PurposeThe second planned interim analysis (median follow-up 12.5 months) in a phase III trial of postoperative adjuvant chemotherapy for stage III gastric cancer revealed significant improvement in relapse-free survival (RFS) for S-1 plus docetaxel over S-1 alone. Although enrollment was terminated on the recommendation of the independent data and safety monitoring committee, we continued follow-up and herein report on 3-year RFS, the primary endpoint. Patients and methods Patients with histologically confirmed stage III gastric cancer who underwent gastrectomy with D2 lymphadenectomy were randomly assigned to receive adjuvant chemotherapy with either S-1 plus docetaxel or S-1 alone. In the S-1 plus docetaxel group, S-1 was given orally for 2 weeks followed by 1 week of rest for seven courses, and docetaxel was given intravenously on day 1 of the second to seventh courses. The combination therapy was followed by S-1 monotherapy for up to 1 year. ResultsThe 3-year RFS rate of the S-1 plus docetaxel group was 67.7%. This was significantly superior to that of 57.4% in the S-1 group (hazard ratio [HR] 0.715, 95% CI 0.587-0.871, P = 0.0008). This translated into a significant benefit in the 3-year overall survival (OS) rate in the S-1 plus docetaxel group (77.7% versus 71.2%, HR 0.742, 95% CI 0.596-0.925, P = 0.0076). Conclusion On 3-year follow-up data, postoperative adjuvant therapy with S-1 plus docetaxel was confirmed to improve both RFS and OS and can be recommended as a standard of care for patients with stage III gastric cancer treated by D2 dissection.

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A 70-year-old woman presented with hypogastric pain. Computed tomography and magnetic resonance imaging revealed a retroperitoneal tumor 18.0 cm in diameter with fatty tissue density, ventrally compressing the pancreatic head. We suspected a well-differentiated liposarcoma compressing the pancreas. At laparotomy, the tumor mass was the size of an infant’s head; its center was located in the area corresponding to the pancreatic uncus. It was continuous with the pancreatic parenchyma through a poorly demarcated border, and we resected as much of the tumor mass as possible while conserving the pancreatic capsule. Histopathological examination indicated lipomatous pseudohypertrophy of the pancreas with proliferation of mature fatty tissue as the main constituent. At the periphery, islands of acinar tissue were retained among the fatty infiltration, which also contained branches of the pancreatic duct and islets of Langerhans. Previous reports have stated that this disorder only causes fatty replacements throughout the pancreas or in the pancreatic body and tail; however, in this patient, imaging and macroscopic examination revealed no fatty replacements in the pancreatic body and tail. We report this case, which we consider extremely rare, along with a brief review of the literature.

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