Cell-free DNA (cfDNA) has emerged as a promising non-invasive biomarker for cancer detection, including non-small cell lung cancer (NSCLC). While these approaches have demonstrated high diagnostic accuracy in controlled settings, their performance in real-world clinical populations remains uncertain. This study aimed to evaluate the diagnostic performance of a plasma cfDNA assay for early-stage NSCLC detection and to explore its association with clinicopathological parameters.

This was a single-center, crosssectional study involving 61 patients with radiologically suspected lung lesions, of whom 52 were confirmed NSCLC. Plasma samples were analyzed using a shallow genomewide sequencing-based cfDNA assay incorporating fragmentomic and copy number features. cfDNA results were compared against histopathological diagnosis to determine sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). Associations between cfDNA detection and clinical variables were evaluated using appropriate statistical tests.

The cfDNA assay demonstrated a sensitivity of 75% and a PPV of 84.8% with a specificity of 22.2% and NPV of 13.3%. cfDNA detection rates increased with advancing disease stage, although a relatively high sensitivity was observed even in stage I disease (79.4%). No statistically significant associations were found between cfDNA positivity and conventional markers of tumour burden, including tumour size, serum carcinoembryonic antigen, and SUVmax.

The cfDNA assay evaluated in this study demonstrated limited clinical utility as a standalone screening tool due to its low specificity and NPV in a realworld early-stage NSCLC population. Future efforts should focus on improving assay specificity through the incorporation of multi-omic tumour-specific biomarkers and validation that includes early-stage lung cancer cases and benign pulmonary conditions.

Cervical cancer is the fourth most common malignancy in women. Approximately 15% of the patients have metastatic disease. The Malaysian National Cancer Registry (MNCR) 2017-2021 reported that over the five-year period, there were 2654 new cases. 47.1% of the patients presented with late stages (stages 3 and 4), slightly higher compared to 41% in the MNCR 2012-2016 report. There were no standard approaches to the management of metastatic/recurrent cervical cancer. Therefore, this study aimed to determine the survival outcomes of patients with metastatic/recurrent cervical cancer and to evaluate the clinicopathological factors based on demographic and tumour characteristics that may affect survival outcomes. Besides that, we would like to outline the management patterns in this cohort of patients.

This was a retrospective observational cohort study looking at the 35 patients diagnosed with metastatic/recurrent cervical cancer at the Department of Clinical Oncology, Universiti Malaya Medical Centre (UMMC) over the five-year period from 1st of January 2016 until 31st of December 2020. Data were obtained from the electronic medical record. The Kruskal-Wallis H and Mann-Whitney U non-parametric tests, Spearman correlation, and Kaplan-Meier survival analysis were conducted to analyse the survival outcomes and clinicopathological factors that may affect the survival outcomes in the form of progression-free survival (PFS) and overall survival (OS). Descriptive analysis was used to describe the prevalence of metastatic/recurrent cervical cancer and the patterns of management.

Out of the total 94 cervical cancer patients registered at the Department of Clinical Oncology, UMMC, 37.2% had metastatic/recurrent disease. Survival analysis demonstrated that median PFS and OS for metastatic/recurrent cervical cancer were six and 12 months, respectively, which were consistent with the global populations. Nonparametric multivariate tests and survival analysis showed that the presence of metastatic disease at less common sites had worse survival. Most of the patients received active oncological treatments, i.e., chemotherapy, radiotherapy or combinations of both.

This study showed that a significant portion of the patients were diagnosed at a late stage, with poor survival outcomes, indicating the necessity for enhanced initiatives in the screening and education programmes to increase awareness of early diagnosis and detection, hence improving survival outcomes of cervical cancer patients.

