Background: Long working hours have been associated with adverse physical and mental health outcomes; however, evidence regarding their relationship with satisfaction with work environment remains limited, particularly when long working hours are defined using a specific daily threshold. This study examined the association between working ≥10 hours per day and satisfaction with work environment among Korean wage workers, focusing on the cumulative number of such workdays per month. Methods: This cross-sectional study analyzed data from the 7th Korean Working Conditions Survey. A total of 24,269 wage workers aged ≥18 years were included after excluding self-employed workers, unpaid family workers, shift workers, and respondents with missing data. Working ≥10 hours per day was categorized as 0, 1–9, and ≥10 days per month. Satisfaction with work environment was categorized as satisfied or dissatisfied. Multiple logistic regression analyses were conducted to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for dissatisfaction with work environment according to the number of long working days, adjusting for demographic and occupational characteristics. Results: Compared with workers who did not work ≥10 hours per day, those who worked 1–9 days and ≥10 days per month showed progressively higher levels of dissatisfaction with work environment. After adjustment for demographic and occupational factors, the odds of dissatisfaction with work environment were significantly higher among workers who worked ≥10 hours per day for 1–9 days per month (OR: 1.380; 95% CI: 1.145–1.665) and ≥10 days per month (OR: 2.106; 95% CI: 1.627–2.725), demonstrating a dose–response relationship. Conclusions Among the analytic sample of Korean wage workers included in this study, working ≥10 hours per day was associated with greater dissatisfaction with work environment, with a dose–response pattern according to the number of long working days per month.

Objective: This study aimed to assess the association between exposure to gadolinium-based contrast agents (GBCAs) and the risk of parkinsonism according to the GBCA type. Materials and Methods: Individuals aged ≥40 years who underwent first-ever magnetic resonance imaging (MRI) examinations between 2011 and 2014 were identified from the Korean nationwide population-based health insurance claims database and followed up until 2022. Individuals were divided into those who underwent at least one GBCA-enhanced MRI, and those who underwent only non-enhanced MRI. GBCA-exposed individuals were further categorized into those exposed only to linear or macrocyclic GBCAs, after excluding those exposed to both types. The primary event of interest was allcause parkinsonism. Secondary events included all-cause parkinsonism requiring medication, Parkinson’s disease (PD), atypical parkinsonism, and secondary parkinsonism. Hazard ratios (HRs) were estimated using multivariable Cox proportional hazard regression models for exposure to linear and macrocyclic GBCAs, with the non-enhanced MRI group serving as a reference. The models were adjusted for age, sex, smoking status, alcohol consumption, regular exercise, body mass index, estimated glomerular filtration rate, and comorbidities. Subgroup analyses were performed according to age, sex, renal function, and history of cancer. Results: A total of 222,977 individuals were included in this study. Among them, 92,230, 48,335, and 82,412 individuals underwent non-enhanced, linear GBCA-enhanced, and macrocyclic GBCA-enhanced MRI, respectively. Exposure to linear GBCAs slightly increased the risk of all-cause parkinsonism (adjusted HR, 1.13 [97.5% confidence interval, 1.08–1.19]), while exposure to macrocyclic GBCAs did not increase the risk (adjusted HR, 1.00 [97.5% confidence interval, 0.95–1.05]).The results were similar for all-cause parkinsonism requiring medication, PD, and secondary parkinsonism, whereas no significant association was observed for atypical parkinsonism. Conclusion Exposure to linear GBCAs may slightly increase the risk of parkinsonism in adults, whereas exposure to macrocyclic GBCAs may not. Caution should be exercised when using linear GBCAs until further evidence emerges.

Purpose: To develop the 2025 update to the Korean colorectal cancer (CRC) screening guidelines by systematically evaluating recent evidence, integrating domestic data, and addressing changes since the 2015 guideline revision, thereby providing an evidence-based standard for clinicians and policymakers. Methods: A multidisciplinary committee developed the guidelines using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) methodology. The process included formulation of three key questions addressing screening efficacy, diagnostic accuracy, and optimal screening age and interval. A systematic review of international guidelines and primary literature was conducted, yielding 327 eligible studies. In addition, a utility-based analysis using a Markov model was performed to determine optimal screening ages and intervals. Results: The evidence synthesis identified high-certainty evidence supporting the use of the fecal immunochemical test (FIT) for reducing CRC mortality and moderate-certainty evidence for colonoscopy. Evidence for computed tomographic colonography (CTC) and stool DNA testing was rated as very low certainty. Based on the evidence review and cost-utility analysis, the committee conditionally recommends CRC screening for asymptomatic, average-risk adults aged 45–74 years using either colonoscopy every 10 years or FIT every 1–2 years. CTC and stool DNA testing were not recommended owing to insufficient evidence. Conclusion The 2025 Korean Guidelines for Colorectal Cancer Screening present updated, evidence-based recommendations tailored to the domestic healthcare context. By conditionally endorsing both colonoscopy and FIT for individuals aged 45–74 years, these guidelines aim to improve population-level screening effectiveness and reduce the burden of CRC in South Korea.

