A novel tyrosine kinase switch is a mechanism of imatinib resistance in gastrointestinal stromal tumors (Q38304282)

1 September 2017

A novel tyrosine kinase switch is a mechanism of imatinib resistance in gastrointestinal stromal tumors (English)

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1 September 2017

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12

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D Mahadevan

1

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L Cooke

2

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C Riley

3

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R Swart

4

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B Simons

5

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K Della Croce

6

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L Wisner

7

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M Iorio

8

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K Shakalya

9

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H Garewal

10

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R Nagle

11

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1 September 2017

language of work or name

English

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publication date

26 February 2007

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1 September 2017

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26

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3909-3919

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27

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1210173

1 September 2017

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Acquired resistance to imatinib in gastrointestinal stromal tumor occurs through secondary gene mutation

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A missense mutation in KIT kinase domain 1 correlates with imatinib resistance in gastrointestinal stromal tumors

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Mechanisms of resistance to imatinib mesylate in gastrointestinal stromal tumors and activity of the PKC412 inhibitor against imatinib-resistant mutants

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Imatinib binding and cKIT inhibition is abrogated by the cKIT kinase domain I missense mutation Val654Ala

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Identification of BMP and activin membrane-bound inhibitor (BAMBI), an inhibitor of transforming growth factor-beta signaling, as a target of the beta-catenin pathway in colorectal tumor cells

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The anticoagulation factor protein S and its relative, Gas6, are ligands for the Tyro 3/Axl family of receptor tyrosine kinases

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Multidrug resistance proteins in gastrointestinal stromal tumors: site-dependent expression and initial response to imatinib

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STI571 inactivation of the gastrointestinal stromal tumor c-KIT oncoprotein: biological and clinical implications

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Neuroectodermal differentiation of the gastrointestinal tumors in the Carney triad. An ultrastructural and immunohistochemical study

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Identifiers

DOI

10.1038/SJ.ONC.1210173

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Dimensions Publication ID

1 September 2017

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