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Molecular Oncology Programme

Director: Vacancy
Secretary: Paloma Olave

It is my pleasure to introduce the highlights of the Molecular Oncology Programme in 2016. First of all, my enthusiastic and warm welcome to Alejo Efeyan, who joined the CNIO early this year to lead the Metabolism & Cell Signalling Junior Group. Alejo is a brilliant young scientist who trained as a postdoctoral fellow with David Sabatini, at the Massachusetts Institute of Technology, Cambridge. Cancer cells are metabolically hyperactive and an exciting discovery in recent years has been the realisation that cancer cells have mutations in the pathways that detect nutrient availability. Understanding how the nutrient sensing mechanisms contribute to cancer is the main goal of the Metabolism & Cell Signalling Junior Group. Alejo’s outstanding career and his original project have been awarded with a prestigious and generous grant from the European Research Council. His Group is now settled and fully operative. We are all very proud of having him here with us and we wish him all the best!

It is also very gratifying that the two other Junior Groups that joined the CNIO during 2015 have continued to successfully consolidate their teams and their projects throughout 2016. The Brain Metastasis Junior Group, led by Manuel Valiente, now has promising candidate small compounds that inhibit metastasis initiation in brain slices. Likewise, the Microenvironment & Metastasis Junior Group, led by Héctor Peinado is making impressive progress towards detecting how the vesicles shed by tumours (known as exosomes) are distributed throughout the organism, modifying it, and thereby making it more receptive for metastatic seeding.

In the following pages, you will read about several surprising discoveries that expand our understanding of cancer and that might pinpoint new therapeutic strategies in the near future. For example, a protein that regulates mRNA stability, CEBP4, and contributes to cancer progression (Melanoma Group, Nat. Commun. 2016); or telomere-derived transcripts that play a key role in chromosomal integrity through the stabilisation of telomeres (Telomeres & Telomerase Group, Nat. Commun. 2016).

Other discoveries concern basic mechanisms that are altered in cancer. For example, it has been found that the infliction of damage to tissues triggers cell plasticity in the surrounding cells and that cytokine IL-6 is a key factor in this process (Tumour Suppression Group, Science 2016). You will also read about a rather unique DNA polymerase named PrimPol (DNA Replication Group); about how cohesins regulate transcription, an unsuspected role for these proteins traditionally involved in sister chromatid cohesion (Chromosome Dynamics Group); and about a kinase named MASTL that is upregulated in cancer and its inhibition blocks the proliferation of some cancer cells (Cell Division & Cancer Group).

The identification of preclinical anti-cancer treatments is the ultimate goal of the Molecular Oncology Programme. In this regard, we are proud of two relevant contributions: a novel therapeutic approach for lung adenocarcinoma based on two inhibitory molecules that are effective even against aggressive cancers lacking p53 (Experimental Oncology Group, Nat. Med. 2016); and the identification of compounds that block DNA repair with therapeutic efficacy against acute myeloid leukaemia (Genomic Instability Group, Sci. Signal. 2016).