Gastric cancer (GC) remains a major global health concern, particularly in East Asia, Central Asia, and Eastern Europe, where its incidence and mortality rates are high. Helicobacter pylori infection is the primary cause of GC and leads to carcinogenic progression from nonatrophic gastritis to cancer. Although screening programs have been implemented in high-risk countries, such as Japan and South Korea, comprehensive strategies remain limited globally. This study reviewed the status of GC screening worldwide and prevention strategies in regions with different risks. Various GC screening methods have been developed, including H. pylori serology, serum pepsinogen testing, upper gastrointestinal contrast radiography, and endoscopy. Endoscopic screening has shown superior sensitivity and specificity, reducing GC mortality by up to 47% in South Korea and demonstrating higher detection rates than upper gastrointestinal contrast radiography and pepsinogen testing. However, cost-effectiveness remains a challenge, particularly in Western countries where the overall GC prevalence is lower. Risk stratification using a combination of H. pylori serology and pepsinogen testing has been adopted in Japan to optimize screening efficiency. Additionally, H. pylori eradication has been recognized as a cost-effective strategy to reduce the incidence of GC with economic benefits demonstrated in Japan and other high-risk regions. In the United States, targeted screening of high-risk immigrant populations has been suggested to enhance cost-effectiveness. GC screening strategies should consider developing epidemiological trends, cost-effectiveness, and risk-based approaches. Future efforts should focus on expanding targeted screening initiatives to high-risk groups to improve early detection and survival rates.

Cancer diagnosis and therapy cause stress to the body. Preclinical studies have shown that stress hormones can stimulate tumor progression and metastasis by interacting with β-adrenergic receptors, and that β-blockers can inhibit those processes. We assessed if β-blocker use was associated with survival in a nationwide cohort of women with epithelial ovarian cancer (EOC). We identified all women aged ≥40 years who underwent EOC surgery in 2004-2018 in Norway through the Cancer Registry of Norway. We estimated the association between peri-diagnostic and post-diagnostic β-blocker use and survival. We used Cox models, adjusted for sociodemographic and health factors, and reported hazard ratios (HRs) and 95% confidence intervals (CIs). The difference in overall survival time between β-blocker users and non-users was estimated as the difference in restricted mean survival time at 5 years after diagnosis using flexible parametric models. We included 3911 women with EOC; 540 (14%) used β-blockers at diagnosis, 1672 (43%) died of the disease, and 1882 (48%) died overall. We found an association between peri-diagnostic β-blocker use and longer EOC-specific survival (HR = 0.85, 95%CI 0.73-1.00; p-value = 0.048), and an indication of an association with overall survival (HR = 0.89, 95%CI 0.77-1.02; p-value = 0.101). Analysis of post-diagnostic β-blocker use, which included only women who survived 12 months or longer (n = 3344), found similar associations. At 5 years from diagnosis, peri-diagnostic β-blocker users lived on average 1.28 months longer than non-users (95%CI 0.01-2.60 months). The results support the hypothesis that β-blocker use improves EOC-specific survival in women with EOC.

Long non‑coding RNAs (lncRNAs) are key regulators of gene expression, that can regulate a range of carcinogenic processes. Moreover, they exhibit stability in biological fluids, with some displaying tissue specificity. As their expression depends on specific conditions or is linked to the regulation of particular signaling pathways, lncRNAs are promising candidates for providing insights into the likely progression of the disease. This allows for the stratification of patients based on their risk of progression, making them potential prognostic biomarkers in various types of cancer. In addition, the tissue‑specific expression profile of lncRNAs renders them ideal candidates for detection, prognosis and monitoring of cancer progression. The present study aims to provide an overview of differentially expressed lncRNAs in Mexican patients with triple‑negative breast cancer (TNBC), a subtype of breast cancer. The aim was to identify potential prognostic biomarkers that can be applied to improve the clinical management of Mexican patients with TNBC. Human Transcriptome Array 2.0 microarrays were used to analyze the transcriptome of TNBC and luminal tumors, which are reported to have a good prognosis amongst aggressive tumor types. Subsequently, results from these microarrays were validated in a cohort from The Cancer Genome Atlas, an independent cohort of Mexican patients and in breast cancer cell lines (MCF7, ZR75, T47D, MDA‑MB‑231, MDA‑MB‑468 and BT20). A total of 746 differentially expressed transcripts were identified, including 102 lncRNAs in TNBC compared with luminal tumors. Among the lncRNAs with the most significant changes in expression levels, SOX9‑AS was highly expressed in TNBC, whereas the expression of Lnc‑peroxidasin‑3:1 (Lnc‑PXDN‑3:1), Lnc‑RNA Synapse Defective Rho GTPase Homolog (Lnc‑SYDE) and long intergenic non‑coding RNA (LINC)01087 were decreased. In addition, the low expression of lncRNA LINC01087, LINC02568, ACO22196, and lncRNA eosinophil granule ontogeny transcript (Lnc‑EGOT) was associated with poor overall survival (OS). Further analysis revealed that the high expression levels of Lnc‑PXDN‑3:1, Lnc RNA fibrous sheath interacting protein 1‑6:3 and (LINC)00182 were associated with reduced survival in patients with the luminal subtype of breast cancer. Similarly, low expression levels of lncRNAs such as GATA binding protein 3‑1 (Lnc‑GATA‑3‑1), LINC01087, and BX679671.1 in luminal subtypes of breast cancer, as well as LINC00504 and LncRNA rho guanine nucleotide exchange factor 38 intronic transcript 1 (Lnc‑ARHGEF38‑IT1) in basal subtypes have been linked to poorer survival. The interactions and functions of LINC01087 were then investigated, revealing the interaction of LINC01087 with RNAs and transcription factors, highlighting their potential involvement in the estrogen receptor pathway. The present study provided a detailed analysis of the expression of lncRNAs in TNBC, which highlights the role of lncRNAs as a biomarker in the survival outcomes of patients with breast cancer to improve the understanding of transcriptional regulation in TNBC.

Gastric cancer-associated mesenchymal stem cells (GC-MSCs) as integral components of the tumor microenvironment potentiate gastric cancer growth and metastasis. SALL4 is aberrantly upregulated in gastric cancer and pivotal for malignant progression. Whether GC-MSCs is responsible for SALL4 upregulation and the underlying mechanisms remains elusive.

Cancer growth and metastasis capacities were assessed by cell colony formation assay, transwell assay, and epithelial-mesenchymal transition protein detection in vitro as well as subcutaneous xenograft and peritoneal metastasis models in vivo. SALL4 was measured by qPCR, western blot and immunohistochemistry staining. Gain- and loss-functional analysis were performed for miRNA and target gene. β-catenin signaling was assessed by immunofluorescence staining and Top/FopFlash luciferase assay. Transcriptional regulation was conducted using chemicals, luciferase reporter and ChIP assay. Clinical tissues and TCGA-STAD database were included for expression profile, correlation and clinical relevance analysis.

