High-level IGF1R expression is required for leukemia-initiating cell activity in T-ALL and is supported by Notch signaling.
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Notch signaling: its roles and therapeutic potential in hematological malignanciesTargeting leukemia stem cells: which pathways drive self-renewal activity in T-cell acute lymphoblastic leukemia?Crosstalk of the Insulin-Like Growth Factor Receptor with the Wnt Signaling Pathway in Breast CancerLong non-coding RNAs in normal and malignant hematopoiesisThe relevance of PTEN-AKT in relation to NOTCH1-directed treatment strategies in T-cell acute lymphoblastic leukemiaNOTCH1 signaling promotes human T-cell acute lymphoblastic leukemia initiating cell regeneration in supportive nichesGrowth factor independence 1 antagonizes a p53-induced DNA damage response pathway in lymphoblastic leukemia.Angiocrine factors deployed by tumor vascular niche induce B cell lymphoma invasiveness and chemoresistanceMolecular Checkpoint Decisions Made by Subverted Vascular Niche Transform Indolent Tumor Cells into Chemoresistant Cancer Stem CellsGenome-wide mapping and characterization of Notch-regulated long noncoding RNAs in acute leukemia.A novel antisense long noncoding RNA within the IGF1R gene locus is imprinted in hematopoietic malignancies.Two hits are better than one: targeting both phosphatidylinositol 3-kinase and mammalian target of rapamycin as a therapeutic strategy for acute leukemia treatment.Interleukin-18 produced by bone marrow-derived stromal cells supports T-cell acute leukaemia progressionA parallel-arm phase I trial of the humanised anti-IGF-1R antibody dalotuzumab in combination with the AKT inhibitor MK-2206, the mTOR inhibitor ridaforolimus, or the NOTCH inhibitor MK-0752, in patients with advanced solid tumours.Growth factor independent-1 maintains Notch1-dependent transcriptional programming of lymphoid precursors.Insulin growth factor 1 receptor expression is associated with NOTCH1 mutation, trisomy 12 and aggressive clinical course in chronic lymphocytic leukaemia.Inhibition of type I insulin-like growth factor receptor tyrosine kinase by picropodophyllin induces apoptosis and cell cycle arrest in T lymphoblastic leukemia/lymphoma.Role of IGF1R in Breast Cancer Subtypes, Stemness, and Lineage DifferentiationThe transcription factors Ik-1 and MZF1 downregulate IGF-IR expression in NPM-ALK⁺ T-cell lymphomaThe role of Notch receptors in transcriptional regulationInhibition of IGF1-R overcomes IGFBP7-induced chemotherapy resistance in T-ALL.Leukemia stem cells in T-ALL require active Hif1α and Wnt signalingRegulation of gene expression dynamics during developmental transitions by the Ikaros transcription factor.IGF1R Derived PI3K/AKT Signaling Maintains Growth in a Subset of Human T-Cell Acute Lymphoblastic Leukemias.HES1 opposes a PTEN-dependent check on survival, differentiation, and proliferation of TCRβ-selected mouse thymocytes.Defined, serum-free conditions for in vitro culture of primary human T-ALL blasts.Endogenous dendritic cells from the tumor microenvironment support T-ALL growth via IGF1R activation.Activated Notch counteracts Ikaros tumor suppression in mouse and human T-cell acute lymphoblastic leukemia.The NOTCH signaling pathway: role in the pathogenesis of T-cell acute lymphoblastic leukemia and implication for therapy.The expression and significance of insulin-like growth factor-1 receptor and its pathway on breast cancer stem/progenitors.MicroRNA-100/99a, deregulated in acute lymphoblastic leukaemia, suppress proliferation and promote apoptosis by regulating the FKBP51 and IGF1R/mTOR signalling pathwaysPhenothiazines induce PP2A-mediated apoptosis in T cell acute lymphoblastic leukemia.The emerging role of insulin and insulin-like growth factor signaling in cancer stem cells.c-Myc inhibition prevents leukemia initiation in mice and impairs the growth of relapsed and induction failure pediatric T-ALL cells.IGF-IR signaling in epithelial to mesenchymal transition and targeting IGF-IR therapy: overview and new insightsPPAR-γ Agonists As Antineoplastic Agents in Cancers with Dysregulated IGF Axis.Type I insulin-like growth factor receptor signaling in hematological malignancies.Insulin-like growth factors and insulin: at the crossroad between tumor development and longevity.Outlook on PI3K/AKT/mTOR inhibition in acute leukemia.Targeting the mTOR Pathway in Leukemia.
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P2860
High-level IGF1R expression is required for leukemia-initiating cell activity in T-ALL and is supported by Notch signaling.
description
2011 nî lūn-bûn
@nan
2011 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
High-level IGF1R expression is ...... supported by Notch signaling.
@ast
High-level IGF1R expression is ...... supported by Notch signaling.
@en
type
label
High-level IGF1R expression is ...... supported by Notch signaling.
@ast
High-level IGF1R expression is ...... supported by Notch signaling.
@en
prefLabel
High-level IGF1R expression is ...... supported by Notch signaling.
@ast
High-level IGF1R expression is ...... supported by Notch signaling.
@en
P2093
P2860
P50
P356
P1476
High-level IGF1R expression is ...... supported by Notch signaling.
@en
P2093
Andrew P Weng
Hongfang Wang
Jen-Chieh Tseng
Joan Carboni
Jon C Aster
Marco Gottardis
Michael Pollak
Oksana Nemirovsky
Samuel Gusscott
P2860
P304
P356
10.1084/JEM.20110121
P407
P577
2011-08-01T00:00:00Z