing, a mechanism known as non-homologous end-joining. On the other hand, DSBs can be processed and engaged in a more complex repair pathway called homologous recombination. This pathway uses the information present in a homologue sequence. The balance between these two pathways is exquisitely controlled. Alterations in the DSBs repair pathways facilitate tumor progression and are selected early on during cancer development. On the other hand, DSBs are the molecular base of radiotherapies and several chemotherapies. Little is known about how cells chose between these two repair pathways, or the relevance of such choice in cancer initiation, progression or treatment. A main player for this election is the protein known as CtIP, which has been loosely implicated with cancer. We are studying the role of CtIP as a tumor suppressor and its importance in tumor initiation, progression, prognosis and treatment using cancer samples and cancer cell models.Peer Reviewe