Partial trisomy 21 contributes to T-cell malignancies induced by JAK3-activating mutations in murine models

Author:

Rivera-Munoz Paola1,Laurent Anouchka P.123,Siret Aurelie12,Lopez Cecile K.124,Ignacimouttou Cathy123,Cornejo Melanie G.5,Bawa Olivia2,Rameau Philippe6,Bernard Olivier A.12,Dessen Philippe12,Gilliland Gary D.57,Mercher Thomas1258,Malinge Sébastien129

Affiliation:

1. INSERM U1170, Villejuif, France;

2. Gustave Roussy Institute, Villejuif, France;

3. Ecole doctorale “Hématologie, Oncogenèse et Biothérapies,” Université Paris VII–Denis Diderot, Paris, France;

4. Ecole doctorale “Cancérologie, Biologie, Médecine, Santé,” Université Paris Saclay, Saint-Aubin, France;

5. Division of Hematology, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA;

6. INSERM Unité mixte de service 3655 Centre national de la recherche scientifique/Unité de service 23, Gustave Roussy Cancer Campus, Villejuif, France;

7. Howard Hughes Medical Institute, Boston, MA;

8. Equipe Labellisée Ligue Contre le Cancer, Paris, France; and

9. Telethon Kids Institute, Perth, Australia

Abstract

Key Points Jak3A572V-induced CTCL-like disorders are mutant Jak3 dose-dependent, transplantable, and phenotypically heterogeneous. Trisomy 21, somatically acquired in human CTCL, functionally cooperates with activated Jak3 to enhance the CTCL-like phenotype in vivo.

Publisher

American Society of Hematology

Subject

Hematology

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