Molecular Pathology of Myeloid Neoplasms: Molecular Pattern Recognition.


Journal

Surgical pathology clinics
ISSN: 1875-9157
Titre abrégé: Surg Pathol Clin
Pays: United States
ID NLM: 101491209

Informations de publication

Date de publication:
Sep 2021
Historique:
entrez: 10 8 2021
pubmed: 11 8 2021
medline: 29 10 2021
Statut: ppublish

Résumé

Despite the apparent complexity of the molecular genetic underpinnings of myeloid neoplasms, most myeloid mutational profiles can be understood within a simple framework. Somatic mutations accumulate in hematopoietic stem cells with aging and toxic insults, termed clonal hematopoiesis. These "old stem cells" mutations, predominantly in the epigenetic and RNA spliceosome pathways, act as "founding" driver mutations leading to a clonal myeloid neoplasm when sufficient in number and clone size. Subsequent mutations can create the genetic flavor of the myeloid neoplasm ("backseat" drivers) due to their enrichment in certain entities or act as progression events ("aggressive" drivers) during clonal evolution.

Identifiants

pubmed: 34373100
pii: S1875-9181(21)00047-7
doi: 10.1016/j.path.2021.05.013
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

517-528

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

Auteurs

Sam Sadigh (S)

Department of Pathology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA.

Annette S Kim (AS)

Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA. Electronic address: askim@bwh.harvard.edu.

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Classifications MeSH