Gastric cancer is one of the most common cancers in both Korea and worldwide. Since 2004, the Korean Practice Guidelines for Gastric Cancer have been regularly updated, with the 4th edition published in 2022. The 4th edition was the result of a collaborative work by an interdisciplinary team, including experts in gastric surgery, gastroenterology, endoscopy, medical oncology, abdominal radiology, pathology, nuclear medicine, radiation oncology, and guideline development methodology. The current guideline is the 5th version, an updated version of the 4th edition. In this guideline, 6 key questions (KQs) were updated or proposed after a collaborative review by the working group, and 7 statements were developed, or revised, or discussed based on a systematic review using the MEDLINE, Embase, Cochrane Library, and KoreaMed database. Over the past 2 years, there have been significant changes in systemic treatment, leading to major updates and revisions focused on this area.Additionally, minor modifications have been made in other sections, incorporating recent research findings. The level of evidence and grading of recommendations were categorized according to the Grading of Recommendations, Assessment, Development and Evaluation system. Key factors for recommendation included the level of evidence, benefit, harm, and clinical applicability. The working group reviewed and discussed the recommendations to reach a consensus. The structure of this guideline remains similar to the 2022 version.Earlier sections cover general considerations, such as screening, diagnosis, and staging of endoscopy, pathology, radiology, and nuclear medicine. In the latter sections, statements are provided for each KQ based on clinical evidence, with flowcharts supporting these statements through meta-analysis and references. This multidisciplinary, evidence-based gastric cancer guideline aims to support clinicians in providing optimal care for gastric cancer patients.

Gastric cancer is one of the most common cancers in both Korea and worldwide. Since 2004, the Korean Practice Guidelines for Gastric Cancer have been regularly updated, with the 4th edition published in 2022. The 4th edition was the result of a collaborative work by an interdisciplinary team, including experts in gastric surgery, gastroenterology, endoscopy, medical oncology, abdominal radiology, pathology, nuclear medicine, radiation oncology, and guideline development methodology. The current guideline is the 5th version, an updated version of the 4th edition. In this guideline, 6 key questions (KQs) were updated or proposed after a collaborative review by the working group, and 7 statements were developed, or revised, or discussed based on a systematic review using the MEDLINE, Embase, Cochrane Library, and KoreaMed database. Over the past 2 years, there have been significant changes in systemic treatment, leading to major updates and revisions focused on this area.Additionally, minor modifications have been made in other sections, incorporating recent research findings. The level of evidence and grading of recommendations were categorized according to the Grading of Recommendations, Assessment, Development and Evaluation system. Key factors for recommendation included the level of evidence, benefit, harm, and clinical applicability. The working group reviewed and discussed the recommendations to reach a consensus. The structure of this guideline remains similar to the 2022 version.Earlier sections cover general considerations, such as screening, diagnosis, and staging of endoscopy, pathology, radiology, and nuclear medicine. In the latter sections, statements are provided for each KQ based on clinical evidence, with flowcharts supporting these statements through meta-analysis and references. This multidisciplinary, evidence-based gastric cancer guideline aims to support clinicians in providing optimal care for gastric cancer patients.

Gastric cancer is one of the most common cancers in both Korea and worldwide. Since 2004, the Korean Practice Guidelines for Gastric Cancer have been regularly updated, with the 4th edition published in 2022. The 4th edition was the result of a collaborative work by an interdisciplinary team, including experts in gastric surgery, gastroenterology, endoscopy, medical oncology, abdominal radiology, pathology, nuclear medicine, radiation oncology, and guideline development methodology. The current guideline is the 5th version, an updated version of the 4th edition. In this guideline, 6 key questions (KQs) were updated or proposed after a collaborative review by the working group, and 7 statements were developed, or revised, or discussed based on a systematic review using the MEDLINE, Embase, Cochrane Library, and KoreaMed database. Over the past 2 years, there have been significant changes in systemic treatment, leading to major updates and revisions focused on this area.Additionally, minor modifications have been made in other sections, incorporating recent research findings. The level of evidence and grading of recommendations were categorized according to the Grading of Recommendations, Assessment, Development and Evaluation system. Key factors for recommendation included the level of evidence, benefit, harm, and clinical applicability. The working group reviewed and discussed the recommendations to reach a consensus. The structure of this guideline remains similar to the 2022 version.Earlier sections cover general considerations, such as screening, diagnosis, and staging of endoscopy, pathology, radiology, and nuclear medicine. In the latter sections, statements are provided for each KQ based on clinical evidence, with flowcharts supporting these statements through meta-analysis and references. This multidisciplinary, evidence-based gastric cancer guideline aims to support clinicians in providing optimal care for gastric cancer patients.

