Secondary resistance of extra-gastrointestinal stromal tumors to imatinib mesylate: Report of a case

• Published in: Surgery today (Tokyo, Japan) Vol. 41; no. 9; pp. 1290 - 1293
• Main Authors: Ando, Koji, Oki, Eiji, Sugiyama, Masahiko, Zhao, Yan, Kojima, Aya, Yamamoto, Hidetaka, Yamashita, Yoichi, Saeki, Hiroshi, Taketomi, Akinobu, Morita, Masaru, Kakeji, Yoshihiro, Tsujitani, Shunichi, Maehara, Yoshihiko
• Format: Journal Article
• Language: English
• Published: Japan Springer Japan 01.09.2011
• Subjects: Abdominal Neoplasms - drug therapy; Abdominal Neoplasms - genetics; Abdominal Neoplasms - pathology; Antineoplastic Agents - therapeutic use; Benzamides; Case Report; Drug Resistance, Neoplasm; Humans; Imatinib Mesylate; Liver Neoplasms - genetics; Liver Neoplasms - secondary; Male; Medicine; Medicine & Public Health; Middle Aged; Neoplasm Recurrence, Local - genetics; Neoplasms, Connective Tissue - drug therapy; Neoplasms, Connective Tissue - genetics; Neoplasms, Connective Tissue - pathology; Neoplasms, Multiple Primary - drug therapy; Neoplasms, Multiple Primary - genetics; Neoplasms, Multiple Primary - pathology; Piperazines - therapeutic use; Pyrimidines - therapeutic use; Surgery; Surgical Oncology; Secondary resistance; gene mutation; Extra-gastrointestinal stromal tumor; Imatinib mesylate
• ISSN: 0941-1291; 1436-2813
• DOI: 10.1007/s00595-010-4477-8

Extra-gastrointestinal stromal tumors (EGISTs) that do not originate in the digestive tract are rare. We report a case of multiple EGISTs, which was monitored closely by KIT gene mutation analysis and other investigations. The patient was a 52-year-old man in whom multiple tumors in the abdominal cavity were diagnosed as EGISTs. Immunohistochemical analysis revealed positive staining for c-kit; however, no mutations were found in the KIT gene. The tumors decreased in size remarkably following treatment with imatinib mesylate, but after 2 years of this treatment, multiple liver metastases and some regrowth of the abdominal masses were found simultaneously. The liver metastasis and the abdominal masses were excised, and further analysis of the KIT gene revealed the same mutation in exon 11 in the KIT gene in the metastatic tumors. We speculate that the treatment might have triggered development of the imatinib mesylate-resistant clone, which may have existed in the primary lesion as a KIT gene mutant. This report provides valuable insight into the mechanisms of recurrent GISTs after treatment with imatinib mesylate.