NDLI: Surgical intervention for imatinib and sunitinib-resistant gastrointestinal stromal tumors

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Surgical intervention for imatinib and sunitinib-resistant gastrointestinal stromal tumors

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kikuchi, Hirotoshi Setoguchi, Tomohiko Miyazaki, Shinichiro Yamamoto, Masayoshi Ohta, Manabu Kamiya, Kinji Sakaguchi, Takanori Konno, Hiroyuki
Description	Country affiliation: Japan Author Affiliation: Kikuchi H ( Second Department of Surgery, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu 431-3192, Japan. kikuchih@hama-med.ac.jp)
Abstract	Imatinib mesylate is an effective treatment for recurrent or metastatic gastrointestinal stromal tumors (GISTs), but secondary resistance has been reported. The tyrosine kinase inhibitor sunitinib malate has shown efficacy in imatinib-resistant GISTs, and has been used as second-line therapy for recurrent or metastatic GISTs. However, it is often difficult to treat patients with imatinib- and sunitinib-resistant GISTs. In this report, we describe a case of surgically resected liver and peritoneal recurrences of GISTs that arose polyclonally and were resistant to imatinib and sunitinib. A 67-year-old man was referred to our hospital with multiple recurrent GISTs after failed imatinib treatment. Sunitinib was administered at 50 mg/day for 4 weeks with 2-week intervals between treatments. Some of the recurrent GISTs were sensitive, but others were resistant, and progressive disease was diagnosed. Extended left hepatectomy and peritoneal tumorectomy were performed. Histologically, tumors sensitive to sunitinib showed degenerative changes, while the resistant tumors consisted of KIT-positive, viable GIST cells. The primary mutation in all the tumors consisted of a deletion at nucleotides 555–560 with an E554D point mutation at exon 11 of the c-kit gene. The sunitinib-resistant liver and peritoneal tumors had different point mutations: T to G and T to A, respectively, although both resulted in an N822K amino acid alteration, indicating the polyclonal evolution of recurrent GISTs. Thus, if R0 resection is expected, surgical intervention under the control of imatinib or sunitinib should be considered for the control of metastatic or recurrent GISTs.
File Format	HTM / HTML
ISSN	13419625
Issue Number	6
Volume Number	16
e-ISSN	14377772
Journal	International Journal of Clinical Oncology
Language	English
Publisher	Springer
Publisher Date	2011-12-01
Publisher Place	Japan
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Oncology Drug Resistance, Neoplasm Gastrointestinal Neoplasms Surgery Gastrointestinal Stromal Tumors Hepatectomy Liver Neoplasms Drug Therapy Aged Antineoplastic Agents Therapeutic Use Benzamides Pathology Humans Imatinib Mesylate Indoles Secondary Male Mutation Neoplasm Metastasis Neoplasm Recurrence, Local Piperazines Proto-oncogene Proteins C-kit Genetics Pyrimidines Pyrroles Radiography Case Reports Journal Article
Content Type	Text
Resource Type	Case study Article
Subject	Hematology Surgery Oncology

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