| Literature DB >> 31142838 |
Michaela Gruber1,2,3,4, Ivana Bozic5, Ignaty Leshchiner2, Dimitri Livitz2, Kristen Stevenson6, Laura Rassenti7, Daniel Rosebrock2, Amaro Taylor-Weiner2, Oriol Olive1, Reaha Goyetche1, Stacey M Fernandes1, Jing Sun1, Chip Stewart2, Alicia Wong2, Carrie Cibulskis2, Wandi Zhang1, Johannes G Reiter8, Jeffrey M Gerold8, John G Gribben9, Kanti R Rai10, Michael J Keating11, Jennifer R Brown1,12,13, Donna Neuberg6, Thomas J Kipps7, Martin A Nowak8,14, Gad Getz15,16,17,18, Catherine J Wu19,20,21,22.
Abstract
How the genomic features of a patient's cancer relate to individual disease kinetics remains poorly understood. Here we used the indolent growth dynamics of chronic lymphocytic leukaemia (CLL) to analyse the growth rates and corresponding genomic patterns of leukaemia cells from 107 patients with CLL, spanning decades-long disease courses. We found that CLL commonly demonstrates not only exponential expansion but also logistic growth, which is sigmoidal and reaches a certain steady-state level. Each growth pattern was associated with marked differences in genetic composition, the pace of disease progression and the extent of clonal evolution. In a subset of patients, whose serial samples underwent next-generation sequencing, we found that dynamic changes in the disease course of CLL were shaped by the genetic events that were already present in the early slow-growing stages. Finally, by analysing the growth rates of subclones compared with their parental clones, we quantified the growth advantage conferred by putative CLL drivers in vivo.Entities:
Mesh:
Year: 2019 PMID: 31142838 PMCID: PMC6630176 DOI: 10.1038/s41586-019-1252-x
Source DB: PubMed Journal: Nature ISSN: 0028-0836 Impact factor: 49.962