Enterococcus faecium, particularly in its multidrug-resistant forms, causes invasive nosocomial infections. Given the limited data comparing the effectiveness of the European Committee on Antimicrobial Susceptibility Testing (EUCAST) and the CLSI clinical breakpoints (CBPs) for quinupristin–dalfopristin (QD) resistance and the need to evaluate their practical application, we retrospectively investigated the susceptibility patterns of 287 E.faecium bloodstream isolates from Korean hospitals to QD using the updated EUCAST and CLSI CBPs and two antimicrobial susceptibility testing methods: disk diffusion (DD) and Sensititre broth microdilution (Sensititre). QD resistance rates were 5.9% (CLSI) and 18.8% (EUCAST) for DD and 22.6% (CLSI) and 28.2% (EUCAST) for Sensititre. The most prevalent QD resistance gene types among QD-resistant isolates were ermB+msrC+ or ermB– msrC+. Categorical agreement between DD and Sensititre ranged from 77.7% to 90.7%, depending on the testing method and CBPs applied. The EUCAST zone diameter CBPs more effectively help identify QD-resistant E. faecium isolates using the DD method than the CLSI zone diameter CBPs. In comparison, the CLSI minimum inhibitory concentration (MIC) CBPs provide more reliable results for resistance classification in the Sensititre method than EUCAST MIC CBPs. These findings would help improve clinical decision-making for treating multidrug-resistant E. faecium infections.

Objectives: . Although mandibular advancement device (MAD) treatment is effective for obstructive sleep apnea (OSA), some concerns remain regarding its potential therapeutic impact and side effects. Thus, we developed a novel MAD that auto-titrates depending on its position in patients with OSA. We conducted a clinical trial to determine the efficacy of an auto-titrating mandibular advancement device (AMAD) for treating OSA. Methods: . Fourteen patients diagnosed with OSA participated in this study. Polysomnography (PSG) was performed at the beginning of the clinical trial, and after 3 months of treatment, PSG with AMAD in situ was conducted. Results: . The mean scores for the Epworth Sleepiness Scale (ESS) and STOP-Bang were 8.21±4.21 and 5.00±1.00, respectively. After 3 months of AMAD treatment, the STOP-Bang scores improved to 3.75±1.06; however, the ESS scores did not show a significant change. Additionally, we observed statistically significant improvements in several respiratory parameters in the PSG data following AMAD treatment. These included reductions in the apnea-hypopnea index (AHI) (from 32.85±21.71 to 12.93±10.70), supine AHI (from 45.91±23.58 to 15.59±12.76), and lateral AHI (from 13.94±10.95 to 5.49±7.40). Improvements were also noted in the lowest O2 saturation (from 79.71±6.22 to 84.00± 5.71), total arousal number (from 191.14±112.07 to 86.57±48.80), and arousal index (from 33.76±21.00 to 15.05± 8.42). However, there were no significant changes in total sleep time, sleep efficiency, or mean oxygen saturation. Additionally, no major side effects were observed during treatment, specifically related to tooth or jaw pain. Conclusion . Our clinical trial found that AMAD improved PSG parameters and reduced the incidence of common side effects. Therefore, AMAD may be an effective alternative treatment for OSA.