Chondroblastoma (CB) is a benign but locally aggressive bone tumor that may present histopathologic diagnostic challenges, particularly in atypical locations and limited biopsy specimens. Recent studies have identified recurrent mutations in the H3F3B and, less frequently, H3F3A genes, suggesting their potential diagnostic value. This study aimed to evaluate the prevalence and diagnostic utility of H3F3A and H3F3B mutations in a multicenter cohort of CB patients.

Forty-three patients with histopathologically confirmed CB were included in a retrospective analysis. All cases were re-evaluated by 2 pathologists, and mutation analysis of H3F3A and H3F3B genes was performed using polymerase chain reaction-based Sanger sequencing.

H3F3B mutations were detected in 41 cases (95.3%), all corresponding to the Lys36Met substitution. One case (2.3%) harbored an H3F3A Gly34Trp mutation, whereas 1 case (2.3%) showed no detectable mutation. No significant histopathological differences were observed between mutation-positive and mutation-negative cases. A notable case involved a 72-year-old patient with frontal bone involvement, highlighting the diagnostic difficulty in unusual locations and older age groups.

The findings demonstrate that H3F3B mutation analysis is an extremely sensitive and reliable molecular tool for confirming the diagnosis of CB. It is particularly valuable in challenging cases and especially in small biopsy samples where pathognomonic findings, such as chicken-wire calcification and chondroid matrix are not visible. Incorporation of molecular testing into targeted diagnostic workflows may improve diagnostic accuracy and assist in distinguishing CB from its histological mimics.   Cite this article as: Tosun I, Yilmaz I, Cakir A, et al. H3F3B gene mutation in chondroblastomas: a multicenter study. Acta Orthop Traumatol Turc.,2026; 60(4), 0277, doi: 10.5152/j.aott.2026.25277.

This study aims to assess the histopathological and clinical characteristics of chondroblastomas (CBs), with particular emphasis on the correlation between local invasion and mitotic activity, cytological atypia, and recurrence.

A retrospective analysis was performed on 26 cases of CB diagnosed between 2016 and 2024 and pathologically evaluated at a tertiary oncology center, with surgical procedures performed across 2 tertiary oncology referral centers. Clinical, radiological, and histopathological data were reviewed. For comparative analysis, tumors were grouped as non-infiltrative (confined to the bone) or infiltrative (showing invasion of the bone cortex and/or extracortical connective tissues). Tumors were assessed for cytological atypia, mitotic index, matrix production, calcification, aneurysmal bone cyst formation, and invasion pattern. Immunohistochemical staining for S100, DOG1, and Ki-67 was conducted. Statistical analyses included t-tests, Mann-Whitney U, chi-square, and correlation analyses.

The mean age at diagnosis was 17.7 years, with a male-to-female ratio of 1.36 : 1. The femur was identified as the most common site. Invasion beyond the bone cortex was observed in 16 patients (61.5%), including 4 instances of soft tissue involvement. Invasive tumors showed significant association with moderate cytological atypia (P = .022), higher mitotic index (P = .023), and lower extremity location (P = .02). A positive correlation was identified between mitotic index and both atypia (P = .001) and tumor invasiveness. Recurrence occurred in four patients (15.4%), all presenting invasive tumors. No metastases were reported during the mean follow-up period of 38.9 months.

Although CB typically manifests benign behavior, a subset of these tumors demonstrates locally aggressive characteristics, such as cortical and soft tissue invasion. Elevated mitotic activity and moderate cytological atypia may serve as histopathological markers for local aggressiveness.   Cite this article as: Aygün MİŞ, .omunoğlu C, Doğan B, Adaş M, Tanrıtanır R. Chondroblastoma: the relationship between local invasiveness, recurrence, and histopathological features. Acta Orthop Traumatol Turc., 2026; 60(4), 0407, doi: 10.5152/j.aott.2026.25407.

