Background/Objectives: Colorectal cancer (CRC) is one of the most commonly diagnosed malignancies worldwide and a leading cause of cancer-related mortality. Surgical resection remains the cornerstone of curative treatment. Over the past two decades, robotic-assisted surgery has emerged as an evolution of minimally invasive surgery, aiming to overcome several limitations of conventional laparoscopy. This narrative review summarizes the current state of the art of robotic surgery in CRC. Methods: A narrative review of the literature was conducted using PubMed/MEDLINE and Scopus databases, focusing on publications from 2015 to 2026. The review provides an overview of robotic platforms and summarizes the available clinical evidence. Priority was given to randomized controlled trials, meta-analyses, large observational studies, and clinical practice guidelines. The review focuses on major commercially available robotic systems, including the da Vinci^®, Hugo™ RAS, and Versius^® platforms, as well as emerging robotic technologies. Results: Robotic colorectal surgery showed potentially favorable perioperative and oncological outcomes compared with laparoscopy. In rectal cancer, robotic approaches were associated with improved total mesorectal excision quality, lower conversion rates, and improved postoperative functional outcomes. Emerging evidence also suggested potential improvements in disease-free survival and local disease control following robotic rectal surgery. In colon cancer, robotic colectomy were associated with lower conversion rates, reduced blood loss, and faster postoperative recovery, with comparable long-term oncological outcomes. However, robotic procedures showed longer operative times and higher procedural costs. Conclusions: Robotic colorectal surgery appears to be a safe and effective minimally invasive approach, particularly in rectal cancer surgery. The development of new robotic platforms and increasing market competition may improve cost sustainability and expand its future role in colorectal cancer management.

Background and Objectives: Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer-related mortality, largely due to late-stage diagnosis and the absence of effective population-based screening. Intrapancreatic fat deposition (IPFD) has emerged as a potential risk phenotype. This narrative review critically appraises the clinical, metabolic, epidemiologic, and mechanistic evidence linking IPFD to PDAC and discusses its implications for risk stratification and prevention. Materials and Methods: A structured literature search was conducted in PubMed/MEDLINE and Scopus for studies published between 2007 and 2025 using predefined terms related to pancreatic steatosis and pancreatic cancer. After duplicate removal and screening according to predefined inclusion and exclusion criteria, 42 articles were included. Evidence was synthesized focusing on epidemiologic associations, mechanistic pathways, and imaging-based quantification methods. Results: A strong association between IPFD and PDAC was found. Although definitive causality remains unproven, some studies support temporal correlation between IPFD and PDAC, suggesting that IPFD precedes PDAC. A possible pathophysiological explanation to this correlation has been advanced in experimental models indicating IPFD as a pro-inflammatory factor cooperating with oncogenic KRAS to facilitate neoplastic progression. Finally, variability in IPFD definitions and heterogeneity in imaging assessment limit interpretability. Conclusions: Current evidence links IPFD to PDAC risk, suggesting a strong suspicion that pancreatic steatosis may represent an independent risk factor for PDAC. Still robust causal inference remains unproven. Well-designed prospective studies, standardized imaging protocols, and mechanistic investigations are required to clarify causality and determine whether pancreatic steatosis can be incorporated into risk-based screening and preventive strategies.

Background/Objectives: Surveillance of intraductal papillary mucinous neoplasms (IPMNs) provides a clinically relevant window in which biological changes associated with pancreatic ductal adenocarcinoma (PDAC) development may potentially be investigated before advanced disease occurs. Nanoparticle-enabled protein corona (PC) fingerprinting has shown analytical potential in PDAC, but the extent to which different nanoplatforms recover distinct information across the biologically proximate IPMN-PDAC spectrum remains unclear. This exploratory study compared three nanoplatform configurations to identify a candidate workflow for subsequent validation. Methods: Plasma from 22 patients with de novo PDAC (n = 11), IPMN (n = 6), or IPMN-derived PDAC (n = 5) was incubated with graphene oxide (GO) nanosheets, gold nanoparticles (AuNPs), or cationic DOTAP-DOPE liposomes. Wash-resistant PCs were analyzed by SDS-PAGE, quantified across predefined molecular weight (MW) regions, and evaluated using exploratory linear discriminant analysis with repeated stratified cross-validation. Results: The three nanoplatforms generated non-equivalent electrophoretic PC architectures. In this small exploratory cohort, GO showed the broadest pattern of nominal clinical-group-associated variation in relative MW-region contributions and yielded internal cross-validation AUC estimates of 0.955 for IPMN versus de novo PDAC, 0.767 for IPMN versus IPMN-derived PDAC, and 0.927 for IPMN-derived versus de novo PDAC. Corresponding AUCs were 0.606–0.700 for AuNPs and 0.621–0.691 for liposomes. Conclusions: GO provided the broadest group-associated variation and numerically highest internal discrimination estimates, supporting its prioritization for independent validation and prospective longitudinal evaluation in IPMN surveillance.

Background/Objectives: The absence of pancreatic fibrosis is a known risk factor for post-operative pancreatic fistula (POPF) following pancreaticoduodenectomy (PD). Emerging evidence suggests inflammation plays a role in anastomotic healing. This study aimed to assess the role of chronic lymphomononuclear inflammatory infiltrate (CLII) and fibrosis at the pancreatic resection margin (PRM) on POPF development and explored a method for its intraoperative prediction. Materials and Methods: Data from 141 patients who underwent PD between 2014 and 2022 were retrospectively analyzed. PRM were histologically evaluated for fibrosis and CLII. Univariate and multivariate analyses were performed to identify potential predictors of postoperative pancreatic fistula (POPF) and clinically relevant postoperative pancreatic fistula (CR-POPF). Results: The histopathological analysis of intraoperative frozen sections of the PRM showed a strong association between the absence of fibrosis and CLII and increased risk of POPF and CR-POPF (OR 7.51, p < 0.0001; OR 4.30, p < 0.0001). Multivariate analysis further identified a main pancreatic duct diameter of less than 3 mm, as well as the combined presence of fibrosis and inflammation, as independent risk factors for developing POPF (OR 4.22, p = 0.001) and CR-POPF (OR 4.83, p = 0.020). Conclusion: The absence of fibrosis and CLII at the PRM significantly increases the risk of POPF and CR-POPF. This study validated a reproducible method for intraoperative assessment of fibrosis and CLII, enabling the identification of high-risk cases. Such a tool could guide surgical strategies to mitigate POPF-related complications, improving patient outcomes after PD.