Purpose: Bladder cancer is a common genitourinary malignant disease worldwide. Dasatinib is a small molecule inhibitor of Src family kinases. We investigated the anticancer effect and putative molecular mechanisms of dasatinib on T24 and cisplatin-resistant T24R2 human bladder cancer cells. Materials and Methods: Cell proliferation was measured using Cell Counting Kit-8 (CCK-8) and colony formation in dasatinib treated bladder cancer cells. Flow cytometry was used to determined cell cycle arrest and apoptosis. The expression of apoptosis and autophagy related proteins were detected by western blot analysis. Results: In bladder cancer cells, dasatinib significantly reduced cell proliferation, colony formation, and induced G1-phase arrest.Dasatinib triggered apoptosis along with an increased expression of apoptosis-related genes (caspases, PARP, and cytochrome c).Down-regulation of Bcl-2 and up-regulation of Bad, which are hallmarks of apoptosis, were found to play a dominant role in mediating the effects of dasatinib treatment. We further showed that dasatinib inhibits p-Src, p-PI3K, p-Akt, and p-mTOR in bladder cancer cells. Dasatinib also increased the expression of markers of autophagy flux such as LC3-II and p62. Conclusions These results confirmed that dasatinib is a potent chemotherapeutic drug which induces apoptosis and autophagy by suppressing the PI3K/Akt/mTOR pathway in bladder cancer cells.

Purpose: T1 high grade (T1HG) bladder cancer (BC) is a type of non-muscle invasive BC (NMIBC) that is recognized as an aggressive subtype with a heightened propensity for progression. Current risk stratification methods for NMIBC rely on clinicopathological indicators; however, these approaches do not adequately capture the aggressive nature of T1HG BC. Thus, new, more accurate biomarkers for T1HG risk stratification are needed. Here, we enrolled three different patient cohorts and investigated expression of collagen type VI alpha 1 (COL6A1), a key component of the extracellular matrix, at different stages and grades of BC, with a specific focus on T1HG BC. Materials and Methods: Samples from 298 BC patients were subjected to RNA sequencing and real-time polymerase chain reaction. Results: We found that T1HG BC and muscle invasive BC (MIBC) exhibited comparable expression of COL6A1, which was significantly higher than that by other NMIBC subtypes. In particular, T1HG patients who later progressed to MIBC had considerably higher expression of COL6A1 than Ta, T1 low grade patients, and patients that did not progress, highlighting the aggressive nature and higher risk of progression associated with T1HG BC. Moreover, Cox and Kaplan–Meier survival analyses revealed a significant association between elevated expression of COL6A1 and poor progression-free survival of T1HG BC patients (multivariate Cox hazard ratio, 16.812; 95% confidence interval, 3.283–86.095; p=0.001 and p=0.0002 [log-rank test]). Conclusions These findings suggest that COL6A1 may be a promising biomarker for risk stratification of T1HG BC, offering valuable insight into disease prognosis and guidance of personalized treatment decisions.

Objectives: . Although mandibular advancement device (MAD) treatment is effective for obstructive sleep apnea (OSA), some concerns remain regarding its potential therapeutic impact and side effects. Thus, we developed a novel MAD that auto-titrates depending on its position in patients with OSA. We conducted a clinical trial to determine the efficacy of an auto-titrating mandibular advancement device (AMAD) for treating OSA. Methods: . Fourteen patients diagnosed with OSA participated in this study. Polysomnography (PSG) was performed at the beginning of the clinical trial, and after 3 months of treatment, PSG with AMAD in situ was conducted. Results: . The mean scores for the Epworth Sleepiness Scale (ESS) and STOP-Bang were 8.21±4.21 and 5.00±1.00, respectively. After 3 months of AMAD treatment, the STOP-Bang scores improved to 3.75±1.06; however, the ESS scores did not show a significant change. Additionally, we observed statistically significant improvements in several respiratory parameters in the PSG data following AMAD treatment. These included reductions in the apnea-hypopnea index (AHI) (from 32.85±21.71 to 12.93±10.70), supine AHI (from 45.91±23.58 to 15.59±12.76), and lateral AHI (from 13.94±10.95 to 5.49±7.40). Improvements were also noted in the lowest O2 saturation (from 79.71±6.22 to 84.00± 5.71), total arousal number (from 191.14±112.07 to 86.57±48.80), and arousal index (from 33.76±21.00 to 15.05± 8.42). However, there were no significant changes in total sleep time, sleep efficiency, or mean oxygen saturation. Additionally, no major side effects were observed during treatment, specifically related to tooth or jaw pain. Conclusion . Our clinical trial found that AMAD improved PSG parameters and reduced the incidence of common side effects. Therefore, AMAD may be an effective alternative treatment for OSA.

