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The genetic basis of early T-cell precursor acute lymphoblastic leukaemia
The mutational spectrum is similar to myeloid tumours, and moreover, the global transcriptional profile of ETP ALL was similar to that of normal andMyeloid leukaemia haematopoietic stem cells, suggesting that addition of myeloids-directed therapies might improve the poor outcome of E TP ALL.
Genetic alterations activating kinase and cytokine receptor signaling in high-risk acute lymphoblastic leukemia.
JAK-STAT pathway activation in malignant and nonmalignant cells contributes to MPN pathogenesis and therapeutic response.
It is demonstrated that JAK-STAT3-mediated cytokine production from malignant and nonmalignant cells contributes to MPN pathogenesis and thatJAK inhibition in both populations is required for therapeutic efficacy, providing novel insight into the mechanisms by which JAK kinase inhibition achieves therapeutic efficacy in MPNs.
Mutation of the receptor tyrosine phosphatase PTPRC (CD45) in T-cell acute lymphoblastic leukemia.
It is demonstrated that down-regulation of CD45 expression sensitizes T cells to cytokine stimulation, as observed by increased JAK/STAT signaling, whereas overexpression of CD43 decreases cytokine-induced signaling, and identifies a tumor suppressor role for CD45 in T-cell acute lymphoblastic leukemia.
CHZ868, a Type II JAK2 Inhibitor, Reverses Type I JAK Inhibitor Persistence and Demonstrates Efficacy in Myeloproliferative Neoplasms.
Toll-like receptor alterations in myelodysplastic syndrome
Findings indicate that TLR2-centered signaling is deregulated in MDS, and that its targeting may have potential therapeutic benefit in M DS.
TYK2-STAT1-BCL2 pathway dependence in T-cell acute lymphoblastic leukemia.
RNAi technology is used to identify a novel oncogenic pathway that involves aberrant activation of the TYK2 tyrosine kinase and its downstream substrate, STAT1, which ultimately promotes T-ALL cell survival through the upregulation of BCL2 expression.
Deletion of the protein tyrosine phosphatase gene PTPN2 in T-cell acute lymphoblastic leukemia
The identification of focal deletions of PTPN2 in human T-cell acute lymphoblastic leukemia (T-ALL) is described and genetic and functional evidence for a tumor suppressor role is provided and it is suggested that expression of P TPN2 may modulate response to treatment.
Dual Targeting of Oncogenic Activation and Inflammatory Signaling Increases Therapeutic Efficacy in Myeloproliferative Neoplasms.
Discovery of Novel Recurrent Mutations in Childhood Early T-Cell Precursor Acute Lymphoblastic Leukemia by Whole Genome Sequencing - a Report From the St Jude Children's Research Hospital -…
Results of whole genome sequencing of tumor and normal DNA from 12 children with ETP ALL show a high frequency of activating mutations in genes regulating cytokine receptor and Ras signalling are identified, including GATA3 regulates early T cell development, and mutations in this gene were observed exclusively in ETP All.