Gastric cancer remains a leading cause of cancer-related mortality worldwide. Helicobacter pylori (Hp) infection is a major risk factor, but the diagnostic performance of serum biomarkers may vary according to Hp infection status. This study aimed to evaluate the diagnostic value of serum human epididymis protein 4 (HE4), trefoil factor 3 (TFF3), and carbohydrate antigen 72-4 (CA72-4), individually and in combination, for gastric cancer stratified by Hp infection status using a propensity score-matched retrospective case-control design.

This retrospective study was conducted at Jinshazhou Hospital of Guangzhou University of Chinese Medicine, from January 2022 to December 2025. Propensity score matching (1:1 nearest neighbor matching, caliper 0.1) was performed to balance age, sex, body mass index (BMI), smoking history, alcohol consumption history, chronic kidney disease, chronic liver disease, and Hp infection status between groups. After matching, 268 gastric cancer patients and 268 healthy controls were included. Serum levels of HE4, TFF3, and CA72-4 were measured. Between-group comparisons of each marker, stratified by Hp status, were performed. Logistic regression was used to construct combined diagnostic models, and receiver operating characteristic (ROC) curve analysis was performed to evaluate the area under the curve (AUC).

After matching, all covariates achieved good balance with standardized mean differences <0.1. In the total population, serum levels of HE4, TFF3, and CA72-4 were significantly higher in the gastric cancer group than in the control group (all p < 0.001). Multivariate logistic regression identified all three markers as independent risk factors for gastric cancer (HE4: odds ratio [OR] = 1.05, 95% confidence interval [CI]: 1.03-1.06; TFF3: OR = 1.19, 95% CI: 1.13-1.26; CA72-4: OR = 1.46, 95% CI: 1.34-1.62; all p < 0.001). The combined model yielded an AUC of 0.899 (0.872-0.925) in the total population, significantly superior to any single marker (all p < 0.001). After stratification by Hp status, the AUC of TFF3 was significantly higher in Hp-positive individuals than in Hp-negative individuals (p < 0.001); no significant differences were observed for HE4 or CA72-4 between the two strata (p > 0.05).

The diagnostic value of serum HE4, TFF3, and CA72-4 for gastric cancer varies according to Hp infection status. In Hp-positive patients, TFF3 demonstrates significantly higher diagnostic performance compared with Hp-negative individuals. HE4 and CA72-4 demonstrate stable performance across Hp strata, with no statistically significant differences observed. The combined detection of these biomarkers demonstrates favorable diagnostic performance regardless of Hp status. These findings suggest that Hp status-stratified testing provides an auxiliary strategy for optimizing differential diagnosis of gastric cancer.

Lung cancer patients undergoing combined chemoradiotherapy often experience pain, fatigue, sleep disturbances, and decreased quality of life. Among these, pain catastrophizing, as a negative cognitive pattern, can exacerbate symptom experience. Similarly, fatigue and sleep disturbances are also influenced by psychological and cognitive factors, yet conventional supportive care provides limited intervention at the psychological and cognitive levels. This study aims to investigate the impact of electromyographic biofeedback relaxation training on pain catastrophizing and fatigue levels in lung cancer patients undergoing combined chemoradiotherapy.

This study employed a single-center, retrospective cohort design. Through a review of medical records from March 2020 to March 2022, patients who had received structured electromyographic biofeedback relaxation training undergoing chemoradiotherapy were assigned to an observation group (n = 78). Patients without such records, receiving only routine supportive care, were classified as a control group (n = 109). The training consisted of six sessions over two weeks. Outcomes, including pain catastrophizing (Pain Catastrophizing Scale), pain intensity (Visual Analogue Scale), sleep quality (European Organisation for Research and Treatment of Cancer), and quality of life (Functional Assessment of Chronic Illness Therapy-Fatigue), were assessed before and after the intervention period.

After the intervention, the pain catastrophism scores, pain intensity scores, and sleep disturbance scores of the observation group were significantly lower than those of the control group, while the fatigue score was significantly higher than that of the control group (all p < 0.05). Furthermore, the observation group also showed significantly better scores and total scores on multiple dimensions of quality of life (including physical well-being, social/family well-being, emotional health, functional well-being, and fatigue subscales) than the control group (p < 0.05).

