The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
A Missense Mutation in KIT Kinase Domain 1 Correlates with Imatinib Resistance in Gastrointestinal Stromal Tumors
Abstract
KIT gain of function mutations play an important role in the pathogenesis of gastrointestinal stromal tumors (GISTs). Imatinib is a selective tyrosine kinase inhibitor of ABL, platelet-derived growth factor receptor (PDGFR), and KIT and represents a new paradigm of targeted therapy against GISTs. Here we report for the first time that, after imatinib treatment, an additional specific and novel KIT mutation occurs in GISTs as they develop resistance to the drug. We studied 12 GIST patients with initial near-complete response to imatinib. Seven harbored mutations in KIT exon 11, and 5 harbored mutations in exon 9. Within 31 months, six imatinib-resistant rapidly progressive peritoneal implants (metastatic foci) developed in five patients. Quiescent residual GISTs persisted in seven patients. All six rapidly progressive imatinib-resistant implants from five patients show an identical novel KIT missense mutation, 1982T→C, that resulted in Val654Ala in KIT tyrosine kinase domain 1. This novel mutation has never been reported before, is not present in pre-imatinib or post-imatinib residual quiescent GISTs, and is strongly correlated with imatinib resistance. Allelic-specific sequencing data show that this new mutation occurs in the allele that harbors original activation mutation of KIT.
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Citations
Cites
Gain-of-Function Mutations of c- kit in Human Gastrointestinal Stromal Tumors
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Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors
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Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
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PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors
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Kinase Mutations and Imatinib Response in Patients With Metastatic Gastrointestinal Stromal Tumor
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Cited by
EGFR Mutation and Resistance of Non–Small-Cell Lung Cancer to Gefitinib
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“Abbreviations: CML, chronic myelogenous leukemia; CT, computed tomography; del, deletion; EGFR, epidermal growth factor receptor; GIST, gastrointestinal stromal tumor; HES, hypereosinophilic syndrome; NSCLC, non-small cell lung cancer; p-EGFR, phospho-EGFR; PCR-RFLP, PCR restriction fragment length polymorphism; SNP,…”
ResultInfluentialDemetri, G. D., van Oosterom, A. T., Garrett, C. R., Blackstein, M. E., Shah, M. H., Verweij, J., McArthur, G., Judson, I. R., Heinrich, M. C., Morgan, J. A., et al. (2006) · The Lancet · doi:10.1016/s0140-6736(06)69446-4 · Cited by 2,607
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Self-citationGastrointestinal stromal tumours: origin and molecular oncology
Corless, C. L., Barnett, C. M., & Heinrich, M. C. (2011) · Nature Reviews Cancer · doi:10.1038/nrc3143 · Cited by 891
Metadata
- Authors
- Chen, L. L., Trent, J. C., Wu, E. F., Fuller, G. N., Ramdas, L., Zhang, W., Raymond, A. K., Prieto, V. G., Oyedeji, C. O., Hunt, K. K., Pollock, R. E., Feig, B. W., Hayes, K. J., Choi, H., Macapinlac, H. A., Hittelman, W., Velasco, M. A., Patel, S., Burgess, M. A., Benjamin, R. S., & Frazier, M. L.
- Venue
- Cancer Research
- Published
- 2004-09-01
- Volume
- 64
- Issue
- 17
- Pages
- 5913-5919
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2126920848
- Cited by
- 339
- References
- 19
- FWCI
- 26.18
- Type
- journal article
- Language
- en
- Open access
- closed
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- Chen, L. L., Trent, J. C., Wu, E. F., Fuller, G. N., Ramdas, L., Zhang, W., Raymond, A. K., Prieto, V. G., Oyedeji, C. O., Hunt, K. K., Pollock, R. E., Feig, B. W., Hayes, K. J., Choi, H., Macapinlac, H. A., Hittelman, W., Velasco, M. A., Patel, S., Burgess, M. A., . . . Frazier, M. L. (2004). A Missense Mutation in KIT Kinase Domain 1 Correlates with Imatinib Resistance in Gastrointestinal Stromal Tumors. Cancer Research. https://doi.org/10.1158/0008-5472.can-04-0085
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