Joshua S Weinstock, Jayakrishnan Gopakumar, Bala Bharathi Burugula, Md Mesbah Uddin, Nikolaus Jahn, Julia A Belk, Hind Bouzid, Bence Daniel, Zhuang Miao, Nghi Ly, Taralynn M Mack, Sofia E Luna, Katherine P Prothro, Shaneice R Mitchell, Cecelia A Laurie, Jai G Broome, Kent D Taylor, Xiuqing Guo, Moritz F Sinner, Aenne S von Falkenhausen, Stefan Kääb, Alan R Shuldiner, Jeffrey R O'Connell, Joshua P Lewis, Eric Boerwinkle, Kathleen C Barnes, Nathalie Chami, Eimear E Kenny, Ruth J F Loos, Myriam Fornage, Lifang Hou, Donald M Lloyd-Jones, Susan Redline, Brian E Cade, Bruce M Psaty, Joshua C Bis, Jennifer A Brody, Edwin K Silverman, Jeong H Yun, Dandi Qiao, Nicholette D Palmer, Barry I Freedman, Donald W Bowden, Michael H Cho, Dawn L DeMeo, Ramachandran S Vasan, Lisa R Yanek, Lewis C Becker, Sharon L R Kardia, Patricia A Peyser, Jiang He, Michiel Rienstra, Pim Van der Harst, Robert Kaplan, Susan R Heckbert, Nicholas L Smith, Kerri L Wiggins, Donna K Arnett, Marguerite R Irvin, Hemant Tiwari, Michael J Cutler, Stacey Knight, J Brent Muhlestein, Adolfo Correa, Laura M Raffield, Yan Gao, Mariza de Andrade, Jerome I Rotter, Stephen S Rich, Russell P Tracy, Barbara A Konkle, Jill M Johnsen, Marsha M Wheeler, J Gustav Smith, Olle Melander, Peter M Nilsson, Brian S Custer, Ravindranath Duggirala, Joanne E Curran, John Blangero, Stephen McGarvey, L Keoki Williams, Shujie Xiao, Mao Yang, C Charles Gu, Yii-Der Ida Chen, Wen-Jane Lee, Gregory M Marcus, John P Kane, Clive R Pullinger, M Benjamin Shoemaker, Dawood Darbar, Dan M Roden, Christine Albert, Charles Kooperberg, Ying Zhou, JoAnn E Manson, Pinkal Desai, Andrew D Johnson, Rasika A Mathias, Thomas W Blackwell, Goncalo R Abecasis, Albert V Smith, Hyun M Kang, Ansuman T Satpathy, Pradeep Natarajan, Jacob O Kitzman, Eric A Whitsel, Alexander P Reiner, Alexander G Bick, Siddhartha Jaiswal
Mutations in a diverse set of driver genes increase the fitness of haematopoietic stem cells (HSCs), leading to clonal haematopoiesis1 . These lesions are precursors for blood cancers2-6 , but the basis of their fitness advantage remains largely unknown, partly owing to a paucity of large cohorts in which the clonal expansion rate has been assessed by longitudinal sampling. Here, to circumvent this limitation, we developed a method to infer the expansion rate from data from a single time point. We applied this method to 5,071 people with clonal haematopoiesis...
April 12, 2023: Nature