Cancer therapy shapes the fitness landscape of clonal hematopoiesis.
Adolescent
Adult
Aged
Aged, 80 and over
Antineoplastic Agents
/ pharmacology
Cell Transformation, Neoplastic
/ drug effects
Child
Child, Preschool
Clonal Evolution
Clonal Hematopoiesis
/ drug effects
Cohort Studies
Female
Genetic Fitness
Humans
Infant
Infant, Newborn
Leukemia, Myeloid
/ genetics
Male
Middle Aged
Models, Biological
Mutation
Neoplasms
/ drug therapy
Neoplasms, Second Primary
/ genetics
Selection, Genetic
Young Adult
Journal
Nature genetics
ISSN: 1546-1718
Titre abrégé: Nat Genet
Pays: United States
ID NLM: 9216904
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
05
04
2020
accepted:
02
09
2020
pubmed:
28
10
2020
medline:
30
12
2020
entrez:
27
10
2020
Statut:
ppublish
Résumé
Acquired mutations are pervasive across normal tissues. However, understanding of the processes that drive transformation of certain clones to cancer is limited. Here we study this phenomenon in the context of clonal hematopoiesis (CH) and the development of therapy-related myeloid neoplasms (tMNs). We find that mutations are selected differentially based on exposures. Mutations in ASXL1 are enriched in current or former smokers, whereas cancer therapy with radiation, platinum and topoisomerase II inhibitors preferentially selects for mutations in DNA damage response genes (TP53, PPM1D, CHEK2). Sequential sampling provides definitive evidence that DNA damage response clones outcompete other clones when exposed to certain therapies. Among cases in which CH was previously detected, the CH mutation was present at tMN diagnosis. We identify the molecular characteristics of CH that increase risk of tMN. The increasing implementation of clinical sequencing at diagnosis provides an opportunity to identify patients at risk of tMN for prevention strategies.
Identifiants
pubmed: 33106634
doi: 10.1038/s41588-020-00710-0
pii: 10.1038/s41588-020-00710-0
pmc: PMC7891089
mid: NIHMS1626060
doi:
Substances chimiques
Antineoplastic Agents
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
1219-1226Subventions
Organisme : NCI NIH HHS
ID : K12 CA120780
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL069315
Pays : United States
Organisme : NHGRI NIH HHS
ID : R01 HG010480
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA172012
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA076292
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA217694
Pays : United States
Organisme : NCI NIH HHS
ID : K08 CA241318
Pays : United States
Organisme : NCI NIH HHS
ID : R35 CA253125
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA016672
Pays : United States
Organisme : NHLBI NIH HHS
ID : UG1 HL069315
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA016086
Pays : United States
Commentaires et corrections
Type : CommentIn
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