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Research ArticleClinical Studies

Rapid Relapse after Resection of a Sunitinib-resistant Gastrointestinal Stromal Tumor Harboring a Secondary Mutation in Exon 13 of the c-KIT Gene

HIROTOSHI KIKUCHI, SHINICHIRO MIYAZAKI, TOMOHIKO SETOGUCHI, YOSHIHIRO HIRAMATSU, MANABU OHTA, KINJI KAMIYA, TAKANORI SAKAGUCHI and HIROYUKI KONNO
Anticancer Research September 2012, 32 (9) 4105-4109;
HIROTOSHI KIKUCHI
Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan
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  • For correspondence: kikuchih{at}hama-med.ac.jp
SHINICHIRO MIYAZAKI
Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan
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TOMOHIKO SETOGUCHI
Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan
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YOSHIHIRO HIRAMATSU
Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan
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MANABU OHTA
Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan
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KINJI KAMIYA
Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan
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TAKANORI SAKAGUCHI
Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan
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HIROYUKI KONNO
Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan
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    Figure 1.

    Computed-tomographic (CT) scans of the abdomen before (left panel) and after (middle and right panels) sunitinib (SU) treatment. There are multiple liver metastases in the right lobe (top and middle panels, arrows), one of which was sensitive (top panel) and the other of which was resistant (middle panel) to sunitinib. Recurrent tumors were seen in the retroperitoneal space (bottom panel, arrowheads).

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    Figure 2.

    A: Macroscopic findings of the resected liver (left panel) and retroperitoneal gastrointestinal stromal tumors (GISTs) (right panel). B: Histological findings of the resected GISTs. Hematoxylin and eosin staining showed viable GIST cells as well as tumor cells with degenerative changes both in the liver (left panel) and retroperitoneum (right panel). C: DNA sequencing of the c-KIT gene at exon 13. Both liver (left panel) and retroperitoneal tumors (right panel) exhibited a T to C point mutation which resulted in a V654A amino acid alteration.

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    Figure 3.

    Post-operative computed-tomographic (CT) scans of the abdomen before (left two panels) and after (right two panels) sunitinib (SU) treatment. CT images show recurrent tumors in the retroperitoneal space, one of which was sensitive (upper panel, arrows) and the other of which was resistant (lower panel, arrowheads) to sunitinib.

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Anticancer Research
Vol. 32, Issue 9
September 2012
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Rapid Relapse after Resection of a Sunitinib-resistant Gastrointestinal Stromal Tumor Harboring a Secondary Mutation in Exon 13 of the c-KIT Gene
HIROTOSHI KIKUCHI, SHINICHIRO MIYAZAKI, TOMOHIKO SETOGUCHI, YOSHIHIRO HIRAMATSU, MANABU OHTA, KINJI KAMIYA, TAKANORI SAKAGUCHI, HIROYUKI KONNO
Anticancer Research Sep 2012, 32 (9) 4105-4109;

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Rapid Relapse after Resection of a Sunitinib-resistant Gastrointestinal Stromal Tumor Harboring a Secondary Mutation in Exon 13 of the c-KIT Gene
HIROTOSHI KIKUCHI, SHINICHIRO MIYAZAKI, TOMOHIKO SETOGUCHI, YOSHIHIRO HIRAMATSU, MANABU OHTA, KINJI KAMIYA, TAKANORI SAKAGUCHI, HIROYUKI KONNO
Anticancer Research Sep 2012, 32 (9) 4105-4109;
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