Inigo is a group leader at the Sanger Institute investigating somatic mutation in cancer and normal cells.
With a background in molecular biology, bioinformatics and evolutionary genomics, my research focuses on understanding cancer progression as a result of somatic mutation and selection.
Over the past few years, systematic sequencing of tumours has revolutionised our understanding of the genetics of cancer. This has revealed that most cancers carry thousands of mutations in their genomes, accumulated through the lifetime of their cells. However, owing to technical limitations, very little is known about the earliest steps of cancer and how normal cells in our tissues accumulate mutations during ageing and in their progression towards cancer. I investigate these early changes by studying somatic evolution in normal and precancerous tissues.
I also work on adapting evolutionary methods to cancer genomics and on the development of computational methods for discovering new cancer genes and non-coding driver mutations. This includes the development of dNdScv, an evolutionary method to study selection in cancer and identify driver genes from cancer genomics data.
Universal Patterns of Selection in Cancer and Somatic Tissues.
Tumor evolution. High burden and pervasive positive selection of somatic mutations in normal human skin.
Science (New York, N.Y.) 2015;348;6237;880-6
Somatic mutation in cancer and normal cells.
Science (New York, N.Y.) 2015;349;6255;1483-9
Somatic mutations reveal asymmetric cellular dynamics in the early human embryo.
Precision oncology for acute myeloid leukemia using a knowledge bank approach.
Nature genetics 2017;49;3;332-340
Mutational signatures associated with tobacco smoking in human cancer.
Science (New York, N.Y.) 2016;354;6312;618-622
Tissue-specific mutation accumulation in human adult stem cells during life.
Landscape of somatic mutations in 560 breast cancer whole-genome sequences.
Evidence of non-random mutation rates suggests an evolutionary risk management strategy.
Genomic Classification and Prognosis in Acute Myeloid Leukemia.
The New England journal of medicine 2016;374;23;2209-2221
Genome sequencing of normal cells reveals developmental lineages and mutational processes.
Mobile DNA in cancer. Extensive transduction of nonrepetitive DNA mediated by L1 retrotransposition in cancer genomes.
Science (New York, N.Y.) 2014;345;6196;1251343
Transmissible [corrected] dog cancer genome reveals the origin and history of an ancient cell lineage.
Science (New York, N.Y.) 2014;343;6169;437-440
Inactivating CUX1 mutations promote tumorigenesis.
Nature genetics 2014;46;1;33-8
RAG-mediated recombination is the predominant driver of oncogenic rearrangement in ETV6-RUNX1 acute lymphoblastic leukemia.
Nature genetics 2014;46;2;116-25
Recurrent PTPRB and PLCG1 mutations in angiosarcoma.
Nature genetics 2014;46;4;376-379
Somatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2.
The New England journal of medicine 2013;369;25;2391-2405
Direct competition between hnRNP C and U2AF65 protects the transcriptome from the exonization of Alu elements.
Pathway-based dissection of the genomic heterogeneity of cancer hallmarks' acquisition with SLAPenrich.
Scientific reports 2018;8;1;6713