Abstract
BackgroundA number of non-malignant diseases that share similar morphological features as gastrointestinal stromal tumor (GIST) have been reported. Co-existence of GIST with these other diseases is rarely recognized or reported.Case presentationWe report a case of a 62 year-old man with long-term stable control of metastatic GIST with systemic therapy, presented with an apparent intra-abdominal progression but not supported by imaging with positron emission tomography. Subsequent resection of the intra-abdominal tumor identified a non-malignant fibroid.ConclusionDifferentiating localized progression of GIST from other diseases has important prognostic and therapeutic implications. The potential for co-existence of non-malignant soft tissue neoplasm should always be considered.
Highlights
A number of non-malignant diseases that share similar morphological features as gastrointestinal stromal tumor (GIST) have been reported
We present a case of a man who had been treated with imatinib and achieved long-term stable
No specific adjuvant therapy for the soft-tissue tumor was employed post-operatively. In this patient with metastatic GIST, the development of the mesenteric tumor four years after the institution of Immunohistochemistry was positive for C-KIT, which is unusual in Aggressive fibromatosis (AF) or intra-abdominal keloid type fibrocollagenous scar
Summary
The finding of gain-of-function mutation of KIT has revolutionized the treatment of advanced gastrointestinal stromal tumor (GIST). Post-operatively, this man recovered well from his surgery and was commenced on imatinib 600 mg daily; he subsequently required dose-reduction to 400 mg daily due to grade 3 neutropenia He still had residual hepatic metastatic disease which was visible on computerized tomography [CT] scan, and was FDG-avid on positron emission tomography [PET] evaluation. After two years of therapy, a CT scan revealed an increase in size of a dominant segment VI hepatic metastasis which was treated with radiofrequency ablation He was maintained on imatinib at 600 mg daily with subsequent disease control. No abnormal foci of increased metabolism of FDG can be identified This patient underwent surgery with the pre-surgical diagnosis of a localized progression; surgery was aimed to achieve disease control with the elimination of a presumably localized imatinib resistance tumor. No specific adjuvant therapy for the soft-tissue tumor was employed post-operatively
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