The gastrointestinal stromal tumor (GIST) is one of the most common mesenchymal tumors of the gastrointestinal tract. Between the 1990s and early 2000s, GIST was identified as a tumor characterized by KIT or PDGFRA mutations, resulting in imatinib being established as an effective targeted therapy. However, with advances in molecular diagnostics, approximately 10%–15% of GISTs have been reported to harbor alternative mutations, such as those in the succinate dehydrogenase subunit genes and BRAF, leading to the development of additional targeted therapies. GISTs exhibit a wide spectrum of clinical behaviors, ranging from indolent to highly aggressive, prompting the development of diverse risk classification systems. However, multiple systems remain in use, leading to inconsistent pathologic reports. Moreover, the mitotic counting method—a key factor in risk stratification—has become a major source of confusion among pathologists owing to the adoption of digital pathology and discrepancies between updated international guidelines and outdated reimbursement requirements. These inconsistencies have hindered pathologic reporting and communication between pathologists and clinicians. This review comprehensively overviews the historical background, molecular subtypes, and risk classification systems of GIST, focusing on evolving issues in mitotic rate evaluation and the application of risk classification systems in clinical practice.

BACKGROUND/OBJECTIVES: Lutein, a dietary carotenoid, plays a crucial role in protecting eye health as an anti-inflammatory agent and antioxidant. Green leafy vegetables constitute a major source of lutein; however, comparative studies on different consumption methods are limited. Therefore, this study aimed to evaluate the bioavailability of lutein from lutein-rich foods, namely, raw vegetables and raw vegetable juice. SUBJECTS/METHODS: In this study, 18 adults were recruited. They were randomly divided into three groups: commercial lutein supplement (LUT, 20 mg), raw vegetable (RV), and raw vegetable juice (RVJ) groups. Blood was collected at 0-, 4-, 6-, 8-, 12-, 24-, and 30-h intervals after the consumption of each test meal. Participants’ serum lutein levels were analyzed using high-performance liquid chromatography (HPLC). Considering lutein’s wellestablished anti-inflammatory properties, changes in inflammatory status were assessed by measuring serum high-sensitivity C-reactive protein (hs-CRP) levels. Furthermore, urinary metabolomic profiling was conducted using 1 H nuclear magnetic resonance spectroscopy to evaluate metabolic alterations. RESULTS: After consuming each lutein-rich food, participants’ blood lutein levels were analyzed, and the serum concentration peaked at 12 h (0.37 ± 0.13 μg/mL), 24 h (0.61 ± 0.18 μg/mL), and 30 h (0.42 ± 0.16 μg/mL) after RV, LUT, and RVJ consumption, respectively.Additionally, hs-CRP levels decreased following lutein-rich food consumption. Twelve hours after consumption, hs-CRP levels decreased to 0.81 and 0.83 mg/L in the RV and RVJ groups, respectively. Twenty-four hours after consumption, they further decreased to 0.68 and 0.74 mg/L in the LUT and RVJ groups, respectively. Thirty hours after consumption, a reduction to 0.61 mg/L was observed in the RVJ group. Furthermore, after consuming each luteinrich food, N-acetyl glycoprotein levels decreased at 24 h, reflecting metabolic alterations potentially associated with lutein metabolism. CONCLUSION These findings suggest that the short-term consumption of lutein-rich foods, regardless of their type or source, potentially yields health benefits.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Purpose: This study assessed the validity of the hospital standardized mortality ratio (HSMR) risk-adjusted model by comparing models that include clinical information and the current model based on administrative information in South Korea. Materials and Methods: The data of 53976 inpatients were analyzed. The current HSMR risk-adjusted model (Model 1) adjusts for sex, age, health coverage, emergency hospitalization status, main diagnosis, surgery status, and Charlson Comorbidity Index (CCI) using administrative data. As candidate variables, among clinical information, the American Society of Anesthesiologists score, Acute Physiology and Chronic Health Evaluation (APACHE) II, Simplified Acute Physiology Score (SAPS) 3, present on admission CCI, and cancer stage were collected. Surgery status, intensive care in the intensive care unit, and CCI were selected as proxy variables among administrative data. In-hospital death was defined as the dependent variable, and a logistic regression analysis was performed. The statistical performance of each model was compared using C-index values. Results: There was a strong correlation between variables in the administrative data and those in the medical records. The C-index of the existing model (Model 1) was 0.785; Model 2, which included all clinical data, had a higher C-index of 0.857. In Model 4, in which APACHE II and SAPS 3 were replaced with variables recorded in the administrative data from Model 2, the C-index further increased to 0.863. Conclusion The HSMR assessment model improved when clinical data were adjusted. Simultaneously, the validity of the evaluation method could be secured even if some of the clinical information was replaced with the information in the administrative data.