From my early days as a predoctoral student I focused my research on the development of tumor models that can be useful in understanding the mechanisms underlying both the genesis and progression of cancer (metastasis). So, I did my doctoral thesis under the supervision of Dr. Gabriel Capella (Hospital de Sant Pau, Barcelona) studying the molecular basis of pancreatic cancer, for which we generated the first orthotopic models of pancreatic cancer that were made in Spain by orthotopic implantation of primary human tumors. Models also allowed to generate a library of cell lines (NP18, NP9, etc.) that today are used by many laboratories in the field. During my postdoctoral stay at the Memorial Sloan Kettering Cancer Center (MSKCC), New York, USA (Dr Richard Kolesnick) in collaboration with Cold Spring Laboratories (Dr. Michael Hengartner) I focused on the study of the mechanisms of stress response in the model organism C. elegans (worm). In addition we were pioneered on the use of C. elegans for drug studies, using it in the development of new formulations of Gleevec in this organism in close collaboration with Novartis company. After my postdoctoral stay of four years in NY, I joined the Catalan Institute of Oncology (ICO) as a independent researcher of the program Ramon y Cajal (first call) starting my own lab focused on the study of the mechanisms of resistance to standard chemotherapy (cisplatin and 5-FU) treatments. So we decided to do it from two approaches: (1) generating matched models of sensitive vs. resistant drugs (acquired resistance) in athymic mice by orthotopic implantation of primary human tumors (Orthoxenografts o PDOX); and (2) studying in C.elegans the mechanisms of resistance and drug response. In the last 10 years we have specialized in the generation of  orthoxenografts for at least 12 different tumor types, and our research has converged towards the study of the mechanisms of acquiring resistance to cisplatin with the main endpoint  to search drugs  that re- sensitize to cisplatin treatments.  So, we follow to increase the therapeutic window to get the same answers with less cisplatin doses, as well as to offer treatment in refractory cases.  Research that we did integrating the orthoxenografts models, the worm (C. elegans) studies and primary human tumors series. Our models of resistant/refractory epithelial ovarian cancer orthoxenografts have participated successfully in the advanced preclinical development of a new drug from Pharmamar (Lurbinectedin-PM11083) currently in Phase III. This experience/know how with orthoxenografts® (it is a own quality brand protected in Europe) we are using to develop personalized medicine strategies in real time; looking in the mouse the best therapeutic drug that we can offer to a patient at the relapse time. In 2014 I was co-founder of the spin-off Xenopat (www.xenopat.com), a small specialized company in the use of orthoxenografts® for drug development and patient’s personalized medicine strategies in real time. We think that knowing the genes that play an important role in the acquisition of cisplatin resistance will be very important to generate new therapeutic strategies useful for patients, as well as to identify early non-responders/refractory cases. We believe that matched models sensitive vs. cisplatin resistant (same genetic background) that we have generated with a lot of effort over the past years can be very important tools to achieve these goals.