(Q28271726)

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Phase I study of the heat shock protein 90 inhibitor alvespimycin (KOS-1022, 17-DMAG) administered intravenously twice weekly to patients with acute myeloid leukemia

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Phase I study of the heat shock protein 90 inhibitor alvespimycin (KOS-1022, 17-DMAG) administered intravenously twice weekly to patients with acute myeloid leukemia (English)

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acute myeloid leukemia

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author name string

J E Lancet

1

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I Gojo

2

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M Burton

3

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M Quinn

4

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S M Tighe

5

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K Kersey

6

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Z Zhong

7

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M X Albitar

8

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K Bhalla

9

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A L Hannah

10

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M R Baer

11

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language of work or name

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publication date

April 2010

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24

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699-705

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4

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

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HSP90 and the chaperoning of cancer

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Inhibitors of the heat shock response: biology and pharmacology

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The Hsp90 molecular chaperone: an open and shut case for treatment

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Phase I trial of 17-allylamino-17-demethoxygeldanamycin in patients with advanced cancer

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Phase I and pharmacodynamic study of 17-(allylamino)-17-demethoxygeldanamycin in adult patients with refractory advanced cancers

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Antiangiogenic properties of 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin: an orally bioavailable heat shock protein 90 modulator

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Comparison of 17-dimethylaminoethylamino-17-demethoxy-geldanamycin (17DMAG) and 17-allylamino-17-demethoxygeldanamycin (17AAG) in vitro: effects on Hsp90 and client proteins in melanoma models

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Revised recommendations of the International Working Group for Diagnosis, Standardization of Response Criteria, Treatment Outcomes, and Reporting Standards for Therapeutic Trials in Acute Myeloid Leukemia

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Chronic myelogenous leukemia: biology and therapy

1 reference

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A potential role for HSP90 inhibitors in the treatment of JAK2 mutant-positive diseases as demonstrated using quantitative flow cytometry

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

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CD8+ T cells that express CD4 on their surface (CD4dimCD8bright T cells) recognize an antigen-specific target, are detected in vivo, and can be productively infected by T-tropic HIV.

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Simultaneous activation of multiple signal transduction pathways confers poor prognosis in acute myelogenous leukemia

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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

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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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Adverse prognostic significance of KIT mutations in adult acute myeloid leukemia with inv(16) and t(8;21): a Cancer and Leukemia Group B Study

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

1 reference

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Heat shock proteins and acute leukemias

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Unusual expression and localization of heat-shock proteins in human tumor cells

1 reference

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Prolonged exposure to FLT3 inhibitors leads to resistance via activation of parallel signaling pathways

1 reference

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Constitutive activation of mitogen-activated protein kinase pathway in acute leukemia cells

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https://api.crossref.org/works/10.1038%2FLEU.2009.292

7 January 2021

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10.1038/LEU.2009.292

1 reference

Consolidated OpenCitations Corpus – April 2017

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OpenCitations bibliographic resource ID

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Consolidated OpenCitations Corpus – April 2017

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1 reference

Consolidated OpenCitations Corpus – April 2017

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Springer Nature article ID

10.1038/leu.2009.292

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