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Mercedes E. Gorre

University of California, Los Angeles

24

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mutation-dependent and -independent imatinib resistance Adaphostin-induced oxidative stress overcomes BCR/ABL

2013
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Inversion and deletion of 16q22 defined by array CGH, FISH, and RT-PCR in a patient with AML

2011 Cancer Letters
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mutation-dependent and -independent imatinib resistance BCR/ABL Adaphostin-induced oxidative stress overcomes

2010
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of the BCR-ABL chaperone heat shock protein 90 mesylate-resistant chronic myeloid leukemia remain sensitive to inhibitors BCR-ABL point mutants isolated from patients with imatinib

2010
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Array CGH analysis of chronic lymphocytic leukemia reveals frequent cryptic monoallelic and biallelic deletions of chromosome 22q11 that include the PRAME gene

2009 Leukemia Research
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Phosphorylation of the ATP-binding loop directs oncogenicity of drug-resistant BCR-ABL mutants

2006 Proceedings of the National Academy of Sciences of the United States of America
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Altered Oncogenic Fitness of Imatinib- and Dasatinib-Resistant BCR-ABL Mutants Is Due to Differential Intrinsic Kinase Activity and Signaling Pathway Selection Defined by Phosphoproteome Profiling.

2005 Blood
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Imatinib-Resistant BCR-ABL Mutations Alter Oncogenic Potency, Kinase Activity and Substrate Selection.

2004 Blood
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Effects of Adaphostin, a Novel Tyrphostin Inhibitor, in Diverse Models of Imatinib Mesylate Resistance.

2004 Blood
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BCR-ABL point mutants isolated from patients with imatinib mesylate-resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90

2002 Blood
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