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Secondary c-kit Mutation in a Recurrent Gastrointestinal Stromal Tumor Under Long-Term Treatment with Imatinib Mesylate: Report of a Case

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Abstract

Gastrointestinal stromal tumors (GISTs) commonly harbor oncogenic mutations of the c-kit receptor gene, which are targets for imatinib mesylate. However, imatinib resistance is an increasing clinical problem. We herein present such a case with a recurrent GIST, in association with the development of a secondary mutation in the c-kit gene. A 67-year-old man, who had a GIST of the stomach with multiple liver metastases, underwent a partial gastrectomy, distal pancreatectomy, and partial hepatectomy. After surgery, he was treated with imatinib. However, during the approximately 4-year treatment period, a recurrence of the GIST in the liver was detected, for which a partial hepatectomy was again performed. The primary GIST constitutively had a deletion mutation in exon 11. In addition, the recurrent hepatic tumor developed a secondary point mutation (Val654Ala) in exon 13, which may be responsible for the imatinib resistance.

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Utsunomiya, T., Okamoto, M., Yano, S. et al. Secondary c-kit Mutation in a Recurrent Gastrointestinal Stromal Tumor Under Long-Term Treatment with Imatinib Mesylate: Report of a Case. Surg Today 38, 65–67 (2008). https://doi.org/10.1007/s00595-007-3559-8

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  • DOI: https://doi.org/10.1007/s00595-007-3559-8

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