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REVIEW article
Front. Hematol.
Sec. Blood Cancer
Volume 3 - 2024 |
doi: 10.3389/frhem.2024.1473920
This article is part of the Research Topic Myeloproliferative Neoplasms: Updates for Patients and Healthcare Providers View all articles
Clonal Evolution: A landmark of MPN evolution
Provisionally accepted- 1 Service de Biologie Cellulaire, Assistance Publique Hôpitaux de Paris (APHP), Hôpital Saint-Louis, Paris, France, Paris, France
- 2 INSERM U1131 Hémopathies Myéloides : Cellules Souches, Modèles Précliniques et Recherche Translationnelle, Paris, Île-de-France, France
- 3 Hôpital Saint-Louis, APHP, Centre d’Investigations Cliniques (Inserm CIC 1427), Paris, France
Myeloproliferative Neoplasms comprise a heterogeneous group of diseases characterized over the past two decades by the acquisition of somatic mutations in hematopoietic stem cells, leading to a pre-leukemic state. The natural history of the disease is marked by the sequential acquisition of genetic events that play an essential role in the phenotype, evolution and response to treatment of the disease. Indeed, disease progression is as heterogeneous as the variety of genetic abnormalities found in individual patients, some of whom lead to disease evolution with a pejorative prognosis, while others persist in a benign manner. In order to better explore these questions, it is important to better understand: (1) the genetic structure of the tumor through dynamic reconstruction of clonal architecture (2) the factors favoring the development of certain clones and their expansion, some of which are governed by Darwinian laws. These parameters could help explain the heterogeneity between MPN patients with similar genetic profiles, and prevent the emergence of clones identified as aggressive by the use of innovative therapeutic strategies targeting new pathways to prevent early transformations in poor prognosis MPN subtypes.
Keywords: Myeloproliferative neoplasms, Additional mutation, Clonal Evolution, Inflammation, selection
Received: 31 Jul 2024; Accepted: 09 Sep 2024.
Copyright: © 2024 Maslah, Giraudier, Cassinat and Kiladjian. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Nabih Maslah, Service de Biologie Cellulaire, Assistance Publique Hôpitaux de Paris (APHP), Hôpital Saint-Louis, Paris, France, Paris, France
Stephane Giraudier, INSERM U1131 Hémopathies Myéloides : Cellules Souches, Modèles Précliniques et Recherche Translationnelle, Paris, 75010, Île-de-France, France
Jean-Jacques Kiladjian, Hôpital Saint-Louis, APHP, Centre d’Investigations Cliniques (Inserm CIC 1427), Paris, France
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