In patients with differentiated thyroid cancer (DTC), initial recurrence risk stratification based on clinical, histopathological, and perioperative data remains the key determinant for guiding management strategies during the first 1-2 years post-treatment. However, the adoption of ongoing risk stratification (ORS), which dynamically reassesses risk by integrating longitudinal clinical data and treatment response, enables more precise long-term prognostic assessment and facilitates highly individualized management. Building upon recent guidelines, the 2026 KTA guideline has been further refined by incorporating robust evidence from large-scale national cohorts and comprehensive systematic reviews. These updated recommendations outline contemporary concepts of ORS, risk-adapted TSH suppression targets, optimized surveillance modalities for recurrence detection, and disease-specific long-term follow-up strategies. Reflecting the paradigm shift toward de-escalated treatment, this revision integrates evolved perspectives on TSH suppression intensity, the clinical interpretation of thyroglobulin levels, and tailored follow-up intervals. These evidence-based recommendations aim to minimize unnecessary treatment and excessive surveillance in the large proportion of patients with excellent prognosis after initial therapy, while ensuring that each patient receives appropriately tailored and effective long-term management.

Radiofrequency ablation (RFA) is a minimally invasive treatment modality used as an alternative to surgery in patients with benign thyroid nodules, recurrent thyroid cancers (RTCs), and primary thyroid microcarcinomas. The Korean Society of Thyroid Radiology (KSThR) initially developed recommendations for the optimal use of RFA for thyroid tumors in 2009 and revised them in 2012 and 2017. As new meaningful evidence has accumulated since 2017 and in response to a growing global interest in the use of RFA for treating malignant thyroid lesions, the task force committee members of the KSThR decided to update the guidelines on the use of RFA for the management of RTCs based on a comprehensive analysis of current literature and expert consensus.

Purpose: Biliary atresia (BA) is a rare but progressive cholangiopathy and the leading cause of pediatric liver transplantation worldwide. The Korean Association of Pediatric Surgeons (KAPS) has conducted three national surveys (2001, 2011, and 2023) to assess long-term trends in the diagnosis, treatment, and outcomes of BA. This study provides a comparative analysis of the 2nd and 3rd national surveys, with reference to selected findings from the 1st survey. Methods: This study included 453 patients from the 3rd national survey (2011–2021) and 435 patients from the 2nd survey (2001–2010), all of whom underwent Kasai portoenterostomy. Data were collected via electronic case report forms from pediatric surgical centers nationwide. Comparisons were made regarding demographics, clinical features, diagnostic patterns, operative details, follow-up outcomes, and survival. Kaplan–Meier analysis was used to evaluate long-term survival. Results: The mean number of BA patients per year remained stable between surveys (43.5 in the 2nd, 41.18 in the 3rd), though centralization of care increased, with 61.5% of cases managed by two major institutions in the 3rd survey. The median age at surgery decreased, and the use of preoperative imaging (especially magnetic resonance cholangiopancreatography) increased. The 10-year native liver survival rate declined from 59.8% to 53.7%, while overall 10-year survival improved slightly (92.9% to 93.2%). Postoperative complications, such as cholangitis and liver failure, persisted but were better categorized. The 3rd survey also reported improved mortality (4.9%) and reduced follow-up loss (11.5%) compared to the 2nd survey. Conclusion While overall survival after Kasai operation has remained high and even improved, native liver survival has slightly declined. The findings reflect earlier diagnosis, more consistent diagnostic imaging, and increasing centralization of care. These trends underscore the importance of long-term nationwide data collection in guiding future strategies for BA management in Korea.

