Younghoon Kim

Isolated splenic peliosis is an exceptionally rare benign vascular disorder characterized by blood-filled cystic cavities within the splenic parenchyma. Although the condition is frequently asymptomatic, it carries a significant risk of spontaneous rupture leading to hemoperitoneum and hemorrhagic shock. Its imaging features overlap substantially with more common benign or malignant vascular or cystic tumors, posing a diagnostic challenge on cross-sectional imaging. We report a case of incidentally discovered isolated splenic peliosis in a 66-year-old woman, with emphasis on multiphasic CT and gadoxetic acid-enhanced MRI findings, and discuss key imaging features.

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.

Background Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease characterized by immune-mediated hepatocellular injury. Regulatory T cells (Tregs) are crucial for maintaining immune tolerance, but their role in AIH remains unclear. This study aimed to evaluate the phenotype, function, and tissue distribution of Tregs in AIH and examine their potential association with immune dysregulation. Methods Peripheral blood and liver samples were collected from 57 biopsy-confirmed AIH patients. Single-cell RNA sequencing was performed on peripheral blood mononuclear cells (PBMCs) from one individual per group (healthy control, before treatment, and flare after steroid discontinuation). Flow cytometry (PBMCs n = 45; livers n = 37) and immunohistochemistry (IHC, n = 33) assessed Treg frequency and phenotype. Treg suppressive function was evaluated using co-culture assays with effector T cells (Teffs) isolated from PBMCs (n = 25). Results IHC revealed marked immune cell infiltration in AIH liver tissues, and FOXP3 + cell counts correlated positively with serum AST levels (p = 0.0096) and portal-peripheral activity severity (p < 0.05). Single-cell RNA sequencing showed expansion of distinct Tregs and transcriptional changes, including IL-7R upregulation suggesting functional instability. Flow cytometry confirmed significantly increased total and activated Tregs in AIH liver samples (both p < 0.0001). However, co-culture assays demonstrated that Tregs from AIH patients had markedly reduced suppressive capacity compared to healthy controls (p < 0.0001). Conclusions Despite their expansion in liver tissue, Tregs in AIH exhibit impaired suppressive function, indicating functional instability contributes to immune dysregulation in AIH.

KRAS mutations occur in over 90% of pancreatic ductal adenocarcinomas (PDACs), most commonly at codon 12, but the clinical implications of codon-specific subtypes in advanced disease remain unclear. We retrospectively analyzed 269 patients with advanced PDAC who underwent next-generation sequencing between 2020 and 2024 at a single tertiary cancer center. Clinical features, co-mutations, treatment outcomes, and survival were evaluated. KRAS mutations were detected in 92% of patients, most frequently G12V (36%) and G12D (34%), followed by G12R (10%) and non-G12 variants (9%). TP53 was the most frequent co-mutation (67%) and was significantly enriched in G12D tumors compared with wild type (74.2% vs. 31.8%). Mutations in homologous recombination and DNA damage response genes were more common in non-G12 and wild-type tumors, although not statistically significant. Serum CA 19-9 was elevated in most G12-mutant tumors, whereas approximately 40% of non-G12 and wild-type patients showed normal levels despite advanced disease. No significant survival differences were observed among KRAS subtypes in the overall or treated cohorts. However, patients with G12V mutations achieved significantly longer survival with fluorouracil-based than gemcitabine-based chemotherapy. These findings suggest that, while KRAS subtyping alone lacks prognostic value, the G12V subtype may inform chemotherapy selection and warrants further prospective validation.

