AI Article Synopsis
- The study developed a human xenograft model of gastrointestinal stromal tumor (GIST) using tissue from a patient with esophageal GIST implanted in NOD-SCID mice.
- The presence of a KIT mutation in exon 11 was confirmed through cDNA analysis, and c-KIT protein expression was consistently observed in the tumors.
- Both imatinib and sunitinib treatments were effective in significantly reducing the size of the xenograft tumors, indicating the model's potential usefulness for future GIST research.
Article Abstract
Background: The clinical outcome of gastrointestinal stromal tumor (GIST) has been improved by the introduction of molecular-targeting drugs. However, resistance to these drugs appears during the course of treatment. The aim of this study was to establish and characterize a human xenograft model of GIST.
Materials And Methods: GIST tissue from a patient with esophageal GIST was implanted under the skin of a NOD-SCID mouse. The tumor became successfully engrafted and we investigated the effects of imatinib and sunitinib on this model. KIT mutation was investigated by complementary DNA analysis, and c-KIT (CD117) expression was evaluated by immunohistological staining.
Results: cDNA analysis of the tumor revealed a KIT mutation in exon 11. c-KIT expression was observed in each passaged tumor. Both imatinib and sunitinib significantly reduced the size of the xenograft tumor.
Conclusion: We established a novel xenograft model of human GIST in mice. This xenograft model may be useful for studying GIST.
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