Clonal evolution in aplastic anemia: failed tumor surveillance or maladaptive recovery?
Fiche publication
Date publication
juin 2023
Journal
Leukemia & lymphoma
Auteurs
Membres identifiés du Cancéropôle Est :
Dr PAGLIUCA Simona
Tous les auteurs :
Gurnari C, Pagliuca S, Maciejewski JP
Lien Pubmed
Résumé
Clonal evolution to secondary paroxysmal nocturnal hemoglobinuria (PNH) or myeloid neoplasia (MN) represents one of the long-term complications of patients with aplastic anemia (AA). The recent evidence in the field of immunology and the application of next-generation sequencing have shed light on the molecular underpinnings of these clonal complications, revealing clinical and molecular risk factors as well as potential immunological players. Particularly, whether MN evolution represents a failed tumor surveillance or a maladaptive recovery is still a matter of controversy in the field of bone marrow failure syndromes. However, recent studies have explored the precise dynamics of the immune-molecular forces governing such processes over time, generating knowledge useful for potential early therapeutic strategies. In this review, we will discuss the immune pathophysiology of AA and the emergence of clonal hematopoiesis with regard to the adaptive and maladaptive mechanisms at the basis of secondary evolution trajectories operating under the immune pressure.
Mots clés
), Aplastic anemia, clonal evolution, genomic profiling, human leukocyte antigen (HLA, immune escape, paroxysmal nocturnal hemoglobinuria (PNH)
Référence
Leuk Lymphoma. 2023 06 25;64(8):1389-1399