Background : The impact of the RECIST 1.1 on the selection of target lesions and assessment of tumor response was not evaluated in patients with advanced NSCLC who received cytotoxic chemotherapy.Methods: We reviewed medical records of patients with advanced NSCLC who received first-line chemotherapy between January 2004 and December 2013 and compared the selection of target lesions and tumor responses using the two RECIST versions.Results: A total of 88 patients who had at least one target lesion according to the RECIST 1.0 were included in the study. The number of target lesions by the RECIST 1.1 was significantly lower than that by the RECIST 1.0. When adopting the RECIST 1.1 instead of the RECIST 1.0, 40 patients (45.4%) showed a decrease in the number of target lesions. Three patients no longer had target lesion because of the new lymph node (LN) criteria of the RECIST 1.1. Tumor responses showed a high level of concordance between the RECIST 1.0 and RECIST 1.1, with a kappa value of 0.912. Four patients (4.5%) showed disagreement of tumor responses between the two criteria, which were all due to the change of the LN criteria.Conclusion: The RECIST 1.1 showed a high level of concordance with the RECIST 1.0 in the assessment of tumor response in advanced NSCLC patients treated with cytotoxic chemotherapy. The new LN criteria were the major cause of the reduction of target lesions and reclassification of the tumor response.

Only two cases of gastric intramural hematoma (IMH) caused by endoscopic mucosal resection (EMR) have been reported to date. This is the first reported case of gastric IMH caused by EMR, treatment of which required hemoclipping and transcatheter arterial embolization. The patient had a normal coagulation profile and no relevant medical history. About 8 h after completing the EMR, the patient vomited approximately 150 mL fresh blood and complained of abdominal pain. Endoscopy showed a 3 × 7 cm hematoma with active surface bleeding in the gastric antrum. Hemoclipping of the bleeding site on the surface and transcatheter arterial embolization of the left gastric artery were performed. Thereafter, conservative management including administration of a proton pump inhibitor was performed, and the lesion resolved. A review of relevant previous cases and this case suggested vessel damage secondary to the submucosal injection itself to be a reasonable causative mechanism for the gastric IMH.