Small cell lung cancer (SCLC) is a highly aggressive neuroendocrine carcinoma (NEC) with poor prognosis due to chemotherapy resistance. Molecular subtypes, including ASCL1, NEUROD1, YAP1 and POU2F3, have distinct clinical implications. POU2F3, linked to a tuft cell-like lineage, represents a non-neuroendocrine subtype found in SCLC and extrapulmonary NECs. However, its prognostic and clinical significance remain unclear. A meta-analysis was performed to assess the relationship between POU2F3 expression and clinical outcomes in SCLC and NECs. Studies reporting clinicopathological or survival data related to POU2F3 expression, identified via immunohistochemistry, were included. This review was performed following the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and was registered on the International Prospective Register of Systematic Reviews (registration number: CRD42023478789). Sixteen studies involving 2011 patients met inclusion criteria. Pooled analysis revealed that POU2F3 expression in SCLC significantly improved OS (HR = 0.74, 95% CI = 0.61-0.90, p < .01 and PFS/RFS (HR = 0.69, 95% CI = 0.53-0.90, p < .01). Subgroup analyses associated POU2F3 positivity with favourable survival when surgical specimen or whole slide analysis was used, or when studies with chemotherapy regimen were included. POU2F3 expression also correlated with younger age (p = .02) and male sex (p = .03) but not with smoking history, tumour stage, nodal involvement, or vascular invasion. POU2F3 expression is associated with improved survival and correlates with younger age and male sex in SCLC, highlighting distinct clinical and biological characteristics of this tuft cell-originated subtype. Data on extrapulmonary NECs were limited, precluding definitive conclusions for this population.

Objective: Claudin18.2 has been established as a putative therapeutic target in human solid malignancies. The aim of this study is to determine claudin18.2 expression as a clinicopathological and prognostic factor in human solid tumors through a systematic review and meta-analysis. Articles were systematically reviewed for studies that included the correlation between claudin18.2 expression and clinicopathological features and prognosis in solid tumors. Meta-analysis was conducted to estimate either odds ratio and 95% confidence intervals (CIs) of clinicopathological factors or hazard ratio and 95% CIs of survival outcomes for claudin18.2 expression in all available solid tumors.Results: 21 studies including 5,331 patients were identified. Overall proportion of claudin18.2 positivity was 29.7%. Analyses of clinicopathological features demonstrated that claudin18.2 positivity correlated with male predominance, lower T stage, more frequent MUC5AC positivity when all primary tumors included. In subgroup analysis, gastric cancer showed significant correlation between high claudin18.2 expression and frequent EBV infection, male predominance and lower T stage. In lung cancer, claudin18.2 expression was associated with favorable overall survival. However, analyses of survival outcomes in all solid tumors showed that claudin18.2 expression was not associated with overall survival and pooled disease-free survival, tumor-specific survival, progression-free survival and relapse-free survival.Conclusions: Our study emphasizes evaluation of claudin18.2 expression as a potential prognostic factor in lung adenocarcinoma and further exploration in other solid tumors as well.Systematic review registration: https://www.crd.york.ac.uk/prospero/, identifier CRD42023468651.

Determining tumor microsatellite status has significant clinical value because tumors that are microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR) respond well to immune check-point inhibitors (ICIs) and oftentimes not to chemotherapeutics. We propose MSI-SEER, a deep Gaussian process-based Bayesian model that analyzes H&E whole-slide images in weakly-supervised-learning to predict microsatellite status in gastric and colorectal cancers. We performed extensive validation using multiple large datasets comprised of patients from diverse racial backgrounds. MSI-SEER achieved state-of-the-art performance with MSI prediction, which was by integrating uncertainty prediction. We achieved high accuracy for predicting ICI responsiveness by combining tumor MSI status with stroma-to-tumor ratio. Finally, MSI-SEER’s tile-level predictions revealed novel insights into the role of spatial distribution of MSI-H regions in the tumor microenvironment and ICI response.

