Manuel Serrano

Manuel Serrano, investigador del programa de Ciencia de la Fundación Botín

Tumour Supression - Molecular Oncology Programme

Centro Nacional de Investigaciones Oncologicas (CNIO)

Madrid, Spain

Manuel Serrano obtained his PhD in 1991 for his research on DNA replication at the Centro de Biología Molecular 'Severo Ochoa' under the supervision of M. Salas. From 1992 to 1996 he worked as a Postdoctoral Fellow in the laboratory of D. Beach at the Cold Spring Harbor Laboratory, New York, USA.

In 1997, Serrano returned to Spain to start his own research group at the Centro Nacional de Biotecnología, in Madrid. He moved to the CNIO in 2003 to lead the Tumour Suppression Group.

He has contributed greatly to the Oncology field. Among all of his discoveries, the following ones are of special relevance:

  • He is responsible for the discovery, cloning and characterisation of the tumor suppressor p16, which defined a new class of cell cycle regulators and was soon acknowledged as one of the key tumour suppressors.
  • He established for the first time the concept of "oncogene-induced senescence" as a tumour suppression mechanism, thus opening up a new frontier in Molecular Oncology.
  • He has pioneered the generation of cancer-resistant mice with the so-called 'super-mice'.
  • He has received the FEBS Anniversary Prize of the Gesellschaft für Biochemie und Molekularbiologie, the Carcinogenesis Young Investigator Award, the Fundación Echevarne National Award in Oncology, the Fundación Banco de Sabadell National Award in Biomedical Research, and the Fundación Carmen y Severo Ochoa Award. Manuel Serrano is an elected EMBO Member.

Research interest:

  • Understand the mechanisms underlying tumour suppression and identify new regulators of tumour suppressors. They manipulate the mouse genome to create novel alterations that increase or decrease tumour suppression potency.
  • Study the interplay between tumour suppression and ageing. Cellular and genetic lesions are at the origins of cancer appearance and, interestingly, this type of lesions is also the basis of ageing.
  • Characterise cellular senescence as a mechanism of tumour suppressio.
  • Study the involvement of tumour suppressors in the regulation of nuclear reprogramming of differentiated adult cells to induced pluripotent stem (iPS) cells. Reprogramming processes are thought to mimic tumorigenesis.

Most relevant publications:

  • Herranz, D., Muñoz-Martín, M., Cañamero, M., Mulero, F., Martínez-Pastor, B., Fernández-Capetillo, O., Serrano, M. Sirt1 improves healthy ageing and protects from metabolic syndrome-associated cancer. Nat. Commun. 1:3 doi:10.1038/ncomms1001 (2010).
  • Fernández-Marcos, PJ., Pantoja, C., González-Rodríguez, A., Martin, N., Flores, JM., Valverde, AM., Hara, E., Serrano, M. Normal proliferation and tumorigenesis but impaired pancreatic function in mice lacking the cell cycle regulator sei1. PLoS One, 5, e8744 (2010).
  • Collado, M., Serrano, M. Senescence in tumours: evidence from mice and humans. Nat Rev Cancer, 10, 51-57 (2010).
  • Serrano M. Cancer: a lower bar for senescence. Nature, 464, 363-364 (2010).
  • Collado, M., Serrano, M. The TRIP from ULF to ARF. Cancer Cell, 17, 317-318 (2010).
  • Li, H., Collado, M., Villasante, A., Strati, K., Ortega, S., Cañamero, M., Blasco, M.A. and Serrano, M. The Ink4/Arf locus is a barrier for iPS reprogramming. Nature, 460, 1136-1139 (2009).
  • Llanos, S., Cuadrado, A. and Serrano, M. MSK2 inhibits p53 activity in the absence of stress. Sci. Signal., 2, ra57. (2009).
  • Matheu, A., Maraver, A., Collado, M., Garcia-Cao, I., Cañamero, M., Borras, C., Flores, J.M., Klatt, P., Viña, J. and Serrano, M. Anti-aging activity of the Ink4/Arf locus. Aging Cell, 8, 152-161 (2009).
  • Efeyan, A., Murga, M., Martinez-Pastor, B., Ortega-Molina, A., Soria, R., Collado, M., Fernandez-Capetillo, O. and Serrano, M. Limited role of murine ATM in oncogene-induced senescence and p53-dependent tumor suppression. PLoS ONE, 4, e5475. (2009).
  • Fernandez-Marcos, PJ., Abu-Baker, S., Joshi, J., Galvez, A., Castilla, EA., Cañamero, M., Collado, M., Saez, C., Moreno-Bueno, G., Palacios, J., Leitges, M., Serrano, M., Moscat, J., and Diaz-Meco, MT. Simultaneous inactivation of Par-4 and PTEN in vivo leads to synergistic NF-kB activation and invasive prostate carcinoma. Proc. Natl. Acad. Sci. USA, 106,12962-12967 (2009).


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