Esophageal stent complications include stent migration, tumor ingrowth, perforation, a broncho-esophageal fistula, and gastroesophageal reflux. Development of a new stricture at a flange site after stent removal has been predicted but not yet reported. We experienced the first case of a recurrent esophageal stricture induced by a stent flange after stent removal. A fully covered metallic stent, which had been inserted 2 months ago for treatment of an anastomotic stricture, triggered another stricture at the flange site. Although endoscopic balloon dilatations were repeated several times and then the 2nd stent for rescue therapy was inserted, the stricture was refractory to all treatment. Thus, we prescribed oral prednisolone with repeated endoscopic balloon dilation; the stricture eventually improved. The oral steroid seemed to suppress stricture development. If a stent flange-induced refractory stricture is encountered, an oral steroid combined with endoscopic balloon dilation may be helpful.

Esophageal stent complications include stent migration, tumor ingrowth, perforation, a broncho-esophageal fistula, and gastroesophageal reflux. Development of a new stricture at a flange site after stent removal has been predicted but not yet reported. We experienced the first case of a recurrent esophageal stricture induced by a stent flange after stent removal. A fully covered metallic stent, which had been inserted 2 months ago for treatment of an anastomotic stricture, triggered another stricture at the flange site. Although endoscopic balloon dilatations were repeated several times and then the 2nd stent for rescue therapy was inserted, the stricture was refractory to all treatment. Thus, we prescribed oral prednisolone with repeated endoscopic balloon dilation; the stricture eventually improved. The oral steroid seemed to suppress stricture development. If a stent flange-induced refractory stricture is encountered, an oral steroid combined with endoscopic balloon dilation may be helpful.

Purpose: Since accurate lung cancer segmentation is required to determine the functional volume of a tumor in [ 18 F]FDG PET/CT, we propose a two-stage U-Net architecture to enhance the performance of lung cancer segmentation using [ 18 F]FDG PET/CT. Methods: The whole-body [ 18 F]FDG PET/CT scan data of 887 patients with lung cancer were retrospectively used for network training and evaluation. The ground-truth tumor volume of interest was drawn using the LifeX software. The dataset was randomly partitioned into training, validation, and test sets. Among the 887 PET/CT and VOI datasets, 730 were used to train the proposed models, 81 were used as the validation set, and the remaining 76 were used to evaluate the model. In Stage 1, the global U-net receives 3D PET/CT volume as input and extracts the preliminary tumor area, generating a 3D binary volume as output. In Stage 2, the regional U-net receives eight consecutive PET/CT slices around the slice selected by the Global U-net in Stage 1 and generates a 2D binary image as the output. Results: The proposed two-stage U-Net architecture outperformed the conventional one-stage 3D U-Net in primary lung cancer segmentation. The two-stage U-Net model successfully predicted the detailed margin of the tumors, which was determined by manually drawing spherical VOIs and applying an adaptive threshold. Quantitative analysis using the Dice similarity coefficient confirmed the advantages of the two-stage U-Net. Conclusion The proposed method will be useful for reducing the time and effort required for accurate lung cancer segmentation in [ 18 F]FDG PET/CT.

Purpose: Isoform 2 of tight junction protein claudin-18 (CLDN18.2) is a potential target for gastric cancer treatment. A treatment targeting CLDN18.2 has shown promising results in gastric cancer. We investigated the clinical significance of CLDN18.2 and other cell-adherens junction molecules (Rho GTPase-activating protein [RhoGAP] and E-cadherin) in metastatic diffuse-type gastric cancer (mDGC). Materials and Methods: We evaluated CLDN18.2, RhoGAP, and E-cadherin expression using two-plex immunofluorescence and quantitative data analysis of H-scores of 77 consecutive mDGC patients who received first-line platinum-based chemotherapy between March 2015 and February 2017. Results: CLDN18.2 and E-cadherin expression was significantly lower in patients with peritoneal metastasis (PM) than those without PM at the time of diagnosis (P=0.010 and 0.013, respectively), whereas it was significantly higher in patients who never developed PM from diagnosis to death than in those who did (P=0.001 and 0.003, respectively). Meanwhile, CLDN18.2 and E-cadherin expression levels were significantly higher in patients with bone metastasis than in those without bone metastasis (P=0.010 and 0.001, respectively).Moreover, we identified a positive correlation between the expression of CLDN18.2 and E-cadherin (P<0.001), RhoGAP and CLDN18.2 (P=0.004), and RhoGAP and E-cadherin (P=0.001). Conversely, CLDN18.2, RhoGAP, and E-cadherin expression was not associated with chemotherapy response and survival. Conclusions CLDN18.2 expression was reduced in patients with PM but significantly intactin those with bone metastasis. Furthermore, CLDN18.2 expression was positively correlated with other adherens junction molecules, which is clinically associated with mDGC and PM pathogenesis.