Metabolic and bariatric surgery (MBS) is the most effective and durable therapeutic intervention for patients with obesity. In recent years, laparoscopic sleeve gastrectomy (SG) has become the most commonly performed primary MBS procedure owing to its technical feasibility and excellent short-term outcomes. Despite these favorable results and perceived advantages, SG is associated with several unique complications. Complications such as a postoperative leak or bleeding have been more commonly observed and reported than others, and their management approaches are well described. However, other complications following SG are far less familiar to surgeons, which may delay recognition and result in poor patient outcomes. Of these complications, we describe splenic injuries; esophageal perforation; staple line malformations; stapling of intraluminal devices; phytobezoar formation; gastro-colic, gastro-pleural and gastro-bronchial fistula; pancreatic leak; and portomesenteric venous thrombosis. It is paramount for surgeons to be aware of these underreported issues and have the resources to learn how to recognize and manage them when they arise. This review aims to describe rare (i.e., reported incidence <1%) and underdescribed complications after SG, focusing on causes, clinical presentation, prevention strategies, and management.

Metabolic and bariatric surgery (MBS) is the most effective therapeutic intervention for patients with obesity, with sleeve gastrectomy (SG) being the most commonly performed primary MBS procedure. Long-term studies have demonstrated that 15–20% of patients require revisional bariatric surgery (RBS) due to weight-related issues or surgical complications. Despite the gold standard being laparoscopic revision, there are other available approaches such as open or robotic-assisted. An extensive literature review was performed for articles from their inception to February 2024. A descriptive review of MBS procedures (SG, Roux-en-Y gastric bypass (RYGB), single anastomosis duodeno-ileostomy (SADI) and biliopancreatic diversion-duodenal switch (BPD-DS)) was carried out to report and compare outcomes between primary and revisional bariatric surgery. A similar review was conducted to compare outcomes of revisional approaches (open, laparoscopic, robotic). RYGB remains the dominant RBS with a similar safety profile compared to revisional SADI and BPD-DS. In terms of the RBS surgical approach, all three options showed comparable short and long-term outcomes, with robotic RBS being associated with longer operative time and variable length of stay. Additional long-term studies are required to further validate our conclusions.

Objective The columnar cell variant of papillary thyroid carcinoma (PTC-CC) is a rare, malignant tumor of the thyroid gland. This study uses the National Cancer Database (NCDB) to analyze demographic and prognostic factors affecting the overall survival rates of PTC-CC. Methods From 2004 to 2020, 7,079 patients diagnosed with columnar cell papillary thyroid carcinoma were identified in the NCDB. Patient demographics were reviewed based on categories listed in the NCDB participant user file data dictionary. Kaplan-Meier curves, log-rank tests, and multivariable Cox hazard regression models were used to analyze the significance of demographic and prognostic factors on overall survival rates of PTC-CC. Results Multivariate analysis demonstrated each five-year increment in age was associated with a 30% increase mortality (hazard ratio (HR) = 1.30, 95% confidence interval (CI): 1.25-1.36, P < 0.001). Charlson-Deyo scores displayed similar incremental increases, such that patients with a score >= 3 had a 154% increase in mortality risk relative to a score of 0 (HR = 2.54; 95% CI: 1.75-3.68, P < 0.001). Black individuals had a 70% increase mortality compared to White individuals (HR = 1.70, 95% CI: 1.25-2.30, P < 0.001), while all Other races the highest 10-year survival rate of 92.7%. Females had a significant 37% decrease in mortality compared males (HR = 0.63, 95% CI: 0.54-0.73, P < 0.001). Patients in the lowest income quartiles were found to have significant increase in mortality compared to the highest income group (HR = 0.54; 95% CI: 0.41-0.71, P 0.001). Survival rates were negatively correlated with NCDB Analytic Staging increases. Conclusion In general, age, sex, race, education, income, comorbidities, and cancer staging were found to be predictive factors of overall survival rates of PTC-CC. However, insurance status and education levels did not result significant differences.