GC-MSCs promoted gastric cancer growth and metastasis along with elevation of SALL4 and miR-4669 in cancer cells and tissues. Overexpression of miR-4669 mimicked GC-MSC effects, while miR-4669 knockdown eliminated their oncogenic roles. TIMP3 was identified as a target of miR-4669 and mediated its functions. TIMP3 overexpression counteracted GC-MSC-induced cancer progression and SALL4 expression. GC-MSCs activated SALL4 transcription through the miR-4669/TIMP3/β-catenin pathway. The regulatory axis was aberrantly expressed in gastric cancer tissues, correlated with each other in certain cancer tissues and associated with lymph node metastasis.

GC-MSCs transcriptionally upregulate SALL4 to facilitate gastric cancer cell growth and metastasis via miR-4669/TIMP3/β-catenin pathway, highlighting the crucial role of GC-MSCs in the aberrant upregulation of SALL4.

Epidermal growth factor-like proteins (EGFLs) contain more than a single EGF/EGF-like domain within their protein structure. To date, ten EGFL family members (EGFL1-10) have been characterized across diverse tissues and developmental stages under different conditions. In this review, we conclude that EGFLs are instrumental in regulating biological activities and pathological processes. Under physiological conditions, EGFLs participate in angiogenesis, neurogenesis, osteogenesis, and other processes. Under pathological conditions, EGFLs are linked with different diseases, particularly cancers. Furthermore, we highlight recent advancements in the study of EGFLs in biological conditions and cancers. In addition, the regulatory role and key underlying mechanism of EGFLs in mediating tumorigenesis are discussed. This paper also examines potential antagonists that target EGFL family members in cancer therapeutics. In summary, this comprehensive review elucidates the critical role of EGFLs in neoplastic diseases and highlights their potential as therapeutic targets.

Research studies aimed at improving the outcomes of patients with pancreatic ductal adenocarcinoma (PDAC) have brought about limited progress, and in clinical practice, the optimized use of surgery, chemotherapy and supportive care have led to modest improvements in survival that have probably reached a plateau. As a result, PDAC is expected to be the second leading cause of cancer-related death in Western societies within a decade. The development of therapeutic advances in PDAC has been challenging owing to a lack of actionable molecular targets, a typically immunosuppressive microenvironment, and a disease course characterized by rapid progression and clinical deterioration. Yet, the progress in our understanding of PDAC and identification of novel therapeutic opportunities over the past few years is leading to a strong sense of optimism in the field. In this Perspective, we address the aforementioned challenges, including biological aspects of PDAC that make this malignancy particularly difficult to treat. We explore specific areas with potential for therapeutic advances, including targeting mutant KRAS, novel strategies to harness the antitumour immune response and approaches to early detection, and propose mechanisms to improve clinical trial design and to overcome various community and institutional barriers to progress.

Lung cancer (LC) represents the leading cause of cancer-related death and the third in incidence in Argentina. Survival rates are low.

To analyze the spatial distribution of LC incidence in Córdoba-Argentina (2004-2014), explore trends in histological types, and estimate the probability of survival.

A longitudinal ecological study was conducted using data from the Provincial Cancer Registry. Age-specific and standardized incidence rates for LC (ICD-10: C33-34) were calculated, truncated (35-84 years), and stratified by sex, year (2004-2014), and histology (small cell carcinoma and non-small cell: adenocarcinoma, squamous cells, large cells, and other carcinomas). Temporal analysis employed Joinpoint regression models, estimating annual percentage changes (APC). Median times estimated survival curves and semiparametric Cox regression models were employed for survival. Statistical significance: log-rank tests and proportional hazards tests. Software: Joinpoint-Regression-Program and Stata17.

From 2004-2014, 8246 LC cases were diagnosed in individuals aged 35-84. The highest incidence occurred in males aged 75-79 and females aged 80-84. The Age-standardized incidence rates for males and females were 57.9 and 23.6 cases per 100,000 person-years, respectively. In both sexes, the temporal incidence trend was decreasing (APC -3.21 %; p = 0.001), more pronounced in males (APC -3.99 %, p = 0.011), with negative APCs in all histological subtypes. The probability of survival decreased to 32 % (95 %CI: 31 %-34 %) within just 12 months (38 % in females, 30 % in males). The risk of death increased proportionally with age (males HR: 1.007, (95 %CI: 1.004-1.01, p = 0.000); females HR: 1.005, (95 %CI: 1.00-1.01, p = 0.031)) and across all histological types, with lower proportional risks in females and disparities based on histology: in males, the highest risk was in large cells (p = 0.008) and SMCC, while in females, it was SCLC (p = 0.055).

Despite estimating a favorable trend in LC incidence since 2004, the survival prognosis remains unfavorable one-year post-diagnosis, dependent on sex, age, and histological type.

The European Randomized study of screening for prostate cancer (ERSPC) demonstrated a reduction in prostate cancer (PC) mortality via PSA-based screening. We evaluated whether treatments for castration resistant PC vary between the trial arms within the Finnish section (FinRSPC) of the ERSPC.

Clinical data were collected from medical records and national health care databases for all men diagnosed with PC and starting androgen deprivation therapy (ADT) during 1996-2015 at Tampere University Hospital. We evaluated frequencies and durations of treatments for castration resistant PC. Cox regression was used to assess time from ADT initiation to castration resistant PC treatment.

In total, 62 (14.2%) and 116 (15.9%) received at least % cycle of treatment for castration resistant PC in the screening and control-arm, respectively. There were no statistically significant differences in distribution of treatments for castration resistant PC between the study arms at any treatment lines (P-values over 0.05 for first, second and third & later lines of treatment). No difference was found in time to initiation of treatment for castration resistant PC after ADT. (HR: 1.00; 95% [CI], 0.78-1.39; P = 0.998).

Although limited by small sample size and a single-center scope, our findings suggest the mortality result of the FinRSPC is not attributable to differing treatment for castration-resistant PC between the trial arms.

