Fiche publication
Date publication
juin 2021
Journal
Molecular cancer
Auteurs
Membres identifiés du Cancéropôle Est :
Dr MARCAIS Ambroise
Tous les auteurs :
Bellon M, Bialuk I, Galli V, Bai XT, Farre L, Bittencourt A, Marçais A, Petrus MN, Ratner L, Waldmann TA, Asnafi V, Gessain A, Matsuoka M, Franchini G, Hermine O, Watanabe T, Nicot C
Lien Pubmed
Résumé
Human T cell Leukemia virus type 1 (HTLV-I) is etiologically linked to adult T cell leukemia/lymphoma (ATL) and an inflammatory neurodegenerative disease called HTLV-I-associated myelopathy or tropical spastic paraparesis (HAM/TSP). The exact genetic or epigenetic events and/or environmental factors that influence the development of ATL, or HAM/TSP diseases are largely unknown. The tumor suppressor gene, Fragile Histidine Triad Diadenosine Triphosphatase (FHIT), is frequently lost in cancer through epigenetic modifications and/or deletion. FHIT is a tumor suppressor acting as genome caretaker by regulating cellular DNA repair. Indeed, FHIT loss leads to replicative stress and accumulation of double DNA strand breaks. Therefore, loss of FHIT expression plays a key role in cellular transformation.
Mots clés
ATL, ATLL, Cancer, Epigenetic, Epimutation, FHIT, HAM, HTLV-1, Leukemia, Lymphoma, Methylation, TSP, TSP/HAM, Tax
Référence
Mol Cancer. 2021 06 6;20(1):86
