Dr. David Santamaria

Bio

David Santamaría received his PhD from University Autónoma of Madrid (Spain) in 1999, under the guidance of Prof. Jorge B. Schwartzman, studying replication fork barriers. He then joined the laboratory of Prof. Ronald A. Laskey, (1999-2003) at the Wellcome/CRC Institute (Cambridge, UK) where he dealt with the initiation of DNA replication and its connection with cell cycle control. He returned to Spain (2003-2016) as a staff scientist in Prof. Mariano Barbacid group (CNIO, Madrid) where he has used mouse genetics to conduct a comprehensive analysis of the Cyclin Dependent Kinase family and to identify putative therapeutic targets in lung adenocarcinoma. He was recently recruited as a group leader at the IECB to continue his research on novel oncogenic pathways and signalling mediators in lung adenocarcinoma.

Keywords / Expertise / Techniques

Lung adenocarcinoma, signalling pathways, novel oncogenic drivers, pre-clinical modelling

Summary

We have recently utilized mouse models to study the very early stages of lung adenocarcinoma. This approach bypassed the difficulties imposed by tumour heterogeneity in full-blown tumours and also facilitated the identification of novel therapeutic targets with low toxicity and potential clinical applicability. Our study also revealed that cancer cell fate and tumour malignancy are established at an unanticipated early step. We plan to continue using mouse models and tissue organoids to identify and investigate novel signalling pathways and oncogenic functions that govern the onset of lung adenocarcinoma. We also intend to pay particular attention to the significant percentage (up to 40 %) of lung adenocarcinoma patients without identified oncogenic driver to potentially translate this knowledge into novel therapeutic treatments.

Selected publications

• Ambrogio, C., Gómez-López, G., Falcone M., Kim, H.G., Byun, S., Crosetto, N., Blasco, R., Sánchez-Céspedes, M., Ren, X., Wang, Z., Ding, K., Serrano, M., Lee, S., Santamaría, D.* and Barbacid, M.* (2016) Combined inhibition of DDR1 and Notch signaling is a therapeutic strategy for KRAS-driven lung adenocarcinoma. Nature Medicine 22(3), 270-7. * Co-corresponding authors.
• Ambrogio, C., Carmona, F.J., Vidal, A., Falcone, M., Nieto, P., Romero, O.A., Puertas, S., Vizoso, M., Nadal, E., Poggio, T., Sánchez-Céspedes, M., Esteller, M., Voena, C., Chiarle, R., Barbacid, M., Santamaría D.* and Villanueva A*. (2014) Modeling lung cancer evolution and pre-clinical response by orthotopic mouse allografts. Cancer Research 74(21), 5978-88. * Co-corresponding authors.
• Cerqueira, A., Martín, A., Symonds, C.E., Odajima, J., Dubus, P., Barbacid, M and Santamaría, D. (2014) Genetic characterization of the role of the Cip/Kip family of proteins as Cdk inhibitors and assembly factors. Mol Cell Biol. 34(8), 1452-59.
• Ganuza, M., Sáiz-Ladera, C., Cañamero, M., Gómez, G., Schneider, R., Blasco, M., Pisano, D., Paramio, J.M., Santamaría, D.* and Barbacid, M.* (2012) Genetic inactivation of Cdk7 leads to cell cycle arrest and induces premature aging due to adult stem cell exhaustion. EMBO J. 31(11), 2498-510. * Co-corresponding authors.
• Blasco, R.B., Francoz, S., Santamaría, D., Cañamero, M., Dubus, P., Charron, J., Baccarini, M. and Barbacid, M. (2011) c-Raf, but not B-Raf, is essential for development of K-Ras oncogene-driven non-small cell lung carcinoma. Cancer Cell. 19(5), 652-63.

Research team

• Dr. David Santamaria, Team leader

• Dr. Benjamin Drogat, Postdoctoral Fellow

• Oriane Galmar, PhD student

• Sonia San Jose, Technician Assistant (A.I)

• Aurelie Lacouture, M2 Student