An increasing number of studies have shown that circular RNAs (circRNAs) are key regulators of cancer development and progression. RNA-binding proteins (RBPs) play critical roles in the regulation of biological activities, such as RNA synthesis, selective splicing, modification, translocation, and translation; therefore, research on the interactions of circRNAs with RBPs is key to identifying potential targets for cancer treatment. However, the biological roles and mechanisms of circRNAs in gastric cancer (GC) remain largely unknown. We identified differentially expressed circRNAs in GC by analysing Gene Expression Omnibus (GEO) datasets. Concurrently, in vitro functional assays and in vivo animal studies were performed to explore the biological role of circRNAs in GC. We performed western blotting (WB) of labelled proteins, salvage assays, mass spectrometry (MS), and RNA sequencing to investigate the mechanism of circRNAs in GC to explore their effects on GC cell proliferation and metastasis and to validate their potential value as therapeutic targets. Upregulated expression of cyclic RNA EPSTI1 (circEPSTI1; hsa_circ_0000479) was found in GC tissues and was associated with a poor clinical prognosis. hsa_circ_0000479 promotes the proliferation and migration of GC cells in vitro and in vivo. Notably, hsa_circ_0000479 interacts with Ras-GTPase-activated protein-binding protein 1 (G3BP1) in GC cells and inhibits the degradation of G3BP1 via the ubiquitin‒proteasome pathway, whereas hsa_circ_0000479 blocks the binding of G3BP1 to the E3 ligase BTRC. Mechanistic studies suggest that hsa_circ_0000479 promotes GC progression by competitively inhibiting the G3BP1 ubiquitination-mediated degradation facilitated by BTRC. Our results reveal the molecular mechanism by which hsa_circ_0000479 promotes GC progression through BTRC-mediated competitive binding to G3BP1 to inhibit its ubiquitination-mediated degradation, which provides a new theoretical basis for the targeted treatment of GC and elucidates the potential of hsa_circ_0000479-G3BP1-BTRC as a therapeutic target in GC. These findings provide a new direction for the treatment of patients with GC.

Non-invasive diagnostic monitoring techniques have become essential for treating lung cancer (LC), which continues to be the primary cause of cancer-related death worldwide. The new diagnostic biomarkers called tumour-educated platelets (TEPs) show strong prospects for providing vital information about tumor biology, tumor spread pathways, and treatment reaction patterns. Despite lacking a nucleus, platelets exhibit an active RNA profile that develops through interactions with tumor-derived compounds and the tumor microenvironments (TME). This review explains platelet-tumour interaction regulatory mechanisms while focusing on platelet contributions toward cancer development, immune system avoidance, and blood clot formation. The detection and classification of LC show promise through the analysis of RNA molecules extracted from platelets that encompass mRNAs and non-coding RNAs. RNA sequencing technology based on TEP demonstrates excellent diagnostic power by correctly identifying LC patients alongside their oncogenic alterations of EGFR, KRAS, and ALK. Treatment predictions have proven successful using platelet RNA profiles, specifically in immunotherapy and targeted therapy. Integrating next-generation sequencing with machine learning and artificial intelligence enhances TEP-based diagnostic tools, improving detection accuracy. Standardizing platelet extraction methods and vesicle purification from tumor material needs better development for effective and affordable clinical use. Future investigations should combine TEPs with circulating tumor DNA and exosomal RNA markers to enhance both earliest-stage LC diagnosis and patient-specific therapeutic approaches. TEPs introduce a groundbreaking technique in oncology since they can transform non-invasive medical diagnostics and therapeutic monitoring for cancer.

The purpose of this study is to compare a cohort of cancer survivors with a cohort of cancer-free employees (1) with respect to employment prospects over a 15-year period and (2) with respect to the differential impact of working conditions on employment over this time period.

The cancer cohort is retrieved from the Cancer Registry of Norway, while data on the non-cancer cohort are retrieved from register data managed by Statistics Norway. Job exposure matrices were used to remedy the lack of working-conditions information in the register data. We use nearest-neighbor matching to match the non-cancer cohort (the control group) to the cancer-survivor cohort (the treatment group). Cox regression analysis was applied to examine the relationships between working conditions, employment, and cancer. The results are reported separately for mechanical-job exposures and psychosocial exposures, as well as by gender.

Cancer survivors are more likely to experience reduced employment as compared to individuals without a history of cancer. Male cancer survivors in physically demanding occupations have an increased risk of reduced employment after being diagnosed with cancer. This does not apply to female cancer survivors. Regarding the impact of psychosocial exposures on employment, we find no differences over time between cancer survivors and the non-cancer population.

Male cancer survivors in physically demanding occupations have an increased risk of reduced employment after being diagnosed with cancer, whereas this is not the case for female cancer survivors. Psychosocial exposures do not impact the relative risk of reduced employment over time.

We suggest that return to work after cancer should be considered a process rather than only the re-entry step of resuming work. Thus, it is important to provide long-term support for cancer survivors. We recommend providing more attention to working conditions, particularly in occupations that involve a high level of mechanical-job exposures.

In computer-aided diagnosis systems, precise feature extraction from CT scans of colorectal cancer using deep learning is essential for effective prognosis. However, existing convolutional neural networks struggle to capture long-range dependencies and contextual information, resulting in incomplete CT feature extraction. To address this, the PEDRA-EFB0 architecture integrates patch embeddings and a dual residual attention mechanism for enhanced feature extraction and survival prediction in colorectal cancer CT scans. A patch embedding method processes CT scans into patches, creating positional features for global representation and guiding spatial attention computation. Additionally, a dual residual attention mechanism during the upsampling stage selectively combines local and global features, enhancing CT data utilization. Furthermore, this paper proposes a feature selection algorithm that combines autoencoders and entropy technology, encoding and compressing high-dimensional data to reduce redundant information and using entropy to assess the importance of features, thereby achieving precise feature selection. Experimental results indicate the PEDRA-EFB0 model outperforms traditional methods on colorectal cancer CT metrics, notably in C-index, BS, MCC, and AUC, enhancing survival prediction accuracy. Our code is freely available at https://github.com/smile0208z/PEDRA .

A wide inequality exists between high- and low-income countries in the outcome of paediatric acute lymphoblastic leukaemia (ALL). At a tertiary-level hospital in Tanzania, multidimensional approaches have been taken to improve cancer care for children. This study aimed to update the outcomes of paediatric ALL at Muhimbili National Hospital (MNH), Tanzania from 2016 to 2020.

We performed a retrospective chart review of children who were treated with modified UKALL2003 protocol at MNH from January 1, 2016 to December 31, 2020. We used the Cox proportional hazards model to estimate the effect of each prognostic factor on event-free survival (EFS).

We identified 202 patients who had confirmatory diagnoses of ALL and initiated treatment at MNH. Fifty-two patients (26%, 52/202) died (n = 47) or abandoned treatment (n = 5) before the end of remission induction. The main causes of death during this period were infections and bleeding complications. The median EFS was 9 months and 2-year EFS was 36%. Oedema, non-early rapid responder, and non-remission were associated with short EFS in the multivariable analysis.

