Recent genetic studies have indicated relationships between gene mutations and colon cancer phenotypes. However, how physical properties of tumor cells are changed by genetic alterations has not been elucidated. We examined genotype-defined mouse intestinal tumor-derived cells using a high-speed scanning ion conductance microscope (HS-SICM) that can obtain high-resolution live images of nano-scale topography and stiffness. The tumor cells used in this study carried mutations in Apc (A), Kras (K), Tgfbr2 (T), Trp53 (P), and Fbxw7 (F) in various combinations. Notably, high-metastatic cancer-derived cells carrying AKT mutations (AKT, AKTP, and AKTPF) showed specific ridge-like morphology with active membrane volume change, which was not found in low-metastatic and adenoma-derived cells. Furthermore, the membrane was significantly softer in the metastatic AKT-type cancer cells than other genotype cells. Importantly, a principal component analysis using RNAseq data showed similar distributions of expression profiles and physical properties, indicating a link between genetic alterations and physical properties. Finally, the malignant cell-specific physical properties were confirmed by an HS-SICM using human colon cancer-derived cells. These results indicate that the HS-SICM analysis is useful as a novel diagnostic strategy for predicting the metastatic ability of cancer cells.

Claudins are the major component of tight junctions, which form a primary barrier to paracellular diffusion and maintain cell polarity in normal epithelia and endothelia. In cancer cells, claudins play additional roles besides serving as components of the tight junctions, and participate in anoikis or invasion. Among the claudin family proteins, claudin‐1 has the most promising potential, both diagnostically and prognostically, in many types of cancers, including oral, gastric, liver, and colon cancers. However, conflicting results have been reported in relation to the degree of claudin‐1 expression and the prognosis, suggesting that the expression level of claudin‐1 alone is not sufficient to analyze the relationship between claudin‐1 and cancer progression. As endocytic trafficking of claudin‐1 has been reported in several epithelial cell types in vitro, we aimed to determine whether intracellular localization of claudin‐1 is the missing aspect between claudin‐1 and cancer. We investigated the expression of claudin‐1 in 83 tongue squamous cell carcinoma (TSCC) pathological specimens. Although the expression level of claudin‐1 based on immunohistochemistry was not associated with TSCC progression, within the high claudin‐1 expression group, the incidence of intracellular localization of claudin‐1 was correlated with cervical lymph node metastasis. In an in vitro experiment, claudin‐1 was constitutively internalized in TSCC‐derived cells. Motility of TSCC‐derived cells was increased by deficiency of claudin‐1, suggesting that the decrease in cell‐surface claudin‐1 promoted the cell migration. Therefore, intracellular localization of claudin‐1 at the invasion front may represent a promising diagnostic marker of TSCC.

Objective: To investigate the incidence of male sexual dysfunction including erectile dysfunction (ErD) and ejaculatory dysfunction (EjD) after minimally invasive rectal cancer surgery. Background: Male sexual dysfunction significantly affects after rectal cancer surgery quality of life. Current assessments using the International Index of Erectile Function-5 are unsuitable for patients with reduced postoperative sexual activity because it assume sexual intercourse. This study addresses this gap using the Erection Hardness Score and custom ejaculatory questionnaires. Methods: This prospective multicenter open-label phase 2 trial enrolled 399 patients who underwent laparoscopic (Lap), robotic (Ro), or transanal (Ta) rectal cancer surgery. Erection Hardness Score and custom ejaculatory questionnaires assessed ErD, EjD, and potency impairment at 3, 6, and 12 months postoperatively. The rates were assessed in the full analysis set and compared between the Lap and Ro groups after propensity score matching. Results: At 12 months, the overall incidences of ErD and EjD were 34.7% and 29.8%, respectively. The Ro group showed a significantly lower EjD rate (25.0%) than the Lap group (40.9%), with no significant difference in ErD. Potency impairment was lower in the Ro group at 6 months (32.7% vs 22.3%) and 12 months (29.0% vs 17.8%) postoperatively. The Ta group showed relatively high ErD and EjD at 3 months, with some recovery at 12 months. Conclusions: Minimally invasive rectal cancer surgery commonly results in ErD, EjD, and potency impairment. Ro surgery provides lower EjD rates and less potency impairment. Comprehensive sexual function assessments are essential to inform patients and improve quality of life outcomes.

Background: Endoscopic submucosal dissection (ESD) is increasingly applied for early gastric cancer. ESD is a less invasive procedure and could be a radical treatment. However, in some cases, ESD cannot be completed owing to patient or technical factors. In such cases, which could have the potential for curative resection with ESD, standard gastrectomy is excessively invasive. Through closed laparoscopic and endoscopic cooperative surgery (LECS), gastric tumor can be precisely resected without exposing tumor cells to the abdominal cavity. Compared with standard gastrectomy, closed LECS is less invasive for the treatment of early gastric cancer. Case presentation: We performed closed LECS for three cases of early gastric cancer after failed ESD. In all three cases, ESD was interrupted owing to technical and patient factors, including perforation, respiratory failure, and carbon dioxide narcosis. All three cases successfully underwent closed LECS with complete tumor resection and showed an uneventful postoperative course. All three patients remain alive and have experienced no complications or recurrence, with a median follow up of 30 (14–30) months. Conclusions: Closed LECS is less invasive and useful procedure for the treatment of early gastric cancer, particularly in cases with difficulty in ESD.

Introduction: The subvesical bile ducts are located in the peri-hepatic connective tissue of the gallbladder fossa. Injury of the subvesical bile ducts provokes the severe complication of bile leak. Until now, fluorescent cholangiography has been employed during hepatobiliary surgery. Herein, we report the detection of subvesical bile ducts by fluorescent cholangiography during laparoscopic cholecystectomy. Presentation of case: A 63-year-old female was admitted to our department for surgery for symptomatic cholelithiasis. The subvesical bile ducts were not observed on drip-infusion cholangiography with computed tomography. Immediately following induction of anesthesia, 2.5 mg of indocyanine green was intravenously injected. Fluorescent cholangiography demonstrated two thin aberrant bile ducts during dissection of Calot's triangle. We considered them to be subvesical bile ducts. We ligated them with clips, divided them, and then performed laparoscopic cholecystectomy using a standard procedure. The patient had a good post-operative recovery without bile leakage. Postoperative laboratory test results were all within normal limits. Computed tomography revealed no dilatation of the intrahepatic bile duct after laparoscopic cholecystectomy. The patient was discharged on postoperative day 4. Discussion: Injury to the subvesical bile ducts is one of the most common causes of bile leakage associated with cholecystectomy. Fluorescent cholangiography enabled real-time identification of the thin subvesical bile ducts, which were undetectable by drip-infusion cholangiography with computed tomography. Conclusion: Fluorescent cholangiography during laparoscopic cholecystectomy may be useful for preventing postoperative bile leakage. Highlights: