Gastric cancer continues to be a worldwide health crisis because it results in many deaths. The protein Claudin 18.2 (CLDN18.2) exists at higher levels in gastric adenocarcinoma tumors which makes it a promising therapeutic target. This study evaluated CLDN18.2 protein levels in gastric cancer tissues and their relationship with patient and tumor characteristics. This retrospective cohort study analyzed 112 gastric adenocarcinoma patients together with 62 healthy controls. The research team used ELISA to determine CLDN18.2 concentrations in tumor tissue and adjacent normal tissue and control specimens. Patients were stratified based on their Helicobacter pylori infection status, tumor site, tumor grade, and presence of metastasis. Diagnostic performance was assessed using receiver operating characteristic analysis, and Cox regression analysis was performed to evaluate prognostic factors for survival. The cancer tissue contained elevated CLDN18.2 levels which measured at 2.385 ng/mL (median), whereas normal tissue and controls displayed 1.349 ng/mL and 1.260 ng/mL (median) respectively (P < .001). The receiver operating characteristic analysis for diagnosing gastric adenocarcinoma showed 92.4% sensitivity and 100% specificity at 1.675 ng/mL (area under the curve: 0.956). The study found that CLDN18.2 levels were higher in patients with Helicobacter pylori infection and in cases with poor tumor differentiation and metastasis. The risk of metastasis increased by 4.82 times for every 1 ng/mL rise in CLDN18.2 levels (P < .001). This study demonstrates that CLDN18.2 exhibits strong diagnostic performance for gastric adenocarcinoma and shows strong correlation with cancer progression. The Cox regression analysis established CLDN18.2 as an independent prognostic factor for patient survival outcomes.

This study aimed to determine the associations between pretreatment quantitative dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) pharmacokinetic (PK) parameters, post-neoadjuvant systemic therapy (NST) MRI features, and pathologic complete response (pCR) in patients with invasive ductal carcinoma (IDC). Twenty-eight consecutive IDC patients who received NST were retrospectively reviewed. All patients underwent MRI at 3 time points: before NST; after 2 cycles of NST; and before surgery. Continuous and categorical variables were compared between pCR and non-pCR groups using the Mann-Whitney U test and Fisher exact test, respectively, with HER2 status adjusted in PK parameter analyses. Partial correlation assessed associations between MRI features and pCR. Select PK parameters were further evaluated using Firth's penalized-likelihood regression, controlling for covariates. Receiver operating characteristic (ROC) analysis was performed to evaluate predictive performance. Significant differences were detected between groups regarding HER2-positive, luminal B subtype, Miller-Payne, and postoperative lymph node metastasis (P < .05). Pretreatment peritumoural extravascular extracellular volume (Ve), post-NST shrinkage pattern, and residual disease were significantly different between the groups (P < .05). Partial correlation analysis indicated a positive association between the peritumoural flux rate constant (Kep) and pCR (P < .05). Regression analysis identified the peritumoural Kep as a factor influencing the pCR with an area under the curve of 0.756 (95% CI = 0.564-0.947). Our preliminary findings suggested an association between the pCR and pretreatment peritumoural PK parameters, highlighting the potential value of the peritumoural region. These results require further validation in larger prospective studies.

Colorectal cancer (CRC) is a prevalent and increasingly common malignancy that poses significant threats to patient survival and quality of life. This study investigates the role of ubiquitously expressed prefoldin-like chaperone (UXT) in regulating polyamine metabolism, particularly putrescine, and its impact on CRC progression. Through comprehensive bioinformatics analysis, UXT was identified as a key factor positively correlated with putrescine abundance in CRC cell lines. Clinical samples confirmed upregulation of UXT and its positive correlation with putrescine levels. Functional assays revealed that UXT knockdown reduced cell viability, migration, and invasion, while overexpression enhanced these phenotypes. Additionally, UXT knockdown decreased putrescine levels and increased the expression of ornithine decarboxylase antizymes (OAZ1, OAZ2, OAZ3), which negatively regulate polyamine synthesis. Conversely, UXT overexpression exhibited the opposite effects. In vivo experiments using a subcutaneous xenograft tumor model in nude mice showed that UXT overexpression enhanced tumor growth and putrescine levels, and UXT overexpression is associated with an increase in M2 macrophage markers, along with reduced M1-associated markers, while UXT knockdown inhibited these effects. These findings suggest that UXT contributes to CRC progression by regulating polyamine metabolism and macrophage polarization, demonstrating its potential as a therapeutic target to disrupt metabolic pathways essential for cancer cell survival and proliferation.

Colorectal cancer ranks second in cancer-related deaths, but management has significantly evolved over the past two decades with increasing use of systemic therapy, organ preservation, and a lowering of the cancer screening age alongside new threats such as COVID-19. Thus, we explored temporal trends in cause of death (COD) among colon and rectal cancer patients.

To evaluate the prognostic utility of the FIGO 2023 staging system with/without molecular classification vs. FIGO 2009 in endometrial cancer.

Obesity is well-documented to increase the risk and worsen the prognosis of various cancers. This review investigates the relationship between obesity and glioma, as a comprehensive analysis has not been conducted. A literature search was conducted across several databases, including ScienceDirect, PubMed, and Google Scholar, from 2004 to 2025, using the keywords: (glioblastoma OR glioma OR GBM) AND (obesity OR "body mass index" OR BMI OR overweight OR adiposity OR "waist circumference") AND (risk OR association OR prevalence OR incidence OR correlation OR etiology). Inclusion criteria focused on studies in English published from 2004 to 2025. From an initial screening of 606 studies, 26 met the criteria.The role of high BMI or waist circumference (WC) as a risk factor remains unclear, with evidence varying by age, gender, and tumor grade. The compound effect of high BMI with high WC is more pronounced in women. Evidence of linearity between BMI and glioma risk is also stronger in women. Notably, low BMI combined with high waist circumference presents a greater risk than high BMI with high waist circumference. Healthy lifestyle factors may influence glioma risk more significantly than BMI. Additionally, elevated BMI in early life (18-21yo) is more consistently associated with increased glioma risk, while height is identified as a common risk factor. Although several studies associate higher BMI with poorer overall survival (OS) and progression-free survival (PFS), some suggest that being overweight may confer a survival advantage compared to normal or underweight individuals. Obesity impacts prognosis more significantly in MGMT-methylated gliomas. Further research is needed to clarify these complex associations.

Purpose To develop a multiparametric MRI-based radiomics model and deep learning-radiomics (DLR) fusion model for preoperative prediction of lymph node metastasis (LNM) in early-stage cervical cancer. Materials and Methods In this multicenter retrospective study (January 2020-December 2022), preoperative MRI data from patients with early-stage cervical cancer were split into training, internal testing, and external testing cohorts. Radiomic and deep learning (DL) features of both the tumor and lymph node were extracted separately from the MRI scans. Multivariable logistic regression was used to construct predictive models for LNM based on tumor and lymph node radiomic features (Rad_T+LN) and based on radiomic and DL features from both the tumor and lymph node (DLR_T+LN). The models' effectiveness and clinical applicability were evaluated using receiver operating characteristic curves, calibration curves, and decision curve analysis. A two-tailed P value of <.05 was considered statistically significant. Results The overall dataset included 862 patients (median age, 53 years [IQR, 45-60 years]). Rad_T+LN resulted in areas under the receiver operating characteristic curve (AUCs) of 0.81 (95% CI: 0.76, 0.86), 0.79 (95% CI: 0.72, 0.87), and 0.77 (95% CI: 0.71, 0.82) in the training, internal testing, and external testing cohorts, respectively. DLR_T+LN achieved AUCs of 0.83 (95% CI: 0.76, 0.91) and 0.79 (95% CI: 0.74, 0.84) in the internal and external testing cohorts, respectively, and did not improve over Rad_T+LN (P > .05). Both models demonstrated good calibration and positive net benefit on decision curve analysis. Conclusion Rad_T+LN and DLR_T+LN exhibited robust diagnostic performance for LNM prediction. Keywords: MR-Diffusion Weighted Imaging, MR Imaging, Genital/Reproductive, Cervix, Metastases, Decision Analysis, Segmentation, Radiomics, Diagnosis, Uterine Cervical Neoplasms, Lymphatic Metastasis, Magnetic Resonance Imaging, Deep Learning Supplemental material is available for this article. © RSNA, 2026.

Neoplastic diseases are among the most important conditions of morbidity and mortality in companion dogs worldwide. The research was conducted from October 2017 to May 2018 to determine the type and incidence of neoplasms in canines.

Conventional magnetic resonance imaging (MRI) exhibits notable limitations in the diagnosis, grading, and therapeutic assessment of gliomas, making it insufficient to meet the demands of precision medicine. As a chemical exchange saturation transfer MRI technique, amide proton transfer (APT) imaging enables molecular-level visualization by detecting the chemical exchange of amide protons in endogenous mobile proteins and peptides. Previous studies have demonstrated that APT imaging provides substantial advantages over conventional MRI in the diagnosis, grading, and treatment monitoring of gliomas. This review systematically summarizes the development of APT imaging technology, emphasizing its innovative clinical applications, including preoperative grading, differentiation of postoperative recurrence, and dynamic evaluation of radiotherapy and chemotherapy efficacy. Furthermore, it discusses current challenges and future directions for clinical implementation, aiming to offer new perspectives for advancing precision medicine in glioma management.

IntroductionImmunohistochemistry (IHC) plays a crucial role in breast cancer diagnosis, treatment selection, and research. However, manual scoring of IHC whole slide images (WSIs) is time-consuming and suffers from inter- and intra-observer variability.MethodsTo help address these challenges, we present and publicly release a fully automated, compartment-specific (ie, tumor and stroma) H-scoring framework for IHC analysis. The framework consists of three deep learning modules: tumor-stroma segmentation, nuclei segmentation, and H-score estimation for tumor and stroma. It processes WSIs in minutes, delivering consistent and reproducible H-scores with accuracy comparable to expert pathologists. The modular design also allows flexibility for use in other IHC tasks such as cellularity quantification, and supports configuration options to balance accuracy and computational efficiency.ResultsFine-tuned on 87 expert-annotated patches, the framework achieved a Spearman's rank correlation (ρ) in internal validation of 0.84 (95% confidence interval [CI]: 0.77-0.89) across 100 expert-annotated WSIs, outperforming state-of-the-art (ρ = 0.78, 95% CI: 0.68-0.85) and matching the inter-observer variability between two expert pathologists (ρ = 0.84, 95% CI: 0.63-0.94). In external validation, it achieved 86% accuracy in HER2 classification (0-3+) and a mean absolute error of 21 ± 10 (range: [5-46]) in CD73 scoring, where ground truth H-scores were all 0.ConclusionThe framework achieves agreement comparable to that of expert pathologists, underscoring its clinical utility in providing reproducible IHC scores that can reduce diagnostic variability and support consistent treatment decisions. The code is available at https://github.com/YinTuo/AutoIHC.

Thyroid carcinoma is characterized by significant heterogeneity and immune evasion, in which myeloid cells play a pivotal role in tumor microenvironment (TME) remodeling. However, the key regulatory genes and their underlying mechanisms are not yet fully elucidated.

BackgroundSERPINE1 has attracted considerable attention in tumor biology, but its clinical importance in head and neck squamous cell carcinoma (HNSCC) is not yet clear. We therefore examined whether SERPINE1 expression is related to survival in patients with HNSCC.MethodsWe searched three major databases (PubMed, EMBASE, and the Cochrane Library) and identified observational studies reporting survival outcomes in relation to SERPINE1 expression through November 11, 2024. From eligible reports we extracted data on progression-free survival (PFS), overall survival (OS), disease-specific survival (DSS) and disease-free survival (DFS), and calculated pooled hazard ratios (HRs) using random-effects models.ResultsEleven studies including 733 individuals with HNSCC met the inclusion criteria. Across these cohorts, higher SERPINE1 expression was consistently linked with shorter OS (HR 2.81, P = 0.003) and shorter DFS (HR 1.57, P = 0.004). In contrast, no clear associations were observed for PFS or DSS (P ≥ 0.05).ConclusionCurrent evidence suggests that increased SERPINE1 expression is associated with an unfavorable prognosis in HNSCC, particularly for OS and DFS. Larger prospective studies are needed to confirm these findings and to determine how SERPINE1 assessment might be incorporated into risk stratification and treatment planning for patients with HNSCC.

Cervical cytology offers a relatively safe and reliable method for cancer screening, but the tests contain vague grading criteria, such as atypical squamous cells, and cannot exclude high-grade squamous intraepithelial lesions (ASC-H) and atypical squamous cells of undetermined significance (ASC-US).

MutL homolog 1 (MLH1) loss is a defining molecular feature of endometrial cancer (EC) and a principal driver of microsatellite instability (MSI). Ishikawa cells harbor intrinsic MLH1 promoter hypermethylation, resulting in reduced but not abolished MLH1 expression and placing these cells in a vulnerable, partially compromised mismatch repair state. This study explores the effects of MLH1 knockdown (MLH1-KD) on MSI, cellular functions, signaling pathways, and tumor growth in Ishikawa EC cells.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the immunohistochemical images shown in Fig. 1A on p. 1377, the 'DNMT3A' and 'DNMT3B' images for the 'BN' row of data contained an overlapping section, such that date which were intended to show the results from differently performed experiments had apparently been derived from the same original source. In addition, upon performing an independent analysis of the data in this paper in the Editorial Office, it came to light that the same data had been included for the Petri dish images in Fig. 3B on p. 1382 for the DMSO experiments with the T24 and EJ cell lines, albeit the EJ image had been rotated through 90°. The authors were contacted by the Editorial Office to offer an explanation for this apparent duplication of data within these figures; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Oncology Reports 35: 1375‑1384, 2016; DOI: 10.3892/or.2015.4492].

High mobility group box 3 (HMGB3) acts as an essential participator in fundamental biological processes, including transcriptional regulation, chromatin remodeling and DNA repair. HMGB3 is highly expressed and functionally essential during embryonic development, particularly in the hematopoietic and nervous systems, but it is significantly downregulated or silenced in most normal adult tissues. Its aberrant upregulation has been revealed in numerous human malignancies, such as leukemia, as well as breast, bladder, colorectal and gastric cancer, and its expression levels have been established to be closely associated with poor prognosis of specific patients. Accordingly, the present review systematically explores the central roles of HMGB3 in mediating resistance to cancer therapy. This review focuses on its multifaceted mechanisms of maintaining cancer stemness, enhancing DNA damage repair, modulating cell death pathways and remodeling the tumor microenvironment, thereby contributing to the resistance to chemotherapy, radiotherapy, targeted therapy and immunotherapy collectively. HMGB3 can be accepted as a key target in the development of highly promising therapeutic strategies, given its pivotal involvement in multidrug resistance, which may offer novel avenues for overcoming clinical treatment resistance and improving patient outcomes.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the paraffin‑embedded glioma tissue sections shown in Fig. 2A on p. 494, the Ki‑67/Grade III and DTX3L/Grade IV data panels contained an overlapping section, suggesting that these data panels were derived from the same original source where different experimental groups were reported. In addition, GAPDH control western blots featured in Figs. 1C and 4E were found to be strikingly similar, even though the experimental conditions reported for these figure parts were different. The authors have been contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in their paper, and we are awaiting their response. Due to the fact that we have been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of these potential problems while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 40: 491‑498, 2017; DOI: 10.3892/ijmm.2017.3023].