The number of new paediatric ALL admissions at MNH has doubled in the past decade. The prevention of early deaths is critical to improve the long-term survival of paediatric ALL in Tanzania.

This study aims to investigate the efficacy of a combination of ropivacaine hydrochloride and esketamine in paravertebral block (PVB), in providing analgesia and promoting the postoperative recovery of patients undergoing elective thoracoscopic radical lung cancer surgery.

A randomized controlled trial was conducted involving 70 patients scheduled for elective thoracoscopic radical lung cancer surgery.

Participants were randomly assigned to either the esketamine group (K group) or the control group (C group). Patients in the K group were administered a combination of 0.1 mg/kg of esketamine and 0.5% ropivacaine for PVB, while patients in the C group received only 0.5% ropivacaine. The time interval between the patient's discharge from the postanesthesia care unit and the first press of the analgesic pump and the number of presses. Various parameters that were monitored included the patients' mean arterial pressure, heart rate, and oxygen saturation at different time points; levels of interleukin-6, tumor necrosis factor-α, and C-reactive protein in venous blood preoperatively and 6 hours postoperatively; pain assessed using the numeric rating scale scores.

Compared with group C, patients in group K had significantly longer intervals before their first postoperative analgesic pump press and significantly fewer effective analgesic pump presses in the 48-hour postoperative period. Resting numeric rating scale scores were significantly lower in group K at 24 and 48 hours postoperatively (both P < .05). In terms of postoperative recovery, sedation score during extubation was lower in group K compared with group C (P < .05). Patients in group K had significantly improved quality of recovery on the third day postoperatively (both P < .05). The levels of interleukin-6, tumor necrosis factor-α, and C-reactive protein in venous blood were significantly lower in group K than in group C 24 hours postoperatively, and the difference was statistically significant (P < .05).

PVB with ropivacaine hydrochloride combined with esketamine effectively prolonged the time to the first analgesic pump use, reduced the overall analgesic pump requirement, and facilitated rapid recovery in patients undergoing thoracoscopic radical lung cancer surgery.

Population-based, age-standardized net survival estimates provide valuable insights for comparing the effectiveness of cancer treatment and the prospects of cure in an international context. Although numerous studies have previously assessed survival, the choice of life tables may crucially impact the feasibility of such analyses. Therefore, based on available studies, our aim was to understand the critical influence of life tables on net survival estimates.

Record-level data of approximately 50,000 breast, cervical, and ovarian cancer patients were extracted from the Hungarian National Cancer Registry. These patients were diagnosed between 2010 and 2014 and were followed up until December 31, 2019. Life tables for the Hungarian female population were taken from the Human Mortality Database, the Human Life-Table Database and were compiled according to the EUROCARE, CONCORD both multivariable flexible and Ewbank methodology. Regarding the last due to the lack of specific parameters, simulations were performed to assess the missing values​. The calculation of 5-year age-standardized net survival using different life tables revealed limitations in the methodology, highlighting the impact of life table selection on survival estimates.

Minor biases were observed in age-standardized net survival when using life tables from different international databases. However, the net survival of breast cancer, which had the most favorable prognosis of the studied malignancies, showed significant discrepancies. Moreover, this research highlights the extreme sensitivity of the applied κ parameter in the CONCORD Ewbank method, underscoring the need for careful consideration when applying this approach.

Present study shed light on how the choice of life tables can lead to differences in survival estimates for the same cancer population. It also emphasizes the importance of open methodological discussions to improve validity and accuracy of international comparability.

FAM83B is a novel oncogene that mediates transformation. Despite emerging evidence supporting an association between FAM83B and cancer, a holistic view of FAM83B's correlation with pan-cancer is limited and its carcinogenic and radioresistant roles in esophageal squamous cell carcinoma (ESCC) remain to be explored. Using data from the TCGA project, GTEx database, and other online resources, we comprehensively examined FAM83B expression, genetic mutation, copy number variations (CNV), methylation, prognosis, function, immune-associated analyses, and drug sensitivity in pan-cancer. In addition, the biological function of FAM83B in ESCC was verified by CCK-8, colony formation assays, and flow cytometry. We discovered aberrant expression of FAM83B affected prognosis in various malignant tumors. Abnormal FAM83B mRNA expression was associated with CNV and methylation. Significant correlations were also observed between FAM83B expression and immune cell infiltration, immune checkpoints, tumor mutational burden (TMB), and microsatellite instability (MSI) in malignancies. In vitro experiments indicated that FAM83B mRNA and protein were upregulated in ESCC, and knockdown of FAM83B significantly inhibited the proliferation while promoting apoptosis and radiosensitivity of ESCC. These results suggest the multiple functional roles of FAM83B in pan-cancer and provide an attractive diagnostic and therapeutic biomarker for certain cancer types, especially ESCC.

This review systematically reviewed the current guidelines related to radiotherapy for spinal metastases, summarized the relevant recommendations, and assessed the quality of their supporting evidence. The guidelines on radiotherapy for spinal metastases were searched by the keyword "guidelines" and "spinal metastasis". The most updated guidelines on radiotherapy for spinal metastasis were selected based on pre-defined inclusion and exclusion criteria. AGREE II was used to evaluate the quality of these guidelines. In addition, the related recommendations were extracted, and their quality was assessed using an evidence-grading scale. Nine guidelines established between 2013 and 2024 were included in this study. Three of the guidelines had an applicability rating of less than 50%. The difference in scores was the largest in rigor of development (range 48.50-88.03%). A total of 44 recommendations based on indications, re-irradiation, radiation dose and regimen, and emergency radiotherapy, were extracted and evaluated for SM. In conclusion, this study summarizes nine guidelines on radiotherapy for SM and provides useful information for improving treatment outcomes in patients with SM. All nine guidelines scored low in terms of adaptability, and most recommendations were based on a moderate-to-high LOE. The timing of re-radiotherapy varies across guidelines and fractionated radiotherapy regimens are available for specific SM patients. SBRT is more suitable than RBRT for patients with oligo-metastases, but more high-quality evidence is needed to confirm the more advantages of SBRT compared with conventional radiotherapy.

5-Fluorouracil (5-FU) is a primary chemotherapeutic agent for treating gastric cancer (GC), yet resistance to 5-FU frequently limits its effectiveness and contributes to poor patient outcomes. This study investigated the molecular mechanisms by which uridine-cytidine kinase 2 (UCK2) influences 5-FU resistance in GC. Using a genome-wide CRISPR knockout (GeCKO v2) library, we identified UCK2 as a critical gene for 5-FU sensitivity in GC cells. In 5-FU-resistant GC cells, the transcription factor GLI2 and the E3 ubiquitin ligase HRD1 were both upregulated, while UCK2 expression was significantly reduced. Functional assays demonstrated that lowering UCK2 or increasing HRD1 expression enhanced GC cell proliferation and 5-FU resistance, with HRD1 mediating 5-FU resistance through the ubiquitination and degradation of UCK2. Furthermore, GLI2 overexpression promoted cell proliferation and resistance to 5-FU by transcriptionally activating HRD1. In vivo experiments confirmed that GLI2 knockdown effectively reduced tumor growth under 5-FU treatment, an effect that was reversed by HRD1 overexpression. These findings reveal the GLI2-HRD1-UCK2 axis as a crucial pathway for modulating 5-FU resistance in GC, suggesting new potential targets for overcoming chemoresistance in GC therapy.

