BH3 mimetic ABT-737 neutralizes resistance to FLT3 inhibitor treatment mediated by FLT3-independent expression of BCL2 in primary AML blasts. (Q40122807)

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scientific article published on 7 June 2007

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English	BH3 mimetic ABT-737 neutralizes resistance to FLT3 inhibitor treatment mediated by FLT3-independent expression of BCL2 in primary AML blasts.	scientific article published on 7 June 2007

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scholarly article

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31 December 2019

BH3 mimetic ABT-737 neutralizes resistance to FLT3 inhibitor treatment mediated by FLT3-independent expression of BCL2 in primary AML blasts (English)

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31 December 2019

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31 December 2019

Stefan Bohlander

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Kohl TM

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Hellinger C

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Buske C

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Hiddemann W

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Spiekermann K

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publication date

7 June 2007

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1763-1772

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31 December 2019

https://scigraph.springernature.com/pub.10.1038/sj.leu.2404776

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Mutagenesis of the BH3 domain of BAX identifies residues critical for dimerization and killing

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Drug therapy for acute myeloid leukemia

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Genetics of myeloid malignancies: pathogenetic and clinical implications

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Analysis of FLT3 length mutations in 1003 patients with acute myeloid leukemia: correlation to cytogenetics, FAB subtype, and prognosis in the AMLCG study and usefulness as a marker for the detection of minimal residual disease

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Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia: association with FAB subtypes and identification of subgroups with poor prognosis

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The role of FLT3 in haematopoietic malignancies

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FLT3, RAS, and TP53 mutations in elderly patients with acute myeloid leukemia.

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Tandem-duplicated Flt3 constitutively activates STAT5 and MAP kinase and introduces autonomous cell growth in IL-3-dependent cell lines

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FLT3 internal tandem duplication in CD34+/CD33- precursors predicts poor outcome in acute myeloid leukemia

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Finding the next Gleevec: FLT3 targeted kinase inhibitor therapy for acute myeloid leukemia

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Inhibition of mutant FLT3 receptors in leukemia cells by the small molecule tyrosine kinase inhibitor PKC412.

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7 January 2021

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The protein tyrosine kinase inhibitor SU5614 inhibits FLT3 and induces growth arrest and apoptosis in AML-derived cell lines expressing a constitutively activated FLT3.

1 reference

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7 January 2021

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The effects of lestaurtinib (CEP701) and PKC412 on primary AML blasts: the induction of cytotoxicity varies with dependence on FLT3 signaling in both FLT3-mutated and wild-type cases

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7 January 2021

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A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy

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Generalized Equations for the Analysis of Inhibitions of Michaelis-Menten and Higher-Order Kinetic Systems with Two or More Mutually Exclusive and Nonexclusive Inhibitors

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Mutations in the tyrosine kinase domain of FLT3 define a new molecular mechanism of acquired drug resistance to PTK inhibitors in FLT3-ITD–transformed hematopoietic cells

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Variable cytotoxicity of diphtheria toxin 388-granulocyte-macrophage colony-stimulating factor fusion protein for acute myelogenous leukemia stem cells

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An inhibitor of Bcl-2 family proteins induces regression of solid tumours

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Overexpression of Bax sensitizes human pancreatic cancer cells to apoptosis induced by chemotherapeutic agents

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KIT exon 8 mutations associated with core-binding factor (CBF)-acute myeloid leukemia (AML) cause hyperactivation of the receptor in response to stem cell factor.

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KIT-D816 mutations in AML1-ETO-positive AML are associated with impaired event-free and overall survival

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FLT3-ITD-TKD dual mutants associated with AML confer resistance to FLT3 PTK inhibitors and cytotoxic agents by overexpression of Bcl-x(L).

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Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins

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7 January 2021

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'Seed' analysis of off-target siRNAs reveals an essential role of Mcl-1 in resistance to the small-molecule Bcl-2/Bcl-XL inhibitor ABT-737.

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Mcl-1 down-regulation potentiates ABT-737 lethality by cooperatively inducing Bak activation and Bax translocation

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7 January 2021

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Mechanisms of apoptosis sensitivity and resistance to the BH3 mimetic ABT-737 in acute myeloid leukemia

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7 January 2021

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The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized.

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Mule/ARF-BP1, a BH3-only E3 ubiquitin ligase, catalyzes the polyubiquitination of Mcl-1 and regulates apoptosis

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Bim and Bad mediate imatinib-induced killing of Bcr/Abl+ leukemic cells, and resistance due to their loss is overcome by a BH3 mimetic.

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Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737.

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Identifiers

10.1038/SJ.LEU.2404776

1 reference

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31 December 2019

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1 reference

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31 December 2019

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