Nasopharyngeal carcinoma, a malignancy associated with Epstein‑Barr virus, presents a complex immune editing landscape in which T cell fate determination carries out a central role. T cell metabolic exhaustion, Epstein‑Barr virus antigen presentation and tertiary lymphoid structure remodeling are important in the context of tumor immune evasion. Although individual mechanisms have been extensively studied, their interplay and collective contribution to immune editing remain incompletely understood. The present review summarizes the current advances in nasopharyngeal carcinoma immune editing, with a focus on the molecular network underlying T cell fate decisions. How these mechanisms can be leveraged to develop novel immunotherapeutic strategies is further discussed. By integrating recent findings, the present review aims to offer new insights into the intricate immune landscape of nasopharyngeal carcinoma and to provide a theoretical basis for improving immunotherapy efficacy.

Chromodomain helicase DNA‑binding protein 4 (CHD4) is a core adenosine triphosphate (ATP)‑dependent chromatin‑remodeling factor of the nucleosome‑remodeling and deacetylase (NuRD) complex. It plays a crucial role in chromatin structure regulation, gene expression regulation, and DNA damage response. It has been demonstrated that CHD4 has context‑dependent functions in tumor development and progression. It can influence tumor progression via such mechanisms as regulating tumor‑related signaling pathways, maintaining the silencing of tumor suppressor genes, and promoting metabolic adaptation; it can also exert tumor‑suppressive effects in specific transcriptional regulatory environments. Additionally, during DNA damage response, CHD4 participates in chromatin remodeling at damage sites, in cell cycle recovery, and in repair pathway selection. It is also involved in the development of tumor treatment resistance through mechanisms that include regulation of DNA repair, cell cycle progression, drug efflux, the tumor immune microenvironment, and replication fork stability. It has also been shown that various non‑coding RNAs participate in the functional regulation of CHD4 by modulating its expression, localization, and protein stability. In summary, as a key node connecting chromatin regulation, genome stability, and tumor treatment response, CHD4 holds significant importance in tumor progression and treatment.

Pituitary tumors, as common intracranial neoplasms, present challenges in clinical management because of high postoperative recurrence rate, drug resistance and pronounced side effects. Astragaloside IV (AS‑IV), the primary active component of the traditional Chinese herb Astragalus membranaceus, has antitumor activity in numerous types of cancer. However, its effects and mechanisms in pituitary tumors remain unclear. The present study aimed to investigate the effects of AS‑IV on proliferation and apoptosis of pituitary tumor cells and to elucidate its molecular mechanisms. Cell Counting Kit‑8 (CCK‑8), TUNEL, EdU, immunohistochemistry (IHC), and Western blotting, among others, showed that AS‑IV significantly suppressed the viability of the rat pituitary tumor cell lines GH3 and MMQ in a concentration‑ and time‑dependent manner while inducing apoptosis. Tubulin β4B Class IVb (TUBB4B) was highly expressed in pituitary tumor tissue and its overexpression promoted cell proliferation while inhibiting apoptosis. AS‑IV bound TUBB4B with high affinity, forming a stable complex. TUBB4B regulation influenced pituitary tumor cell sensitivity to AS‑IV, with AS‑IV demonstrating enhanced antitumor efficacy in TUBB4B‑overexpressing tumors. TUBB4B activated the ERK/MAPK signaling pathway by upregulating Stathmin 1 (STMN1) expression, which promoted G1/S phase transition. The ERK‑specific inhibitor U0126 reversed this pro-proliferative effect. To the best of our knowledge, the present study is the first to reveal that AS‑IV inhibits pituitary tumor proliferation and promotes apoptosis by targeting TUBB4B to regulate the STMN1‑ERK signaling axis, providing a novel theoretical basis and potential strategies for traditional Chinese medicine treatment and molecular targeted research on pituitary tumors.