Non-small cell lung cancer (NSCLC) is characterized by a complex pathogenesis and high mortality. Targeted drug therapy represents a precise method of treatment. However, Improving sensitivity to targeted agents is currently a major challenge in clinical tumor therapy. Neogambogic acid (NGA), a bioactive compound isolated from the Traditional Chinese Medicine (TCM) Gamboge, has shown potential in NSCLC treatment. Nonetheless, the mechanism by which NGA enhances the sensitivity of NSCLC to the targeted drug Almonertinib remains unclear. This study aimed to elucidate the mechanisms underlying the ability of NGA to enhance the sensitivity of NSCLC to Almonertinib, revealing the synergistic effect exerted by the combination therapy. We established a subcutaneous grafted tumor model of mouse lung cancer by injecting Lewis cells, and evaluated the therapeutic efficacy in vivo. The study demonstrated that NGA combined with Almonertinib effectively suppressed NSCLC tumor growth by promoting cancer cell apoptosis and reducing serum tumor marker levels. In vitro experiments revealed that this combination synergistically inhibited lung cancer cell proliferation and induced apoptosis. Mechanistically, NGA demonstrated the ability to bind to Pregnane X receptor (PXR), regulating the expression of drug-metabolizing enzymes and transporters. We further validated this effect using PXR agonists and inhibitors in A549 cells. Additionally, the combination of NGA with Almonertinib significantly inhibited aberrant EGFR activation and downstream PI3K/AKT signaling, leading to enhanced apoptosis. This study demonstrated that the combination of NGA and Almonertinib inhibited the expression of CYP3A4, P-gp, and BCRP via PXR modulation. Meanwhile, it inhibited the EGFR/PI3K/AKT pathway and enhanced the sensitivity of NSCLC to Almonertinib, exerting synergistic anti-tumor effects. Our findings suggest a promising strategy for integrating active TCM components with targeted therapy in NSCLC management.

Breast cancer patients with similar clinicopathologic characteristics may experience varied outcomes. This urges an increased effort to investigate other prognostic factors. C-reactive protein (CRP)-to-albumin ratio (CAR) is an inflammatory and nutritional biomarker that has been well studied and reported to have an impact on the survival of patients with diverse types of cancer, but limitedly in breast cancer. Therefore, this study aimed to investigate the prognostic significance of CAR in local patients with breast cancer.

This study included 202 stage I-IV breast cancer patients receiving first-line chemotherapy. We calculated inflammatory and nutritional biomarkers including CAR, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), pan-immune-inflammation value (PIV), and prognostic nutrition index (PNI) before treatment. The Kaplan-Meier with log-rank test and Cox proportional hazard regression were used to analyze the prognostic role of clinicopathologic factors and biomarkers on disease-free survival (DFS), progression-free survival (PFS), and overall survival (OS).

The median follow-up period was 46 months (1-77 months). The 3-year DFS and 3-year OS in patients with high CAR (CAR > 1.5) were significantly lower than those with low CAR (CAR ≤ 1.5) (47.0% vs 68.9%, P = 0.022 and 59.5% vs 78.6%, P = 0.009, respectively). Multivariate analysis showed high CAR as prognostic factors for poor DFS (HR 2.10, 95% confidence interval/CI [1.10-3.99], P = 0.023) and OS (HR 2.16, 95% CI [1.27-3.68], P = 0.005), but not for PFS (HR 1.43, 95% CI [0.73-2.80], P = 0.293). In addition, more advanced stage and HER2 positive were correlated with unfavorable DFS and OS, older age predicted poor DFS, and stage was the only prognostic factor of PFS (all P values < 0.05).

Besides age, stage, and molecular subtypes that have been widely observed to have impact on the survival of breast cancer patients, CAR was demonstrated as a promising prognostic marker in our local patients. A high CAR at diagnosis was associated with unfavorable DFS and OS, which can aid in identifying patients at risk and guide personalized treatment planning.

Nigeria has a growing cancer burden, with late presentation and delayed diagnosis contributing to poor outcomes. We explored the durations and causes of the delay in the diagnosis of four common and treatable cancer types (breast, colorectum, head and neck, and uterine cervix) in Nigeria.

Retrospective study based on interviews with cancer patients following the Aarhus framework for designing and reporting such studies. The study focused on the first two of WHO's three main designated stages of cancer diagnosis: duration from symptom to presentation and presentation to histological diagnosis. Our hospital-based study involved 264 patients recruited from tertiary care facilities in the Northwestern (Kano) and Southwestern (Ibadan) regions of Nigeria. We obtained quantitative data to measure the duration of delay by stage, while interview data were collected to explore the causes of delay. We analysed the data by computing the median duration for the two stages of delay, and framework analysis was used to identify themes on the causes of delay.

The median time to receive a cancer diagnosis after noticing the first symptoms was 12 months (interquartile range 5 to 27 months), with head and neck cancer patients reporting the most prolonged (15-month) delay. Patients waited a median of 3 months (interquartile range 12 months) before presenting their first cancer symptom to a healthcare professional. The median time for patients to receive a cancer diagnosis after the first presentation of symptoms to a formal healthcare professional was 5 months (interquartile range 12 months). There was wide variance for all time intervals. Patients reported visiting a median of 3 health facilities before diagnosis in a formal hospital setting. Qualitative findings identified two main reasons patients reported delays in cancer pathway to care: patient-related factors and health system issues.

Long delays were observed, and more than half the delay followed presentation to the local health sector.

Lung cancer remains the leading cause of cancer-related mortality globally, with lung adenocarcinoma (LUAD) being the most prevalent subtype. Despite extensive research efforts, the role of transcription factors in LUAD progression remains largely uncharacterized. In this study, we focused on ZNF266, a transcription factor whose impacts on LUAD have not been investigated.

Using high-throughput sequencing data, we observed a significant downregulation of ZNF266 expression in LUAD tissues. To validate this finding, we conducted a retrospective analysis of nearly three thousand LUAD patients' data from public databases and our institution. Functional studies were performed using cell lines, organoids, and xenograft models to assess the role of ZNF266 in LUAD progression. RNA sequencing, chromatin immunoprecipitation, DNA pull-down assays, and dual-luciferase reporter assays were employed to elucidate the underlying mechanism. Additionally, adeno-associated virus (AAV)-mediated overexpression of ZNF266 was used to evaluate its therapeutic potential.

Patients with low ZNF266 expression had poorer prognosis compared to those with high expression. ZNF266 inhibits the malignant phenotypes of LUAD, including proliferation, migration, and invasion. Mechanistically, ZNF266 binds to the promoter region of CA9, suppressing its transcription. This leads to a reduction in intracellular pH and subsequent inhibition of the mTOR signaling pathway, which is crucial for cancer cell growth and survival. Furthermore, AAV-mediated overexpression of ZNF266 significantly inhibited tumor growth in patient-derived xenograft models.

Our study demonstrated that ZNF266 inhibits LUAD progression in a pH-dependent manner via modulating CA9 expression, uncovering its therapeutic significance for LUAD treatment.

Acute lymphoblastic leukemia (ALL) is the most common pediatric hematologic malignancy. The leukemic cells start in the bone marrow and spread to other vital organs and tissues, including the central nervous system (CNS). Hispanic males are the community with the highest incidence of ALL. Unfortunately, there is limited information on the molecular signatures of leukemic cell infiltration into the CNS, which marks the progression from ALL to central nervous system leukemia (CNSL). To address this knowledge gap, we performed a label-free shotgun proteomics between the cerebrospinal fluid (CSF) from patients with ALL compared to those with confirmed CNSL. We were able to identify 619 proteins, including 340 proteins that had not been reported prevously in the CSF of subjects with CNSL. The major features associated with CNSL included the over-accumulation of cell-adhesion proteins such as L-selectin and several cadherin proteins, along with the modulation of enzymes associated with protein glycosylation, which may provide the appropriate conditions for leukemic cell infiltration into the CNS. The over-accumulation of proteins associated with ROS scavenging processes reveals hypoxic and redox homeostasis microenvironment conditions that favors ALL progression to CNSL. The further characterization of key differential proteins will be essential for establishing reliable molecular markers for CSNL. BIOLOGICAL SIGNIFICANCE: Central nervous system leukemia (CNSL) is a catastrophic progression of ALL defined by leukemic cells reaching the CNS. Limited comparative proteomics studies have been conducted previously between patients with ALL versus CNSL. While these studies were important pioneering steps, they were hindered by difficulties in obtaining the proper amount of protein samples related to CSF. They were based on minimal study subjects, and their proteomics pipelines did not include the depletion of high-abundance proteins. Defining the manners in which the CNSL proteome is perturbed compared to the ALL condition is paramount to understanding the molecular foundations of CNSL and identifying and characterizing protein markers for proper diagnosis. Improving the sensitivity and reliability of diagnosis using molecular markers would help clinicians to maximize patient outcomes and quality of life by implementing aggressive CNSL treatments as soon as possible in cases where infiltration has occurred, while avoiding exposure to toxic chemotherapies in patients where they are not yet necessary.

Platinum-based chemotherapy is limited by drug resistance and severe adverse effects. Although the DNA damage response (DDR) is known to affect drug sensitivity across cancer types, the role of its upstream regulator ATM in modulating cisplatin (DDP) resistance remains unclear. In this study, we investigated the role of the ATM/DDR pathway to DDP resistance and proposed a potential targeted strategy. Bioinformatics analysis revealed significant overexpression of ATM and RAD51 in liver and lung cancers, which correlated with poor survival (p < 0.05). In vitro assays showed that DDP activated ATM to initiate the downstream DDR, thereby promoting chemoresistance; inhibition of ATM using KU-55933 or siRNA enhanced the anticancer effect of DDP. Among screened Shikonin derivatives, acetyl alkannin emerged as the most potent ATM-targeting analogue. Combination treatment with low-dose acetyl alkannin (2.5 μM or 2.6 μM) and DDP increased DDP sensitivity 8.0-fold in Huh-7 liver cancer cells and 22.5-fold in A549 lung cancer cells. Mechanistically, acetyl alkannin targets ATM and induces its caspase-dependent degradation, suppressing DDR signaling and promoting apoptosis. In vivo xenograft experiments confirmed the superior tumor growth inhibition of the combination treatment. These findings establish ATM-mediated DDR activation as a central mechanism of DDP resistance and identify acetyl alkannin as a candidate sensitizer for platinum-based chemotherapy.

While anthracyclines, commonly used in cancer treatment, are well known to cause cardiotoxicity, no validated biomarkers currently exist that can predict the early development of doxorubicin-induced cardiotoxicity (DIC). Therefore, identifying early biomarkers of DIC is urgently needed. Metabolomics approaches have been used to elucidate this relationship and identified related metabolite markers. However, differences in pre-clinical model systems make it challenging to draw definitive conclusions from the discoveries and translate findings into clinical applications.

A systematic literature search on metabolomics studies of DIC was conducted with the goal to identify and compare study results reported using in vitro models, animal models, and studies from clinical patients. Metabolites identified across all studies were pooled to uncover biologically meaningful patterns that are significantly enriched in the data. Finally, pooled metabolites perturbed by DIC were mapped to metabolic pathways to explore potential pathological implications.

We reviewed 28 studies published between 2000 and 2024 that utilized metabolomics approaches to investigate DIC. The included studies used a variety of analytical techniques, including LC-MS, GC-MS, and NMR. The analysis revealed that metabolites such as inosine, phenylalanine, arginine, and tryptophan were commonly perturbed across all study models, with carnitine metabolism and purine and pyrimidine metabolism being the most affected pathways. Metabolite Set Enrichment Analysis (MSEA) using MetaboAnalyst identified the arginine biosynthesis, citrate cycle, and alanine, aspartate, and glutamate metabolism pathways as significantly enriched.

These findings underscore the potential of metabolomics in identifying early biomarkers for DIC, providing a foundation for future studies aimed at preventing cardiotoxicity and improving treatment strategies for cancer patients receiving DOX-containing therapies.

Altogether, metabolomics studies suggest metabolic alterations in DIC, albeit little overlap between studies especially with animal and human studies. Attempts at intercepting these pathways have shown that intervention in DIC may be possible. Future research should focus on developing precise cardiotoxicity models that incorporate cancer metabolism, as these will be crucial in bridging the gap between laboratories (in vitro and animal models) and clinical studies to identify subclinical biomarkers in the early stage of DIC that can effectively identify new targets for interventions to reduce lethal cardiovascular disease risk.

This study demonstrates that the modified frailty index-6 (mFI-6) is a useful tool for predicting the completion of S-1 adjuvant chemotherapy (AC) and associated adverse events (AEs) in patients with pancreatic cancer (PC). mFI-6 is an index that incorporates serum albumin levels into the existing mFI-5, enabling the assessment of patients' ability to complete S-1 therapy and their risk of developing AEs. This study retrospectively analyzed PC patients from two university hospitals between August 2013 and July 2022. Patients from one hospital were assigned to the testing dataset, while those from the other hospital were used as the validation dataset. Patients were classified as frail if they met at least two of the six criteria, including a serum albumin level of < 3.5 g/dL. In the testing cohort (n = 86 PC patients), frailty patients exhibited greater difficulty in completing S-1 therapy compared to non-frail patients, with a significantly lower completion rate (p = 0.003). Additionally, frail patients demonstrated significantly shorter recurrence-free survival (RFS) and overall survival (OS) compared to their non-frail counterparts. The findings were further validated in the validation dataset, where frail patients exhibited a lower S-1 completion rate and significantly shorter RFS (p = 0.023) and overall survival (OS) (p = 0.045). These results suggest that mFI-6 may be an effective tool for postoperative frailty screening, allowing healthcare professionals to assess patients' tolerance to S-1 therapy and adjust treatment plans accordingly. Ultimately, the implementation of this index may contribute to improving clinical outcomes for patients with PC.

Cellular metabolic reprogramming supports tumor proliferation, invasion, and metastasis by enhancing resistance to stress and immune clearance. Understanding these metabolic changes within the tumor microenvironment is vital to developing effective therapies. We conducted single-cell RNA sequencing on 11 gastric cancer (GC) samples and eight metastatic lesions, analyzing 92,842 cells across eight cell types, including cancer cells, stromal cells, and immune cells. Our findings highlight that the mitochondrial ATP synthase subunit ATP5MC2 uniquely alters during early GC metastasis. Experiments and clinical data confirmed that ATP5MC2 upregulation facilitates cancer cell proliferation, invasion, and metastasis. Constructing a single-cell atlas revealed significant immune cell heterogeneity associated with GC metastasis and its molecular subtypes. This study underscores the role of ATP5MC2-driven metabolic changes and diverse immune landscapes in promoting GC metastasis, offering new avenues for anti-metastatic treatment development.

According to the International Agency for Research on Cancer, China had the highest mortality burden of esophageal cancer (EC) globally in 2022.

This study aims to analyze the national and provincial trends, patterns, and risk factors of EC deaths in China.

Data from the National Mortality Surveillance System were used to estimate national and provincial deaths, age-standardized mortality rates (ASMRs), and years of life lost (YLL). An age-period-cohort-based Nordpred model was used to predict trends until 2030. Multilevel Poisson and logistic regression were conductedto assess factors influencing EC mortality and the place of death.

From 2008 to 2021, EC deaths and YLLs decreased from 227,677 to 167,529 and from 5.32 million to 3.50 million, respectively. Meanwhile, the ASMR and age-standardized YLL rate decreased from 24.34 to 11.01 per 100,000 and from 535.91 to 231.08 per 100,000, respectively. By 2030, EC deaths and ASMR are predicted to decline to 150,768 and 7.85 per 100,000, respectively. Nationwide, the average age at death increased from 68.46 to 72.45 years, with an increasing proportion of YLLs in the 65-69 age group. Overall premature mortality was observed to decrease, except for an increase in YLLs among urban populations aged ≥60 years. Higher burdens were observed in rural areas compared to urban areas and among males compared to females. Nationwide, individuals with agriculture-related occupations and lower educational levels exhibited significantly higher risks of EC death. Regions with higher prevalences of smoking and harmful drinking, and lower educational, economic, and medical levels were significantly associated with high mortality. Home was the leading place of EC deaths (80.02 %).

The EC mortality burden in China is decreasing but remains a significant threat to public health. Promoting education, occupational prevention, healthy lifestyles, and medical treatment for targeted populations and regions is essential.

Background: Assessing cancer survival trends is crucial for monitoring progress in cancer management and prevention. As part of the broader HUN-CANCER EPI study, this analysis examined overall survival (OS) in the Hungarian cancer population between 2011 and 2019. Methods: Using data extracted from the Hungarian National Health Insurance Fund (NHIF) database, short- and long-term OS were estimated for various cancer types according to age, sex, and diagnostic period using Kaplan-Meier analysis. The study also identified cancer types with significant early mortality following diagnosis. Results: From 2011 to 2019, a total of 528,808 patients were diagnosed with cancer. During the 2015-2019 diagnostic period, the lowest 5-year OS rates were observed for esophageal (7.0%), pancreatic (10.7%), liver (12.5%), gallbladder (13.9%), and lung cancer (18.4%). Conversely, tumor types with better OS included testicular cancer (91.6%), thyroid cancer (89.0%), Hodgkin's lymphoma (84.0%), melanoma (78.6%), and breast cancer (74.1%). A notable proportion of deaths occurred within 2 months of diagnosis for liver (33.2%), pancreatic (27.9%), and gallbladder cancer (29.0%). Significant early mortality within 6 months post-diagnosis was also noted for esophageal (51.3%), stomach (42.9%), and lung cancer (41.7%). Conclusions: The HUN-CANCER EPI study conducted between 2011 and 2019 provides valuable insights into cancer survival patterns in Hungary, emphasizing the importance of early detection and targeted interventions to improve patient outcomes.

Targeting base excision repair (BER) has been an attractive strategy in cancer therapeutics. RNA-binding motif protein 39 (RBM39) modulates the alternative splicing of numerous genes involved in cancer occurrence and progression. However, whether and how RBM39 regulates BER in hepatocellular carcinoma (HCC) remain unclear. Here, we found that under oxidative stress, RBM39 degradation or knockdown decreased BER efficiency in HCC cells using a well-designed BER reporter. Further assays showed that RBM39 promoted HCC cell proliferation, migration, and invasion, enhancing cell survival and inhibiting apoptosis. Mechanistically, RBM39 interacted with the mRNA of the essential glycosidase 8-oxoguanine-DNA glycosylase 1 (OGG1), thereby stabilising OGG1 mRNA. This in turn increases OGG1 expression and promotes BER efficiency in HCC. Moreover, data suggested that RBM39 degradation, combined with oxidative damage, could be more effective for HCC treatment than monotherapy, both in vitro and in xenograft mice models. Overall, we demonstrated that RBM39 regulated OGG1 stabilisation and improved BER efficiency, suggesting that combining the RBM39 degradant indisulam with the oxidising agent KBrO3 could be an emerging strategy for HCC treatment.

