TY - JOUR
T1 - Secondary c-kit mutation in a recurrent gastrointestinal stromal tumor under long-term treatment with imatinib mesylate
T2 - Report of a case
AU - Utsunomiya, Tohru
AU - Okamoto, Masahiro
AU - Yano, Shuya
AU - Kameyama, Toshihumi
AU - Matsuyama, Ayumi
AU - Kuma, Sosei
AU - Yamamoto, Manabu
AU - Fujiwara, Megumu
AU - Ishida, Teruyoshi
PY - 2008/1
Y1 - 2008/1
N2 - 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.
AB - 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.
KW - Gastrointestinal stromal tumor
KW - Imatinib resistance
KW - Liver metastasis
KW - Recurrence
KW - Secondary mutation
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U2 - 10.1007/s00595-007-3559-8
DO - 10.1007/s00595-007-3559-8
M3 - Article
C2 - 18085368
AN - SCOPUS:37349051430
VL - 38
SP - 65
EP - 67
JO - Japanese Journal of Surgery
JF - Japanese Journal of Surgery
SN - 0941-1291
IS - 1
ER -