Background: Seminoma is a malignant germ cell tumor that most commonly involves the testicles but may involve the mediastinum, the retroperitoneum, and other extra-gonadal sites as well. This study aims to investigate the somatic genomic landscape of seminoma. Methods: Data for a retrospective observational analysis of seminoma was acquired from the American Association for Cancer Research (AACR) Project Genomics Evidence Neoplasia Information Exchange (GENIE) with clinical and genomic data from 2017 and beyond. Using the R and R Studio software (R 4.5.0), analyses for common somatic mutations and copy number alterations were run with a statistical significance of p < 0.05. Results: The most mutated genes included KIT (22.6%), KRAS (17.1%), and MTOR (5.1%), with significant copy number alterations in CDKN1B (17.2%), KRAS (14.7%), CCND2 (10.3%), and H3F3C (9.8%). These suggest involvement within the KIT/RAS/MAPK and PI3K/AKT/mTOR (PAM) pathways for seminoma development. A novel finding within comparative evaluation of PMS1 and AMER1 mutations were found in Black individuals. Additionally, our findings were consistent with a lower testicular cancer rate among individuals with African ancestry than European ancestry. BRD4 mutations were found only in metastatic samples while KMT2C, STAG2, ALK, AXL, and EGFR were only found in primary samples, suggesting a possible association. Conclusions: This study provided a comprehensive molecular and genetic profiling of seminoma including key genetic alterations, affected pathways, and potential therapeutic strategies. Moreover, overlap between pathways and gene mutations provides the potential for alternative treatment options for seminoma via multiple pathways.

Background: Bladder adenocarcinoma (BA) is a rare malignancy, accounting for up to 2% of bladder cancers. Its molecular drivers remain poorly defined, limiting therapeutic options and prognostic assessment. This study characterizes the genomic landscape of BA using a large, multi-institutional sequencing database to identify recurrent alterations and potential therapeutic targets. Methods: Clinical and genomic data for BA were extracted from the AACR Project GENIE® database (accessed July 2025). Samples underwent targeted next-generation sequencing (50–555 genes, >500× coverage). Analyses included somatic mutation frequency, copy number alterations (CNAs), tumor mutational burden (TMB), and stratification by sex, race, and tumor site (primary vs. metastatic). Statistical comparisons used chi-squared, Student’s t-test, or Mann–Whitney U with Benjamini–Hochberg correction. Results: A total of 206 tumor samples from 195 patients were an-alyzed. The cohort was predominantly male (61%) and White (43%). Common somatic point mutations included TP53 (65.0%), KRAS (35.4%), PIK3CA (17.0%), SMAD4 (16.5%), and ARID1A (11.2%). CNAs were frequently affected by CDKN2A (11.6%), CDKN2B (11.6%), and SMAD4 (7.0%). Sex-stratified analysis revealed male enrichment in ARFGAP3, PTEN, LATS2, TSC2, and PRKDC, while CD40, FOXQ1, and WEE1 were observed only in females. Race-based differences included FANCD2 and EGFR en-richment in Asian patients. Co-occurring somatic point mutations were identified between ARID1A–TERT, NSD1–KDM6A, and KRAS–SMAD4, while SMAD4 and KDM6A point mutations demonstrated mutual exclusivity. Discussion: Findings confirm TP53, KRAS, and PIK3CA as recurrently mutated drivers in BA and highlight FGFR3 as a novel re-currently mutated gene, as well as frequent copy number losses involving SMAD4, CDKN2A, and CDKN2B. Subgroup analyses highlight sex- and race-associated muta-tional differences, suggesting potential biologic underpinnings of demographic dispari-ties. Co-occurrence and exclusivity analyses reveal previously unreported interactions, underscoring pathway redundancy and cooperation in tumor progression. Conclusion: This study provides one of the most comprehensive genomic characterizations of BA to date, identifying recurrent drivers, subgroup-specific alterations, and mutational inter-actions. These insights highlight TP53, KRAS, and PIK3CA pathway disruption as central in BA biology and support the development of targeted therapeutics and prospective validation in independent cohorts.