Purpose: Diffuse sclerosing variant papillary thyroid carcinoma (DSV-PTC) is a rare and aggressive subtype of PTC.Preoperative diagnosis is challenging owing to the overlapping of imaging characteristics with those of other thyroid conditions. This study aimed to evaluate the accuracy of preoperative ultrasound (US) in predicting DSV-PTC and to identify significant diagnostic factors. Methods: This retrospective study analyzed 34 patients who were preoperatively suspected of having DSV-PTC based on US findings and later underwent thyroidectomy. Patients were divided into 2 groups based on the final histopathological diagnosis: DSV-PTC and non-DSV-PTC. Demographic, radiological, and pathological characteristics were also compared. Results: Only 32.4% of patients initially suspected of having DSV-PTC were confirmed postoperatively. Among the US features, the Korean Thyroid Imaging Reporting and Data System (K-TIRADS) score 5 was significantly associated with DSV-PTC (P = 0.038), whereas other radiological factors, including echogenicity and microcalcifications, were not. The histopathological features, such as tumor size, BRAF and TERT mutations, vascular invasion, and lymph node metastasis, showed no significant differences between the groups. Conclusion Preoperative US has limited accuracy (32.4%) in diagnosing DSV-PTC. Because of the aggressive treatment recommendations based on preoperative suspicion, clinicians should carefully consider the limitations of imaging. Further studies incorporating fine-needle aspiration or core needle biopsy are required to improve diagnostic accuracy.

Background: Kelch-like ECH-associated protein 1 (KEAP1)–nuclear factor erythroid- 2-related factor 2 (NRF2) pathway is a major regulator protecting cells from oxidative and metabolic stress. Studies have revealed that this pathway is involved in mediating resistance to cytotoxic chemotherapy and immunotherapy; however, its implications in oncogene-addicted tumors are largely unknown. This study aimed to elucidate whether this pathway could be a potential therapeutic target for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. Methods: We measured the baseline expression of NRF2 using EGFR-mutant parental cells and acquired gefitinib resistant cells. We investigated whether NRF2 inhibition affected cell death in vitro and tumor growth in vivo using a xenograft mouse model, and compared the transcriptional changes before and after NRF2 inhibition. Results: Baseline NRF2 expression was enhanced in PC9 and PC9 with gefitinib resistance (PC9/GR) cells than in other cell lines, with a more prominent expression in PC9/ GR. The NRF2 inhibitor induced NRF2 downregulation and cell death in a dose-dependent manner. Cotreatment with an NRF2 inhibitor enhanced osimertinib-induced cell death in vitro, and potentiated tumor growth inhibition in a PC9/GR xenograft model. Finally, RNA sequencing revealed that NRF2 inhibition resulted in the altered expression of multiple genes involved in various signaling pathways. Conclusion We identified that NRF2 inhibition enhanced cell death and inhibited tumor growth in tyrosine kinase inhibitor (TKI)-resistant lung cancer with EGFR-mutation. Thus, NRF2 modulation may be a novel therapeutic strategy to overcome the resistance to EGFR-TKIs.

Background: Kelch-like ECH-associated protein 1 (KEAP1)–nuclear factor erythroid- 2-related factor 2 (NRF2) pathway is a major regulator protecting cells from oxidative and metabolic stress. Studies have revealed that this pathway is involved in mediating resistance to cytotoxic chemotherapy and immunotherapy; however, its implications in oncogene-addicted tumors are largely unknown. This study aimed to elucidate whether this pathway could be a potential therapeutic target for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. Methods: We measured the baseline expression of NRF2 using EGFR-mutant parental cells and acquired gefitinib resistant cells. We investigated whether NRF2 inhibition affected cell death in vitro and tumor growth in vivo using a xenograft mouse model, and compared the transcriptional changes before and after NRF2 inhibition. Results: Baseline NRF2 expression was enhanced in PC9 and PC9 with gefitinib resistance (PC9/GR) cells than in other cell lines, with a more prominent expression in PC9/ GR. The NRF2 inhibitor induced NRF2 downregulation and cell death in a dose-dependent manner. Cotreatment with an NRF2 inhibitor enhanced osimertinib-induced cell death in vitro, and potentiated tumor growth inhibition in a PC9/GR xenograft model. Finally, RNA sequencing revealed that NRF2 inhibition resulted in the altered expression of multiple genes involved in various signaling pathways. Conclusion We identified that NRF2 inhibition enhanced cell death and inhibited tumor growth in tyrosine kinase inhibitor (TKI)-resistant lung cancer with EGFR-mutation. Thus, NRF2 modulation may be a novel therapeutic strategy to overcome the resistance to EGFR-TKIs.