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MLL translocations specify a distinct gene expression profile that distinguishes a unique leukemia
It is proposed that MLL constitute a distinct disease, denoted here as MLL, and it is shown that the differences in gene expression are robust enough to classify leukemias correctly as M LL, acute lymphoblastic leukemia or acute myelogenous leukemia.
A subtype of childhood acute lymphoblastic leukaemia with poor treatment outcome: a genome-wide classification study.
FBW7 mutations in leukemic cells mediate NOTCH pathway activation and resistance to γ-secretase inhibitors
It is shown that all seven leukemic cell lines with FBW7 mutations were resistant to the MRK-003 GSI and most of these resistant lines also failed to down-regulate the mRNA levels of the NOTCH targets MYC and DELTEX1 after treatment with MRk-003, implying that residual NOTCH signaling in T-ALLs with FBw7 mutations contributes to GSI resistance.
Gene expression-based chemical genomics identifies rapamycin as a modulator of MCL1 and glucocorticoid resistance.
Integrated transcript and genome analyses reveal NKX2-1 and MEF2C as potential oncogenes in T cell acute lymphoblastic leukemia.
PHF6 mutations in T-cell acute lymphoblastic leukemia
PHF6 is identified as a new X-linked tumor suppressor in T-ALL and a strong genetic interaction between PHF6 loss and aberrant expression of TLX transcription factors in the pathogenesis of this disease is pointed to.
Oncogenic IL7R gain-of-function mutations in childhood T-cell acute lymphoblastic leukemia
The findings indicate that IL7R mutational activation is involved in human T-cell leukemogenesis, paving the way for therapeutic targeting of IL-7R–mediated signaling in T-ALL.
L‐asparaginase treatment in acute lymphoblastic leukemia
There is an overview of available evidence for optimal use of Erwinia asparaginase in the treatment of ALL and debate on the optimal formulation and dosage of these agents continues.
Biological and therapeutic aspects of infant leukemia.
Leukemias diagnosed in the first 12 months of life are characterized by an equal distribution of lymphoid and myeloid subtypes and account for 2.5% to 5% of acute lymphoblastic leukemias (ALLs) and…
The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia.
It is concluded that SET-NUP214 may contribute to the pathogenesis of T-ALL by enforcing T-cell differentiation arrest by binding in the promoter regions of specific HOXA genes, where it interacts with CRM1 and DOT1L, which may transcriptionally activate specific members of the HOxA cluster.