Objectives: . Although mandibular advancement device (MAD) treatment is effective for obstructive sleep apnea (OSA), some concerns remain regarding its potential therapeutic impact and side effects. Thus, we developed a novel MAD that auto-titrates depending on its position in patients with OSA. We conducted a clinical trial to determine the efficacy of an auto-titrating mandibular advancement device (AMAD) for treating OSA. Methods: . Fourteen patients diagnosed with OSA participated in this study. Polysomnography (PSG) was performed at the beginning of the clinical trial, and after 3 months of treatment, PSG with AMAD in situ was conducted. Results: . The mean scores for the Epworth Sleepiness Scale (ESS) and STOP-Bang were 8.21±4.21 and 5.00±1.00, respectively. After 3 months of AMAD treatment, the STOP-Bang scores improved to 3.75±1.06; however, the ESS scores did not show a significant change. Additionally, we observed statistically significant improvements in several respiratory parameters in the PSG data following AMAD treatment. These included reductions in the apnea-hypopnea index (AHI) (from 32.85±21.71 to 12.93±10.70), supine AHI (from 45.91±23.58 to 15.59±12.76), and lateral AHI (from 13.94±10.95 to 5.49±7.40). Improvements were also noted in the lowest O2 saturation (from 79.71±6.22 to 84.00± 5.71), total arousal number (from 191.14±112.07 to 86.57±48.80), and arousal index (from 33.76±21.00 to 15.05± 8.42). However, there were no significant changes in total sleep time, sleep efficiency, or mean oxygen saturation. Additionally, no major side effects were observed during treatment, specifically related to tooth or jaw pain. Conclusion . Our clinical trial found that AMAD improved PSG parameters and reduced the incidence of common side effects. Therefore, AMAD may be an effective alternative treatment for OSA.

Purpose: Pathologic T3b (pT3b) prostate cancer, characterized by seminal vesicle invasion (SVI), exhibits variable oncological outcomes post–radical prostatectomy (RP). Identifying prognostic factors is crucial for patient-specific management. This study investigates the impact of bilateral SVI on prognosis in pT3b prostate cancer. Materials and Methods: We evaluated the medical records of a multi-institutional cohort of men who underwent RP for prostate cancer with SVI between 2000 and 2012. Univariate and multivariable analyses were performed using Kaplan-Meier analysis and covariate-adjusted Cox proportional hazard regression for biochemical recurrence (BCR), clinical progression (CP), and cancer-specific survival (CSS). Results: Among 770 men who underwent RP without neo-adjuvant treatment, median follow-up was 85.7 months. Patients with bilateral SVI had higher preoperative prostate-specific antigen levels and clinical T category (all p < 0.001). Extracapsular extension, tumor volume, lymph node metastasis (p < 0.001), pathologic Gleason grade group (p < 0.001), and resection margin positivity (p < 0.001) were also higher in patients with bilateral SVI. The 5-, 10-, and 15-year BCR-free survival rates were 23.9%, 11.7%, and 8.5%; CP-free survival rates were 82.8%, 62.5%, and 33.4%; and CSS rates were 96.4%, 88.1%, and 69.5%, respectively. The bilateral SVI group demonstrated significantly lower BCR-free survival rates, CP-free survival rates, and CSS rates (all p < 0.001). Bilateral SVI was independently associated with BCR (hazard ratio, 1.197; 95% confidence interval, p=0.049), CP (p=0.022), and CSS (p=0.038) in covariate-adjusted Cox regression. Conclusion Bilateral SVI is a robust, independent prognostic factor for poor oncological outcomes in pT3b prostate cancer.