Whole-genome sequencing identifies recurrent mutations in chronic lymphocytic leukaemia

Xosé S. Puente(Universidad de Oviedo), Magda Pinyol(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Vı́ctor Quesada(Universidad de Oviedo), Laura Peña Conde(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Gonzalo R. Ordóñez(Universidad de Oviedo), Neus Villamor(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Geòrgia Escaramís(Universitat Pompeu Fabra), Pedro Jares(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Sı́lvia Beà(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Marcos González(Universidad de Salamanca), Laia Bassaganyas(Universitat Pompeu Fabra), Tycho Baumann(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Manel Juan(Hospital Clínic de Barcelona), Mònica López‐Guerra(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Dolors Colomer(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), José M. C. Tubío(Universitat Pompeu Fabra), Cristina López(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Alba Navarro(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Cristian Tornador(Universitat Pompeu Fabra), Marta Aymerich(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Marı́a Rozman(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Jesús María Hernández‐Rivas(Universidad de Salamanca), Diana Puente(Universidad de Oviedo), José M.P. Freije(Universidad de Oviedo), Gloria Velasco(Universidad de Oviedo), Ana Gutiérrez‐Fernández(Universidad de Oviedo), Dolors Costa(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Ana Carrió(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Sara Guijarro(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Anna Enjuanes(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Luís Hernández(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Jordi Yagüe(Hospital Clínic de Barcelona), Pilar Nicolás(Universidad de Deusto), Carlos Romeo-Casabona(Universidad de Deusto), Heinz Himmelbauer(Universitat Pompeu Fabra), Ester Castillo(Universitat Pompeu Fabra), Juliane C. Dohm(Universitat Pompeu Fabra), Silvia de Sanjosé(Institut d'Investigació Biomédica de Bellvitge), Miguel Á. Piris(Spanish National Cancer Research Centre), Enrique de Alava(Universidad de Salamanca), Jesús F. San Miguel(Universidad de Salamanca), Romina Royo(Barcelona Supercomputing Center), Josep Lluis Gelpí(Barcelona Supercomputing Center), David Torrents(Barcelona Supercomputing Center), Modesto Orozco(Barcelona Supercomputing Center), David G. Pisano(Spanish National Cancer Research Centre), Alfonso Valencia(Spanish National Cancer Research Centre), Roderic Guigó(Universitat Pompeu Fabra), Mónica Bayés(Centro Nacional de Análisis Genómico), Simon Heath(Centro Nacional de Análisis Genómico), Marta Gut(Centro Nacional de Análisis Genómico), Peter Klatt(Consejo Superior de Investigaciones Científicas), John Marshall(Wellcome Sanger Institute), Keiran Raine(Wellcome Sanger Institute), Lucy Stebbings(Wellcome Sanger Institute), P. Andrew Futreal(Wellcome Sanger Institute), Michael R. Stratton(Wellcome Sanger Institute), Peter J. Campbell(Wellcome Sanger Institute), Marta Gut(Centro Nacional de Análisis Genómico), Armando López‐Guillermo(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Xavier Estivill(Universitat Pompeu Fabra), Emili Montserrat(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer), Carlos López-Otı́n(Universidad de Oviedo), Elı́as Campo(Consorci Institut D'Investigacions Biomediques August Pi I Sunyer)
Nature
June 3, 2011
Cited by 1,520Open Access
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Abstract

Analysis of the genomes of four patients with chronic lymphocytic leukaemia, and validation in more than 300 patients, has identified four genes — NOTCH1, MYD88, XPO1 and KLHL6 — that are recurrently mutated in the condition. Mutations in NOTCH1, MYD88 and XPO1 are thought to contribute to the clinical evolution of the disease. Evidence that NOTCH1 and MYD88 mutations are activating events highlights them as potential therapeutic targets. Chronic lymphocytic leukaemia (CLL), the most frequent leukaemia in adults in Western countries, is a heterogeneous disease with variable clinical presentation and evolution1,2. Two major molecular subtypes can be distinguished, characterized respectively by a high or low number of somatic hypermutations in the variable region of immunoglobulin genes3,4. The molecular changes leading to the pathogenesis of the disease are still poorly understood. Here we performed whole-genome sequencing of four cases of CLL and identified 46 somatic mutations that potentially affect gene function. Further analysis of these mutations in 363 patients with CLL identified four genes that are recurrently mutated: notch 1 (NOTCH1), exportin 1 (XPO1), myeloid differentiation primary response gene 88 (MYD88) and kelch-like 6 (KLHL6). Mutations in MYD88 and KLHL6 are predominant in cases of CLL with mutated immunoglobulin genes, whereas NOTCH1 and XPO1 mutations are mainly detected in patients with unmutated immunoglobulins. The patterns of somatic mutation, supported by functional and clinical analyses, strongly indicate that the recurrent NOTCH1, MYD88 and XPO1 mutations are oncogenic changes that contribute to the clinical evolution of the disease. To our knowledge, this is the first comprehensive analysis of CLL combining whole-genome sequencing with clinical characteristics and clinical outcomes. It highlights the usefulness of this approach for the identification of clinically relevant mutations in cancer.


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