Recent studies indicate that Secretogranin V (SCG5) is aberrantly expressed in various cancers and may be linked to tumor progression and prognosis. This study aims to evaluate the potential of SCG5 as a prognostic biomarker for non-small cell lung cancer (NSCLC). We employed a combination of bioinformatics analysis, Western blotting, and immunofluorescence techniques to investigate the role of SCG5 in NSCLC. A comprehensive analysis of TCGA and GEO pan-cancer datasets revealed a consistent upregulation of SCG5 across multiple cancer types. In NSCLC, SCG5 expression was significantly higher in tumor tissues compared to normal lung tissues (p < 0.001). Kaplan-Meier survival analysis demonstrated that patients with elevated SCG5 expression exhibited lower overall survival rates, suggesting a strong association with poor prognosis. Univariate and multivariate COX regression analyses, conducted on both TCGA cases and our collected patient data, confirmed SCG5 as an independent prognostic factor for NSCLC. Furthermore, immune infiltration analysis indicated a significant correlation between SCG5 expression and various immune cell subpopulations, underscoring its potential role as a biomarker for adverse outcomes. Western blot analysis further validated the elevated levels of SCG5 in NSCLC tissues and cell lines compared to their normal counterparts. Based on our findings, we hypothesize that SCG5 may serve as a valuable biomarker for predicting the prognosis of non-small cell lung cancer, thereby guiding future research in the fields of diagnosis, progression, therapy, and prognosis of NSCLC.

The COMPASSION-15 trial demonstrated that cadonilimab plus chemotherapy (CAD-CHM) confers clinical benefits over placebo plus chemotherapy (PLA-CHM) as a first-line treatment for human epidermal growth factor receptor 2 (HER2)-negative advanced gastric or gastroesophageal junction (G/GEJ) adenocarcinoma. However, the introduction of cadonilimab substantially elevates treatment costs, and its cost-effectiveness relative to PLA-CHM remains undetermined. This study evaluates the cost-effectiveness of CAD-CHM compared with PLA-CHM from the perspective of the Chinese healthcare system.

A Markov model with three health states was developed to assess the cost-effectiveness of CAD-CHM in HER2-negative advanced G/GEJ adenocarcinoma. Clinical efficacy data were sourced from the COMPASSION-15 trial, while drug costs were calculated based on national tender prices, and additional costs and utility values were extracted from published literature. The analysis encompassed the overall population, as well as subgroups stratified by programmed death ligand 1 (PD-L1) combined positive score (CPS) ≥ 5 and CPS < 5. Outcomes included total costs, quality-adjusted life-years (QALYs), and incremental cost-effectiveness ratios (ICERs). Sensitivity analyses were conducted to evaluate model robustness.

The ICER of CAD-CHM was $67,378.09 per QALY in the overall population, $48,433.34 per QALY in the PD-L1 CPS ≥ 5 subgroup, and $78,463.86 per QALY in the PD-L1 CPS < 5 subgroup. Key determinants influencing model outcomes included patient weight, cadonilimab cost, and the utility value of progression-free survival. Across all groups, CAD-CHM resulted in an ICER exceeding the willingness-to-pay threshold of $41,511 per QALY, with a 0% probability of cost-effectiveness compared with PLA-CHM.

From the perspective of the Chinese healthcare system, CAD-CHM is not cost-effective as a first-line treatment for HER2-negative advanced G/GEJ adenocarcinoma, either in the overall population or in subgroups stratified by PD-L1 CPS status, compared with chemotherapy alone.

The aim of this study was to compare the effects of accommodated jejunal interposition double tract reconstruction (aji-DTR) and Roux-en-Y reconstruction after laparoscopic-assisted total gastrectomy on intraoperative and postoperative indicators in advanced gastric cancer (AGC) patients.

A retrospective analysis was performed on 80 AGC patients, including 43 with aji-ATR and 37 with Roux-en-Y reconstruction. Propensity score matching was performed between the two groups. The primary outcome measures included operative time, intraoperative blood loss, postoperative complications, postoperative hospital stay, total hospitalization costs, and survival rate. The secondary outcome measures were postoperative nutritional status, recovery of digestive function, and postoperative gastrointestinal·symptoms.

There were 24 pairs of patients after matching. There were no significant differences in the operative time, intraoperative blood loss, time of first flatus, time of first defecation, time of liquid diet, time of semi-liquid diet, postoperative complications, postoperative hospital stays, and total hospitalization costs (all P > 0.05). Interestingly, Roux stasis syndrome was significantly more frequent in Roux-en-Y group than aji-DTR group [6 (25.0%) vs 1 (4.2%), P = 0.045]. While no significant difference was observed in survival rates, reflux esophagitis, dumping syndrome and nutritional parameter including hemoglobin, albumin, and prognostic nutritional index (all P > 0.05).

Compared with Roux-en-Y reconstruction, aji-DTR had similar surgical parameters, postoperative digestive function recovery, nutritional parameters, and survival rate, but showed an advantage in reducing Roux stasis syndrome. Therefore, aji-DTR after laparoscopic assisted total gastrectomy may be a safe and feasible alternative for AGC patients.

To update the ASCO evidence-based recommendations on the use of sentinel lymph node biopsy (SLNB) in patients with early-stage breast cancer treated with initial surgery.

ASCO convened an Expert Panel to develop updated recommendations based on a systematic literature review (January 2016-May 2024).

Eleven randomized clinical trials (14 publications), eight meta-analyses and/or systematic reviews, and one prospective cohort study met the inclusion criteria for this systematic review. Expert Panel members used available evidence and informal consensus to develop practice recommendations.

Clinicians should not recommend routine SLNB in select patients who are postmenopausal and ≥50 years of age and with negative findings on preoperative axillary ultrasound for grade 1-2, small (≤2 cm), hormone receptor-positive, human epidermal growth factor receptor 2-negative breast cancer and who undergo breast-conserving therapy. Clinicians may offer postmastectomy radiation (RT) with regional nodal irradiation (RNI) and omit axillary lymph node dissection (ALND) in patients with clinically node-negative invasive breast cancer ≤5 cm who receive mastectomy and have one to two positive sentinel nodes. Clinicians may offer SLNB in patients who have cT3-T4c or multicentric tumors (clinically node-negative) or ductal carcinoma in situ treated with mastectomy, and in patients who are obese, male, or pregnant, or who have had prior breast or axillary surgery. Clinicians should not recommend ALND for patients with early-stage breast cancer who do not have nodal metastases, and clinicians should not recommend ALND for patients with early-stage breast cancer who have one or two sentinel lymph node metastases and will receive breast-conserving surgery and whole-breast RT with or without RNI.Additional information is available at www.asco.org/breast-cancer-guidelines.This guideline has been endorsed by the American Society for Radiation Oncology (ASTRO).