Manuel Serrano obtained his PhD in 1991 for his research at CBM under the supervision of M. Salas and J.M. Hermoso. 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, he returned to Spain to start his own research group at the Centro Nacional de Biotecnología. He moved to the CNIO in 2003 to lead the Tumour Suppression Group. In May 2017 he relocated to IRB Barcelona to establish the Cellular Plasticity and Disease Group within the Molecular Medicine Research Programme. He has accomplished important scientific contributions to the understanding of Ageing from different perspectives: Cancer & Ageing, Metabolism & Ageing, Regeneration & Ageing. Among his discoveries, the following ones have had special impact: CANCER & AGEING 1.- The discovery, cloning and characterisation of the tumour suppressor p16, which defined a new class of cell cycle regulators and was soon acknowledged as one of the key tumour suppressor genes. Together with p53, PTEN and Rb, the tumour suppressor p16 constitutes one of the four most important cancer protecting genes known to date. In addition, the discovery of p16 paved the way to the discovery of p19Arf, another paramount tumour suppressor. The tumour suppressor p16 is also involved in the establishment of cellular senescence and it is today the most widely used gene marker of ageing. 2.- Establishment for the first time of the concept of "oncogene-induced senescence" as a tumour suppression mechanism, thus opening a new frontier in Molecular Oncology. The former concept speedily became an intense research topic in many laboratories; it is a widely-accepted concept upon which a great deal of expectations for future advances have been deposited. 3.- Description for the first time of the identification of senescent tumour cells in vivo. His original discovery of oncogene-induced senescence triggered a cascade of in vitro studies in numerous laboratories. Nevertheless, the question of whether senescence could take place in vivo remained a hotly debated issue. 4.- Identification of the function of p19Arf as an oncogenic sensor. This is a seminal work, which characterised p19Arf as the main sensor of the oncogenic signalling for the activation of p53. This initial observation has been the basis of subsequent research that have solidly established p19Arf as the main pathway for p53 activation. 5.- Identification of a DNA regulatory element that controls the expression of the tumour suppressor p16/p19Arf locus, which under normal conditions is silent and activates upon the presence of oncogenes. This identification constituted the first step towards the understanding of which ones are the switches activating these important tumour suppressor genes. 6.- Pioneering the generation of cancer-resistant mice with the so-called “super-mice”. These works have positively demonstrated the possibility of increasing cancer resistance in the absence of deleterious secondary effects. He also demonstrated that tumour suppressor genes also protect against ageing, thanks to the capacity of these genes to eliminate cellular damage in general. METABOLISM & AGEING 7.- Study of the role of SIRT1 in longevity, cancer and metabolic protection from high-fat diets. 8.- Identification that inhibition of PI3K extends longevity in mice and protects from obesity in mice and monkeys. REGENERATION & AGEING 9.- Identification of the tumour suppressor locus Ink4/Arf as one of the main barriers for the nuclear reprogramming of adult cells to induced pluripotent stem cells (iPS), which has also helped in the understanding the cellular mechanisms of defence. Artificial iPS generation by addition of a defined set of transcription factors is an inefficient process and the motives of the resistance to iPS conversion were unknown. MS reasoned that since the tumour suppressor genes prevent that normal cells convert into cancer ones, they could al
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Evolution over the last 10 years of activity
Aggregated career metrics
477
Total documents
5.11
Normalized Impact
157
Highly Cited Papers (10%)
33.33
International Collab. (%)
Most cited publications
Main coauthors
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