C-KIT mutation cooperates with full-length AML1-ETO to induce acute myeloid leukemia in mice - Wikidata - wikimedia - TriplyDB

C-KIT mutation cooperates with full-length AML1-ETO to induce acute myeloid leukemia in mice

C-KIT mutation cooperates with full-length AML1-ETO to induce acute myeloid leukemia in mice

http://www.wikidata.org/entity/Q34572894

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Contribution of an aged microenvironment to aging-associated myeloproliferative disease.Clathrin assembly protein CALM plays a critical role in KIT signaling by regulating its cellular transport from early to late endosomes in hematopoietic cells.A histone acetyltransferase p300 inhibitor C646 induces cell cycle arrest and apoptosis selectively in AML1-ETO-positive AML cells STAT activation status differentiates leukemogenic from non-leukemogenic stem cells in AML and is suppressed by arsenic in t(6;9)-positive AML RUNX1 mutations in clonal myeloid disorders: from conventional cytogenetics to next generation sequencing, a story 40 years in the making KIT with D816 mutations cooperates with CBFB-MYH11 for leukemogenesis in mice.Distinct classes of c-Kit-activating mutations differ in their ability to promote RUNX1-ETO-associated acute myeloid leukemia.Bortezomib interferes with C-KIT processing and transforms the t(8;21)-generated fusion proteins into tumor-suppressing fragments in leukemia cells.Elucidating the identity of resistance mechanisms to prednisolone exposure in acute lymphoblastic leukemia cells through transcriptomic analysis: A computational approach.Negative effects of GM-CSF signaling in a murine model of t(8;21)-induced leukemia.Overexpression and knockout of miR-126 both promote leukemogenesis JMJD1C is required for the survival of acute myeloid leukemia by functioning as a coactivator for key transcription factors.A novel SAHA-bendamustine hybrid induces apoptosis of leukemia cells.UBASH3B/Sts-1-CBL axis regulates myeloid proliferation in human preleukemia induced by AML1-ETO.Characterization of gene mutations and copy number changes in acute myeloid leukemia using a rapid target enrichment protocol Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation.Kinase-associated gene mutation pattern and clinical relevance in 205 patients with core binding factor leukemias.New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.JAK inhibitors suppress t(8;21) fusion protein-induced leukemia.Molecular pathogenesis of core binding factor leukemia: current knowledge and future prospects.New agents for acute myeloid leukemia: is it time for targeted therapies?Targeted therapy: The new lease on life for acute promyelocytic leukemia, and beyond.AML1-ETO driven acute leukemia: insights into pathogenesis and potential therapeutic approaches.Therapeutic targeting of c-KIT in cancer.Novel therapies for children with acute myeloid leukaemia.Pontin is a critical regulator for AML1-ETO-induced leukemia.Novel approaches to pediatric leukemia treatment.MicroRNAs in Myeloid Hematological Malignancies.VENTX induces expansion of primitive erythroid cells and contributes to the development of acute myeloid leukemia in mice.A minicircuitry of microRNA-9-1 and RUNX1-RUNX1T1 contributes to leukemogenesis in t(8;21) acute myeloid leukemia.Enhanced Fructose Utilization Mediated by SLC2A5 Is a Unique Metabolic Feature of Acute Myeloid Leukemia with Therapeutic Potential.Neutralization of KIT Oncogenic Signaling in Leukemia with Antibodies Targeting KIT Membrane Proximal Domain 5.Regulatory B cells promote graft-versus-host disease prevention and maintain graft-versus-leukemia activity following allogeneic bone marrow transplantation.Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression Precision and prognostic value of clone-specific minimal residual disease in acute myeloid leukemia.Silencing AML1-ETO gene expression leads to simultaneous activation of both pro-apoptotic and proliferation signaling.Alantolactone induces apoptosis in chronic myelogenous leukemia sensitive or resistant to imatinib through NF-κB inhibition and Bcr/Abl protein deletion.Next-generation sequencing with a myeloid gene panel in core-binding factor AML showed KIT activation loop and TET2 mutations predictive of outcome.Cytokines secreted by bone marrow stromal cells protect c-KIT mutant AML cells from c-KIT inhibitor-induced apoptosis.Activating c-KIT mutations confer oncogenic cooperativity and rescue RUNX1/ETO-induced DNA damage and apoptosis in human primary CD34+ hematopoietic progenitors.

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C-KIT mutation cooperates with full-length AML1-ETO to induce acute myeloid leukemia in mice

http://www.wikidata.org/entity/Q34572894

description

2011 nî lūn-bûn

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2011 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2011 թվականի հունվարին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年论文

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C-KIT mutation cooperates with ...... acute myeloid leukemia in mice

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C-KIT mutation cooperates with ...... acute myeloid leukemia in mice

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Proceedings of the National Academy of Sciences of the United States of America

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C-KIT mutation cooperates with ...... acute myeloid leukemia in mice

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Chuan-Feng Wu

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Jian-Qing Mi

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Li-Juan Zhao

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Lin Shi

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Ping Liu

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Ruibao Ren

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Sai-Juan Chen

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Shu-Min Xiong

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Yang Liang

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Zhu Chen

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P2860

Structural mechanism for STI-571 inhibition of abelson tyrosine kinase

Prognostic impact of c-KIT mutations in core binding factor leukemias: an Italian retrospective study.

Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors

Overriding imatinib resistance with a novel ABL kinase inhibitor

Bcr-Abl with an SH3 deletion retains the ability To induce a myeloproliferative disease in mice, yet c-Abl activated by an SH3 deletion induces only lymphoid malignancy

AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec.

The AML1-ETO fusion gene and the FLT3 length mutation collaborate in inducing acute leukemia in mice.

AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations

Focus on acute leukemias.

An activated receptor tyrosine kinase, TEL/PDGFbetaR, cooperates with AML1/ETO to induce acute myeloid leukemia in mice.

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