Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia (Q29615030)

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scientific article (publication date: August 2002)

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English	Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia	scientific article (publication date: August 2002)

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scholarly article

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Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia (English)

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30 April 2017

chronic myeloid leukemia

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author name string

Shah NP

1

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30 April 2017

Nicoll JM

2

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30 April 2017

Nagar B

3

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Gorre ME

4

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Paquette RL

5

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Kuriyan J

6

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Sawyers CL

7

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language of work or name

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30 April 2017

publication date

August 2002

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30 April 2017

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2

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117-25

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2

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An activating mutation in the ATP binding site of the ABL kinase domain.

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7 January 2021

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Roots of clinical resistance to STI-571 cancer therapy

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High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance

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Transformation of an interleukin 3-dependent hematopoietic cell line by the chronic myelogenous leukemia-specific P210bcr/abl protein

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Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome

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Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome

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Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia

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bcr-abl, the hallmark of chronic myeloid leukaemia in man, induces multiple haemopoietic neoplasms in mice.

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SETOR: hardware-lighted three-dimensional solid model representations of macromolecules

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Role of alpha1 acid glycoprotein in the in vivo resistance of human BCR-ABL(+) leukemic cells to the abl inhibitor STI571

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Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification

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Ph(+) acute lymphoblastic leukemia resistant to the tyrosine kinase inhibitor STI571 has a unique BCR-ABL gene mutation

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Crystal structure of the activated insulin receptor tyrosine kinase in complex with peptide substrate and ATP analog

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Alpha1-acid glycoprotein expressed in the plasma of chronic myeloid leukemia patients does not mediate significant in vitro resistance to STI571.

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Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia

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Induction of a chronic myelogenous leukemia-like syndrome in mice with v-abl and BCR/ABL.

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Functional interaction between DNA-PK and c-Abl in response to DNA damage

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Increase in mutant frequencies in mice expressing the BCR-ABL activated tyrosine kinase.

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Chronic myeloid leukemia

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Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study.

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Structural mechanism for STI-571 inhibition of abelson tyrosine kinase

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Interaction between ATM protein and c-Abl in response to DNA damage

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Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study

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BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome-positive leukaemia to STI571: a prospective study

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Structural basis for activation of human lymphocyte kinase Lck upon tyrosine phosphorylation

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c-Abl tyrosine kinase regulates the human Rad9 checkpoint protein in response to DNA damage

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