Hepatic graft-versus-host disease (GVHD) significantly impacts morbidity and mortality among allogeneic hematopoietic stem cell transplant recipients. However, the relationship between clinical and immunopathological phenotypes and their influence on clinical outcomes in hepatic GVHD is not well understood. In this study, we aimed to study the implications of portal T-cell infiltration on the clinical outcomes in hepatic GHVD and its similarities to autoimmune liver disease. We analyzed 78 patients with biopsy-confirmed hepatic GVHD (n = 38) or autoimmune liver disease (n = 40) between 2016 and 2021. The cholestatic variant was defined by an R-value < 2.0, based on the ratio of alanine aminotransferase to alkaline phosphatase. The primary outcome was the biochemical response at 4 (early) and 8–12 (late) weeks after corticosteroid treatment. In hepatic GVHD patients, the hepatitic variant (n = 19) showed greater CD3⁺ T-cell infiltration than the cholestatic variant (n = 19; p < 0.001). No significant differences were observed in the infiltration of CD20⁺, CD38⁺, or CD68⁺ cells. The hepatitic variant had significantly better early and late responses and higher liver-related event-free survival than the cholestatic variants (p < 0.05). Concerning autoimmune liver diseases, the autoimmune hepatitis (AIH) group had significantly more portal T-cell infiltration and better treatment responses than the primary biliary cholangitis (PBC) group. In conclusion, higher portal T-cell infiltration may be associated with better clinical outcomes in patients with hepatic GVHD. Additionally, this study highlights similarities in portal T-cell infiltration and treatment response patterns between AIH and the hepatitic variant, as well as PBC and the cholestatic variant.

Adenocarcinoma of the ampulla of Vater (AAC) is a rare malignancy with heterogeneous tumors arising from various histologic subtypes, necessitating new therapeutic strategies. This study examines epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2), and c-Met expression in AAC, given their potential as druggable targets. Among 87 patients who underwent curative resection, EGFR overexpression was found in 87.4%, HER2 in 11.5%, and c-Met in 50%. EGFR overexpression was more common in the pancreatobiliary subtype (p = 0.018) and associated with a higher histologic grade (p = 0.008). HER2 did not correlate with clinicopathological features, while c-Met was more common in node-negative groups (p = 0.004) and often co-expressed with EGFR (p = 0.049). EGFR-positive patients had worse disease-free (HR = 2.89; 95% CI, 1.35–6.20; p = 0.061) and overall survival (HR = 6.89; 95% CI, 2.94–16.2; p = 0.026) than EGFR-negative patients. HER2-positive AAC showed a trend towards shorter survival, although not statistically significant, and c-Met had no impact on survival outcomes. In the context of systemic disease, survival outcomes did not vary according to EGFR, HER2, and c-Met expression, but the HER2-positive group showed a trend towards inferior progression-free survival (HR = 1.90; 95% CI, 0.56–6.41; p = 0.166). This study underscores the potential of EGFR, HER2, and c-Met as targets for personalized therapy in AAC, warranting further research to evaluate targeted treatments.

Pancreatic ductal adenocarcinoma (PDAC) is notorious for its aggressive progression and dismal survival rates, with this study highlighting elevated interleukin 6 (IL-6) levels in patients as a key marker of increased disease severity and a potential prognostic indicator. Analyzing pre-treatment serum from 77 advanced PDAC patients via ELISA, the research determined optimal cutoff values for IL-6 and the IL-6:sIL-6Rα ratio using receiver operating characteristic curve analysis, which then facilitated the division of patients into low and high IL-6 groups, showing significantly different survival outcomes. Notably, high IL-6 levels correlated with adverse features such as poorly differentiated histology, higher tumor burden, and low albumin levels, indicating a stronger likelihood of poorer prognosis. With a median follow-up of 9.28 months, patients with lower IL-6 levels experienced markedly better median overall survival and progression-free survival than those with higher levels, underscoring IL-6’s role in predicting disease prognosis. Multivariate analysis further confirmed IL-6 levels, alongside older age, and elevated neutrophil-to-lymphocyte ratio, as predictors of worse outcomes, suggesting that IL-6 could be a critical biomarker for tailoring treatment strategies in advanced PDAC, warranting further investigation into its role in systemic inflammation and the tumor microenvironment.