The evolutionary dynamics and fitness landscape of clonal hematopoiesis

Author:

Watson Caroline J.12ORCID,Papula A. L.3ORCID,Poon Gladys Y. P.12ORCID,Wong Wing H.4ORCID,Young Andrew L.4ORCID,Druley Todd E.4ORCID,Fisher Daniel S.3ORCID,Blundell Jamie R.12ORCID

Affiliation:

1. Department of Oncology, University of Cambridge, Cambridge, UK.

2. Early Detection Programme, CRUK Cambridge Cancer Centre, University of Cambridge, Cambridge, UK.

3. Department of Applied Physics, Stanford University, Stanford, CA, USA.

4. Department of Pediatrics, Division of Hematology and Oncology, Washington University School of Medicine, St. Louis, MO, USA.

Abstract

Evolutionary dynamics in hematopoiesis Cells accumulate mutations as we age, and these mutations can be a source of diseases such as cancer. How cells containing mutations evolve, are maintained, and proliferate within the body has not been well characterized. Using a quantitative framework, Watson et al. applied population genetic theory to estimate mutation accumulation in cells in blood from sequencing data derived from nearly 50,000 healthy individuals (see the Perspective by Curtis). By evaluating how mutations differ between blood cell populations, a phenomenon known as clonal hematopoiesis, the researchers could observe how recurrent mutations can drive certain clonal lineages to high frequencies within an individual. The risk of specific mutations, some of which are associated with leukemias, rising to high frequencies may therefore be a function of cellular selection and the age at which the mutation originated. Science , this issue p. 1449 ; see also p. 1426

Funder

National Science Foundation

National Cancer Institute

Stand Up To Cancer

UK Research and Innovation

Cancer Research UK Cambridge Centre

Bei Shan Tang Foundation

Cancer Research UK

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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