1C). These two patients resumed screening libraries imatinib therapy, and their metastatic lesions subsequently became smaller and homogeneous on the follow-up CT scans. DISCUSSION Conventional chemotherapeutic agents are rarely effective against gastrointestinal stromal tumors. The new chemotherapeutic agent, imatinib, has been applied and the results are extremely encouraging. The rationale behind imatinib treatment for gastrointestinal stromal tumors lies in the fact that the KIT (encodes the human homolog of the proto-oncogene c-kit) gene mutation has been detected frequently in gastrointestinal stromal tumors. This mutation induces the constitutive activation of the tyrosine kinase receptor, causing the proliferation of tumor cells (2). Imatinib is highly effective in bringing about a reduction in KIT tyrosine kinase activity.

Gastrointestinal stromal tumors frequently spread to the liver and the peritoneum (4). On the CT scan of the portal venous phase, the metastases within the liver are usually heterogeneous and peripherally enhanced, similar to primary tumors (4). The low attenuation in the center of these metastatic lesions often indicates the presence of necrosis in the center of the solid mass. The peripheral enhanced portion represents viable solid tumor. Peritoneal metastasis shows a CT appearance similar to that of metastasis in the liver. In the peritoneum, metastatic lesions treated with imatinib may appear as ascites or fluid collection. In reviewing the original CT reports, we found that the cystic change of the tumor was described as ascites or fluid collection in three patients.

Although long-term follow-up is needed, metastatic lesions in the peritoneum gradually decrease in size, although they may persist for months or years, which is not the case for ascites. The density of the metastases decreased to 15-51 H on the first CT scan after the treatment and then to 15-28 H on the follow-up CT scan, which is close to that of ascites. Metastases can be distinguished from ascites by reviewing the change in the attenuation value and the previous CT scan. Ideally, the scans should be interpreted by a radiologist who is familiar with scans of peritoneal metastases from gastrointestinal stromal tumors following imatinib treatment, in order to avoid the underestimation of the extent of the tumors. The mechanism that induces the cystic change after imatinib treatment is not clear.

In several reported cases, histological examination of the tumors treated with imatinib showed areas with extensive necrosis, hyalinized areas with sparse, scattered tumor cells containing small, condensed nuclei and areas with viable tumor cells (10-12). The optimal duration of the treatment is not yet known (13). It is not clear whether viable tumor cells with malignant potential GSK-3 persist within the cystic lesions and, consequently, the continuous maintenance of imatinib treatment is required.