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Purpose: This study assessed the validity of the hospital standardized mortality ratio (HSMR) risk-adjusted model by comparing models that include clinical information and the current model based on administrative information in South Korea. Materials and Methods: The data of 53976 inpatients were analyzed. The current HSMR risk-adjusted model (Model 1) adjusts for sex, age, health coverage, emergency hospitalization status, main diagnosis, surgery status, and Charlson Comorbidity Index (CCI) using administrative data. As candidate variables, among clinical information, the American Society of Anesthesiologists score, Acute Physiology and Chronic Health Evaluation (APACHE) II, Simplified Acute Physiology Score (SAPS) 3, present on admission CCI, and cancer stage were collected. Surgery status, intensive care in the intensive care unit, and CCI were selected as proxy variables among administrative data. In-hospital death was defined as the dependent variable, and a logistic regression analysis was performed. The statistical performance of each model was compared using C-index values. Results: There was a strong correlation between variables in the administrative data and those in the medical records. The C-index of the existing model (Model 1) was 0.785; Model 2, which included all clinical data, had a higher C-index of 0.857. In Model 4, in which APACHE II and SAPS 3 were replaced with variables recorded in the administrative data from Model 2, the C-index further increased to 0.863. Conclusion The HSMR assessment model improved when clinical data were adjusted. Simultaneously, the validity of the evaluation method could be secured even if some of the clinical information was replaced with the information in the administrative data.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Purpose: This study assessed the validity of the hospital standardized mortality ratio (HSMR) risk-adjusted model by comparing models that include clinical information and the current model based on administrative information in South Korea. Materials and Methods: The data of 53976 inpatients were analyzed. The current HSMR risk-adjusted model (Model 1) adjusts for sex, age, health coverage, emergency hospitalization status, main diagnosis, surgery status, and Charlson Comorbidity Index (CCI) using administrative data. As candidate variables, among clinical information, the American Society of Anesthesiologists score, Acute Physiology and Chronic Health Evaluation (APACHE) II, Simplified Acute Physiology Score (SAPS) 3, present on admission CCI, and cancer stage were collected. Surgery status, intensive care in the intensive care unit, and CCI were selected as proxy variables among administrative data. In-hospital death was defined as the dependent variable, and a logistic regression analysis was performed. The statistical performance of each model was compared using C-index values. Results: There was a strong correlation between variables in the administrative data and those in the medical records. The C-index of the existing model (Model 1) was 0.785; Model 2, which included all clinical data, had a higher C-index of 0.857. In Model 4, in which APACHE II and SAPS 3 were replaced with variables recorded in the administrative data from Model 2, the C-index further increased to 0.863. Conclusion The HSMR assessment model improved when clinical data were adjusted. Simultaneously, the validity of the evaluation method could be secured even if some of the clinical information was replaced with the information in the administrative data.

Purpose: Given the notable increase in the incidence of multiple myeloma (MM) in Asia and advent of innovative treatments, this study aims to provide a comprehensive understanding of the treatment patterns, outcomes, and eco‑ nomic burden of MM across the lines of therapy (LOTs) in South Korea. Methods: This retrospective cohort study was conducted using data from the National Health Insurance claims data provided by the Health Insurance Review and Assessment Database. An identification algorithm was developed to detect the regimens and LOTs. Treatment patterns and outcomes were assessed as real-world treatment sequence, treatment duration (rwTD), time to next-line treatment (rwTTNT), and overall survival (rwOS). Economic burden was assessed as healthcare resource utilization (HCRU) and the cost incurred per person per month. Results: This study included 11,450 patients who were newly diagnosed with MM between January 2010 and December 2019. The observed real-world LOT patterns reflect the changes in South Korea’s reimburse‑ ment scheme. Mean treatment-free intervals decreased from 11.59 months (SD 16.23) to 2.77 months (SD 6.14) from the first LOT (LOT 1) to LOT 5. Median rwTTNT decreased from 26.61 months (95% CI: 25.69-27.57) to 12.40 months (95% CI: 11.55-13.49), and median rwOS decreased from 61.88 months (95% CI: 59.11-65.46) to 13.65 months (95% CI: 11.88-16.22). The HCRU and associated costs increased substantially with the LOT advancement. Conclusion This large-scale observational study offers comprehensive insights into the real-world treatment of MM in South Korea. The study findings highlight the progressive nature of MM and increasing economic burden of advanced lines of treatment, underscoring the necessity for optimized treatment strategies.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.