The original Reproductive Concerns After Cancer (RCAC) scale is a well-validated instrument. However, its gender-specific nature hinders direct comparison of scores across genders and limits its efficiency in clinical practice. The study was conducted in two phases. First, items from the original female and male RCAC scales were rigorously evaluated and consolidated using a Delphi expert panel and face validity testing, resulting in a preliminary 7-item version. Second, psychometric validation was performed on a sample of 1,049 young cancer survivors (609 males, 440 females) recruited from two specialist oncology hospitals in China. Participants were diagnosed with a range of cancers, including colorectal, lung, breast, thyroid, gastric, and ovarian tumors. The psychometric evaluation encompassed item analysis, content validity, confirmatory factor analysis (CFA), convergent validity with the Patient Health Questionnaire-9 (PHQ-9), internal consistency reliability, and test-retest reliability. The original 18-item scale was successfully reduced to a 7-item unisex instrument, the RCAC-7. Psychometric testing demonstrated that the RCAC-7 has satisfactory internal consistency (Cronbach's α = 0.770; McDonald's ω = 0.889) and excellent test-retest reliability (r = 0.930-0.970). The content validity index was good. Convergent validity was supported by a strong positive correlation with the PHQ-9 (r = 0.783, p < 0.01). Furthermore, confirmatory factor analysis confirmed a robust one-factor structure, indicating good model fit. The RCAC-7 is a valid and reliable unisex tool for measuring reproductive concerns in young cancer survivors. Its brevity and strong psychometric properties make it highly suitable for rapid screening and use in both clinical practice and large-scale research settings.

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, with incidence and mortality projected to rise. Most patients present with advanced or unresectable disease, where treatment efficacy is often constrained by frailty and impaired physical function. As physical function has emerged as a key determinant of treatment eligibility and survival, there is growing interest in physical activity as a supportive intervention in HCC care. This narrative review synthesises observational, pre-clinical, and trial evidence on the role of physical activity in patients with HCC, examining its potential to improve treatment tolerance, quality of life, and survival. A literature search was conducted across four databases (PubMed, Scopus, Web of Science, Embase) using keywords related to HCC, physical activity, exercise, and survivorship. Pre-clinical studies reveal multiple mechanisms through which physical activity may enhance anti-tumour responses, including metabolic reprogramming, modulation of oncogenic signalling and immune activation. Observational studies suggest that frailty and sarcopenia - markers of reduced physical function, are possibly associated with early treatment discontinuation and shorter survival in HCC. Preliminary interventional data suggest that structured exercise programmes, delivered in hospital, outpatient, telehealth, or mobile formats, can improve frailty, preserve muscle mass, and may potentially support survival. However, clinical studies to date are limited by small sample sizes, non-randomised designs, and short follow-up periods. Current evidence provides a biologically plausible and clinically promising rationale for integrating physical activity into HCC care pathways. While findings are encouraging, robust randomised trials are needed to establish efficacy, define optimal exercise regimens, and evaluate long-term outcomes.

Tumor budding (TB) in colorectal cancer (CRC) has been associated with poor prognosis. TB has been considered a form of epithelial–mesenchymal transition (EMT). Additional discovery of proteins involved in TB can help suppress the aggressiveness of CRC. This study focused on examining whether S100A10, which has been implicated in TB and EMT, qualifies as a biomarker for TB. Formalin-fixed, paraffin-embedded tissue sections from 339 low-grade adenocarcinomas were used. TB was assessed using the recommended hotspot method. Immunohistochemical analysis focused on S100A10 expression on both the tumor buds at the hotspot and tumor glands (TGs), which serve as the direct background for TB, with the stroma-facing membrane (SFM) being the target for the evaluation. Among the 339 patients analyzed, 190 (56.0%) were confirmed to have TB. S100A10 positivity in the tumor buds was detected in 153 patients (80.5%) and was significantly correlated with high-grade TB and high S100A10 positivity in background TGs. S100A10 positivity in background TGs was significantly correlated with high-grade TB, node metastasis, and poor pStage. S100A10 positivity in TGs was often observed in the portions having an irregular border with the stroma, especially ones protruding toward the stroma. In CRC, S100A10 expression at the SFMs of the TGs likely promotes TB from its earliest stage and remains active during TB. The increase in the number of S100A10-expressing tumor cells was associated with poor biological behavior in CRC. Overall, our findings suggest that S100A10 could be a potential biomarker for TB of CRC.

Pancreatoduodenectomy (PD) remains the cornerstone surgical treatment for resectable periampullary and pancreatic malignancies, with improving survival due to advances in oncologic surgery and perioperative management. Emerging evidence, however, identifies metabolic dysfunction-associated steatotic liver disease (MASLD) as a relevant postoperative complication that may adversely influence long-term outcomes. This review aims to summarizethe incidence, pathophysiology, clinical implications, and management strategies of de novo MASLD following PD in patients with gastrointestinal malignancies. A narrative review of clinical and translational studies was conducted focusing on hepatic steatosis, metabolic derangements, pancreatic exocrine and endocrine insufficiency, and chemotherapy-related liver injury after PD. Particular attention was given to studies evaluating postoperative nutritional status, liver-related morbidity, and implications for oncologic therapy. De novo MASLD develops in approximately 8-37% of patients within the first year after PD. Unlike classical metabolic MASLD, postoperative disease is predominantly driven by exocrine pancreatic insufficiency, malabsorption, intestinal dysbiosis, and altered gut-liver signaling, leading to hepatic lipotoxicity and inflammation. Progression to metabolic dysfunction-associated steatohepatitis, fibrosis, or cirrhosis has been reported, potentially limiting tolerance to adjuvant chemotherapy. Early pancreatic enzyme replacement therapy improves nutritional parameters and may reduce hepatic steatosis, while duodenum-preserving pancreatic head resection appears to attenuate metabolic sequelae. MASLD represents a distinct and clinically significant postoperative complication following PD with potential impact on oncologic outcomes. Systematic hepatic monitoring and multidisciplinary management should be integrated into postoperative care pathways for patients with gastrointestinal cancers.