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PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors.

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Title: PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors.
Authors: Heinrich, Michael C., Corless, Christopher L., Duensing, Anette, McCreevey, Laura, Chen, Chang-Jie, Joseph, Nora, Singer, Samuel, Griffith, Diana J., Haley, Andrea, Town, Ajia, Demetri, George D., Fletcher, Christopher D. M., Fletcher, Jonathan A.
Source: Science (pre-March 2025). 1/31/2003, Vol. 299 Issue 5607, p708-710. 3p. 3 Diagrams, 1 Chart, 1 Map.
Subjects: Intestinal tumors, Genetic mutation, Protein-tyrosine kinases
Abstract: Most gastrointestinal stromal tumors (CISTs) have activating mutations in the KIT receptor tyrosine kinase, and most patients with CISTs respond well to Cleevec, which inhibits KIT kinase activity. Here we show that -35% (14 of 40) of CISTs lacking KIT mutations have intragenic activation mutations in the related receptor tyrosine kinase, platelet-derived growth factor receptor a (PDGFRA). Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression. Thus, KIT and PDGFRA mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs. [ABSTRACT FROM AUTHOR]
Copyright of Science (pre-March 2025) is the property of American Association for the Advancement of Science and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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PubType: Academic Journal
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  Data: PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors.
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  Data: <searchLink fieldCode="AR" term="%22Heinrich%2C+Michael+C%2E%22">Heinrich, Michael C.</searchLink><br /><searchLink fieldCode="AR" term="%22Corless%2C+Christopher+L%2E%22">Corless, Christopher L.</searchLink><br /><searchLink fieldCode="AR" term="%22Duensing%2C+Anette%22">Duensing, Anette</searchLink><br /><searchLink fieldCode="AR" term="%22McCreevey%2C+Laura%22">McCreevey, Laura</searchLink><br /><searchLink fieldCode="AR" term="%22Chen%2C+Chang-Jie%22">Chen, Chang-Jie</searchLink><br /><searchLink fieldCode="AR" term="%22Joseph%2C+Nora%22">Joseph, Nora</searchLink><br /><searchLink fieldCode="AR" term="%22Singer%2C+Samuel%22">Singer, Samuel</searchLink><br /><searchLink fieldCode="AR" term="%22Griffith%2C+Diana+J%2E%22">Griffith, Diana J.</searchLink><br /><searchLink fieldCode="AR" term="%22Haley%2C+Andrea%22">Haley, Andrea</searchLink><br /><searchLink fieldCode="AR" term="%22Town%2C+Ajia%22">Town, Ajia</searchLink><br /><searchLink fieldCode="AR" term="%22Demetri%2C+George+D%2E%22">Demetri, George D.</searchLink><br /><searchLink fieldCode="AR" term="%22Fletcher%2C+Christopher+D%2E+M%2E%22">Fletcher, Christopher D. M.</searchLink><br /><searchLink fieldCode="AR" term="%22Fletcher%2C+Jonathan+A%2E%22">Fletcher, Jonathan A.</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Science+%28pre-March+2025%29%22">Science (pre-March 2025)</searchLink>. 1/31/2003, Vol. 299 Issue 5607, p708-710. 3p. 3 Diagrams, 1 Chart, 1 Map.
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  Data: <searchLink fieldCode="DE" term="%22Intestinal+tumors%22">Intestinal tumors</searchLink><br /><searchLink fieldCode="DE" term="%22Genetic+mutation%22">Genetic mutation</searchLink><br /><searchLink fieldCode="DE" term="%22Protein-tyrosine+kinases%22">Protein-tyrosine kinases</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Most gastrointestinal stromal tumors (CISTs) have activating mutations in the KIT receptor tyrosine kinase, and most patients with CISTs respond well to Cleevec, which inhibits KIT kinase activity. Here we show that -35% (14 of 40) of CISTs lacking KIT mutations have intragenic activation mutations in the related receptor tyrosine kinase, platelet-derived growth factor receptor a (PDGFRA). Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression. Thus, KIT and PDGFRA mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Science (pre-March 2025) is the property of American Association for the Advancement of Science and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
PLink https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=pbh&AN=9122772
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        Value: 10.1126/science.1079666
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              Text: 1/31/2003
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