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

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.