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Our group is interested in studying how cell signalling (e.g. MAPK, AKT) can affect the malignant transformation process. To this end, we have developed several lines of research including chemical and genetic approaches applied to in vitro models of cancer cell lines and in vivo mouse models. We are currently focusing on the study of the role of MAPK-dependent signalling in human sarcoma, a pathology with a high incidence in childhood. Using an experimental mouse model based on chemical carcinogenesis, we hope to clarify the role of MAPKs in the development of soft tissue sarcomas. We also studied the role of cell signalling in the response of cancer to chemotherapy and in response to radiotherapy. Our study covers both conventional chemotherapy and new compounds used in targeted therapy, such as Imatinib, Palbociclib or Sorafenib, among others. The main objective is to understand how cell signalling can affect the response to cancer therapy and its involvement in the development of resistant phenotypes. In the case of ionizing radiation, we focus on elucidating the role of cell signalling in the development of radio-resistance of cancer cells. Our group has great interest in the role of cell signalling in the radio-sensitizing potential of various chemotherapeutic agents such as 5-FU or Palbociclib. In addition, our laboratory is also studying the interaction between key proteins in DNA damage response (e.g. ATM, p53) and cell signalling. Finally, our group also maintains a line of research on the molecular mechanisms by which nuclear steroid hormone receptors regulate gene expression, focusing on the characterization of new transcriptional co-regulators of nuclear receptors and studying their possible involvement in the initiation and development of tumours in tissues directly regulated by endocrine signals, such as the mammary gland and prostate.