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JOURNAL ARTICLE
Sagi Abelson, Grace Collord, Stanley W K Ng, Omer Weissbrod, Netta Mendelson Cohen, Elisabeth Niemeyer, Noam Barda, Philip C Zuzarte, Lawrence Heisler, Yogi Sundaravadanam, Robert Luben, Shabina Hayat, Ting Ting Wang, Zhen Zhao, Iulia Cirlan, Trevor J Pugh, David Soave, Karen Ng, Calli Latimer, Claire Hardy, Keiran Raine, David Jones, Diana Hoult, Abigail Britten, John D McPherson, Mattias Johansson, Faridah Mbabaali, Jenna Eagles, Jessica K Miller, Danielle Pasternack, Lee Timms, Paul Krzyzanowski, Philip Awadalla, Rui Costa, Eran Segal, Scott V Bratman, Philip Beer, Sam Behjati, Inigo Martincorena, Jean C Y Wang, Kristian M Bowles, J Ramón Quirós, Anna Karakatsani, Carlo La Vecchia, Antonia Trichopoulou, Elena Salamanca-Fernández, José M Huerta, Aurelio Barricarte, Ruth C Travis, Rosario Tumino, Giovanna Masala, Heiner Boeing, Salvatore Panico, Rudolf Kaaks, Alwin Krämer, Sabina Sieri, Elio Riboli, Paolo Vineis, Matthieu Foll, James McKay, Silvia Polidoro, Núria Sala, Kay-Tee Khaw, Roel Vermeulen, Peter J Campbell, Elli Papaemmanuil, Mark D Minden, Amos Tanay, Ran D Balicer, Nicholas J Wareham, Moritz Gerstung, John E Dick, Paul Brennan, George S Vassiliou, Liran I Shlush
The incidence of acute myeloid leukaemia (AML) increases with age and mortality exceeds 90% when diagnosed after age 65. Most cases arise without any detectable early symptoms and patients usually present with the acute complications of bone marrow failure1 . The onset of such de novo AML cases is typically preceded by the accumulation of somatic mutations in preleukaemic haematopoietic stem and progenitor cells (HSPCs) that undergo clonal expansion2,3 . However, recurrent AML mutations also accumulate in HSPCs during ageing of healthy individuals who do not develop AML, a phenomenon referred to as age-related clonal haematopoiesis (ARCH)4-8 ...
July 2018: Nature
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