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Activating Mutations of NOTCH1 in Human T Cell Acute Lymphoblastic Leukemia
These findings greatly expand the role of activated NOTCH1 in the molecular pathogenesis of human T-ALL and provide a strong rationale for targeted therapies that interfere with NOTCH signaling. Expand
Gene expression signatures define novel oncogenic pathways in T cell acute lymphoblastic leukemia.
It is shown that five different T cell oncogenes are often aberrantly expressed in the absence of chromosomal abnormalities, and HOX11L2 activation is identified as a novel event in T cell leukemogenesis. Expand
tp53 mutant zebrafish develop malignant peripheral nerve sheath tumors.
These mutant zebrafish lines provide a unique platform for modifier screens to identify genetic mutations or small molecules that affect tp53-related pathways, including apoptosis, cell-cycle delay, and tumor suppression. Expand
Oncogenic transcription factors in the human acute leukemias.
  • A. Look
  • Biology, Medicine
  • Science
  • 7 November 1997
The insights gained from studies of translocation-generated oncogenes and their protein products should hasten the development of highly specific, and hence less toxic, forms of leukemia therapy. Expand
NOTCH1 directly regulates c-MYC and activates a feed-forward-loop transcriptional network promoting leukemic cell growth
  • T. Palomero, Wei Keat Lim, +14 authors A. Ferrando
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences
  • 28 November 2006
The NOTCH1 signaling pathway directly links extracellular signals with transcriptional responses in the cell nucleus and plays a critical role during T cell development and in the pathogenesis overExpand
A tissue-scale gradient of hydrogen peroxide mediates rapid wound detection in zebrafish
This work reveals a sustained rise in H2O2 concentration at the wound margin, and shows that this gradient is created by dual oxidase (Duox), and that it is required for rapid recruitment of leukocytes to the wound. Expand
Acute lymphoblastic leukaemia
Advances in understanding of the pathobiology of acute lymphoblastic leukaemia, fuelled by emerging molecular technologies, suggest that drugs specifically targeting the genetic defects of leukaemic cells could revolutionise management of this disease. Expand
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. Expand
Caspase 8 is deleted or silenced preferentially in childhood neuroblastomas with amplification of MYCN
Caspase 8 acts as a tumor suppressor in neuroblastomas with amplification of the oncogene MYCN and is silenced through DNA methylation as well as through gene deletion. Expand
Interplay of pu.1 and gata1 determines myelo-erythroid progenitor cell fate in zebrafish.
Gene knockdown experiments and transplantation assays demonstrated the reciprocal negative regulation of pu.1 and gata1 and their non-cell-autonomous regulation that determines myeloid versus erythroid MPC fate in the distinct blood-forming regions, providing intriguing evidence that this gene can function in the absence of some stem cell genes, such as scl, in governing myelopoiesis. Expand