Heat shock protein 90 inhibition is cytotoxic to primary AML cells expressing mutant FLT3 and results in altered downstream signalling. (Q34765294)

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4 January 2020

title

Heat shock protein 90 inhibition is cytotoxic to primary AML cells expressing mutant FLT3 and results in altered downstream signalling (English)

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4 January 2020

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4

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4 January 2020

Ken I. Mills

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4 January 2020

author name string

Laila Al Shaer

1

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4 January 2020

Elisabeth Walsby

2

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4 January 2020

Amanda Gilkes

3

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4 January 2020

Valerie Walsh

5

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4 January 2020

Alan Burnett

7

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4 January 2020

Clare Rowntree

8

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language of work or name

English

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publication date

27 March 2008

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British Journal of Haematology

4 January 2020

published in

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4 January 2020

volume

141

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4 January 2020

issue

4

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4 January 2020

page(s)

483-493

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Phase I pharmacokinetic and pharmacodynamic study of 17-allylamino, 17-demethoxygeldanamycin in patients with advanced malignancies

4 January 2020

cites work

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Hsp-90-associated oncoproteins: multiple targets of geldanamycin and its analogs

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Proteins regulating Ras and its relatives

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Constitutive activation of Akt by Flt3 internal tandem duplications is necessary for increased survival, proliferation, and myeloid transformation.

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Quantitative analysis of dose-effect relationships: the combined effects of multiple drugs or enzyme inhibitors

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Gene expression profiling of human colon cancer cells following inhibition of signal transduction by 17-allylamino-17-demethoxygeldanamycin, an inhibitor of the hsp90 molecular chaperone.

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Protein kinase C mediates mutant N-Ras-induced developmental abnormalities in normal human erythroid cells.

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Heat shock proteins: endogenous modulators of apoptotic cell death

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Cotreatment with 17-allylamino-demethoxygeldanamycin and FLT-3 kinase inhibitor PKC412 is highly effective against human acute myelogenous leukemia cells with mutant FLT-3.

21 January 2018

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FLT3 internal tandem duplication mutations associated with human acute myeloid leukemias induce myeloproliferative disease in a murine bone marrow transplant model

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Mechanism of constitutive activation of FLT3 with internal tandem duplication in the juxtamembrane domain

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The presence of a FLT3 internal tandem duplication in patients with acute myeloid leukemia (AML) adds important prognostic information to cytogenetic risk group and response to the first cycle of chemotherapy: analysis of 854 patients from the Unite

21 January 2018

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A FLT3 tyrosine kinase inhibitor is selectively cytotoxic to acute myeloid leukemia blasts harboring FLT3 internal tandem duplication mutations

21 January 2018

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Heat shock protein 90 inhibition sensitizes acute myelogenous leukemia cells to cytarabine

21 January 2018

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Selective apoptosis of tandemly duplicated FLT3-transformed leukemia cells by Hsp90 inhibitors

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Hsp90 inhibitors as novel cancer chemotherapeutic agents

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Hsp90: chaperoning signal transduction

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The benzoquinone ansamycin 17-allylamino-17-demethoxygeldanamycin binds to HSP90 and shares important biologic activities with geldanamycin

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Destabilization of Raf-1 by geldanamycin leads to disruption of the Raf-1-MEK-mitogen-activated protein kinase signalling pathway

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The role of FLT3 in haematopoietic malignancies

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The AML1-ETO fusion gene promotes extensive self-renewal of human primary erythroid cells

21 January 2018

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Constitutive activation of FLT3 stimulates multiple intracellular signal transducers and results in transformation.

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The Stress Response: Implications for the Clinical Development of Hsp90 Inhibitors

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Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies

21 January 2018

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Internal tandem duplication of the FLT3 gene is preferentially seen in acute myeloid leukemia and myelodysplastic syndrome among various hematological malignancies. A study on a large series of patients and cell lines

21 January 2018

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FLT3 internal tandem duplication in 234 children with acute myeloid leukemia: prognostic significance and relation to cellular drug resistance

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