José Pedro Vaqué Díez

I am a molecular biologist interested in studying the molecular mechanisms that govern the biology of cancer. Since 2015, I lead my own research thanks to a RyC contract and a PCDTU_I3 appointment at the UC (Laboratory of Molecular Mechanisms Driving Human Cancer). I am a tenured professor at the UC school of medicine and biomedicine since 2015 and have supervised 5 doctoral thesis and 8 master degrees. During the last 10 years, I have obtained and supervised as PI, 4 FIS and 2 PIE projects (these 2 as PI, but under a general coordinator). I believe, my scientific trajectory shows a progression from the basic field (transcriptional and signaling mechanisms) to translationally-oriented research projects in human cancer. Thanks to a multidisciplinary and collaborative research approach, our goal is to detect and explain essential disease mechanisms and further explore their translational potential into the clinic. We focus on aggressive types of skin cancers: Cutaneous T-Cell Lymphomas, Merkel Cell Carcinomas and advanced Melanoma; we also study digestive track cancers (Colorectal Adenocarcinomas and Hepatocellular Carcinomas) and MAFLD. MAIN SCIENTIFIC ACHIEVEMENTS: 1. Precision diagnosis and targeted therapy of Cutaneous T Cell Lymphomas (CTCL): Our team describes an activated network of deregulated signaling mechanisms controlling the biology of CTCLs. Of these, activated PLCG1 induces NFAT activation via calcineurin (CaN) which constitutes a mayor disease mechanism acting in all stages of the disease (Vaqué JP et al. Blood 2014). Also, we showed deregulated JAK/STAT signaling participating in the progression of CTCLs towards advanced stages (Perez C. et al. Haematologica 2015, Perez C. et al.BJD 2020 and García-Díaz N. et al. 2021). Later we discover that PKC-Theta is a mechanistic link between PLCG1-CaN and JAK/STAT signaling, and constitutes a key mechanism controlling CTCL development and dissemination (García-Diaz N. et al. JID, 2022 and Alonso-Alonso R. et al . BJD, 2022) Finally, we show in a clinical trial (phase II), the activity (ORR, 60%) and safety of topical Pimecrolimus (a specific CaN inhibitor) in CTCL patients at initial stages of the disease (Ortiz-Romero PL. et al. Lancet Haematology 2022). 2 . Identification of activated CREB as independent adverse marker for Merkel Cell Carcinoma patients (González-Vela MC and Curiel-Olmo S. et al. JID, 2017) 3. Novel approaches for molecular diagnosis directing targeted therapy of Advanced Cutaneous Melanoma and Hepatocellular Carcinoma (Curiel-Olmo S et al . Oncotarget 2015 and Llerena S and García-Diaz N. Oncotarget 2018). 4. Depicted GNAQ downstream signaling network in Uveal Melanoma (Vaqué JP et al. Molecular Cell, 2013, Feng X. et al. Cancer Cell 2014). 5. Transcriptional control of gene expression by MYC independently of MAX (Vaqué JP et al. MCR, 2008). MYC-mediated transcriptional modulation of exacerbated RAS-oncogenic signaling (Delgado MD et al. Oncogene 2000, Vaqué JP et al. JBC, 2004).