Supplementing routine combined chemoradiotherapy management with electromyographic biofeedback relaxation training was associated with lower levels of pain catastrophizing and fatigue, improved sleep quality, and enhanced overall quality of life in lung cancer patients. This intervention may represent a safe and feasible non-pharmacological support strategy for symptom management in lung cancer patients undergoing combined chemoradiotherapy.

Progressive disease (PD) remains the dominant barrier to cure in high-risk neuroblastoma (HR-NB), driven in part by profound post-transcriptional deregulation that fuels clonal evolution, stemness, immune evasion, and therapy resistance. In this study, we define the molecular architecture of PD-associated microRNA (miR) collapse and demonstrate that radiotherapy (RT) acts as a potent post-transcriptional reprogrammer capable of reversing this trajectory.

miRNome profiling was performed in HR-NB tumors from patients during diagnosis (Dx), intensive multi-modal clinical therapy (IMCT) defiant PD, or residual disease after incorporating RT with IMCT (RD-RT). miRs' expression profiles were validated with selective miR-320a, miR-423, miR-483-3p, miR-122-5p, miR-3184-5p, miR-21-5p qPCR. RT-influenced changes in cell-identity were investigated by assessing histomorphological alterations (H&E) and multiplex immunofluorescence (mIF) for Ki-67, PD-L1, SOX2, CD44 or p53.

IMCT-defying PD displayed a loss of 167 miRs, and none upregulated, corresponding an evolutionary fingerprint for pathways governing cancer stem cell (CSC) maintenance, epithelial to mesenchymal transition (EMT), metabolic rewiring, proliferative fitness, and immune suppression. Strikingly, adding RT reversed 146 of these miRs and induced additional 179 RT-specific miRs, restoring regulatory networks governing apoptosis, p53-mediated DNA-damage response, differentiation/mesenchymal to epithelial transition (MET), and immune visibility. Individual miR-qPCR analysis of miR-320a, miR-483-3p, miR-3184-5p miR-21-5p, and miR-122-5p validated and corroborated the array expression outcomes. Histologic and mIF remarkably substantiated these miR signatures, showing that RT transforms poorly differentiated, plastic, PD-L1⁺/SOX2⁺/CD44⁺ CSC-like PD tumors into differentiated, lineage-stabilized, immune-permissive states characterized by neuropil restoration, ganglioneuroma-like maturation, marginal yet measurable loss of SOX2/CD44, suppression of PD-L1, complete collapse of Ki-67⁺ proliferative compartments, and significant induction of p53.

Collectively, our findings indicated that RT could be a global regulator of tumor state transitions, reinstating miR-mediated governance lost during PD evolution and redirecting tumor fate toward regression. Our results provide proof-of-concept evidence that RT delivers powerful molecular benefits beyond local control, introducing a conceptual framework for miR-guided RT personalization, biomarker development, and rational combination strategies to improve outcomes in HR-NB.

Enhancer RNAs (eRNAs) are important regulators of tumor development and progression. Nevertheless, the diagnostic utility of circulating eRNAs in hepatocellular carcinoma (HCC) remains unclear.

This was a retrospective study. The recently identified eRNA, leucine-rich repeat-containing 3 divergent transcript (LRRC3-DT), was analyzed in serum samples, tissue specimens, and various cell lines. Its diagnostic performance was evaluated alone and in combination with alpha-fetoprotein (AFP) and protein induced by vitamin K absence or antagonist-II (PIVKA-II) using receiver operating characteristic (ROC) curve analysis. Functional investigations were performed to assess the biological role of LRRC3-DT by overexpressing and knocking down this eRNA in HCC cell lines. Furthermore, using transcriptome sequencing, potential target genes of LRRC3-DT were identified.

The serum levels of LRRC3-DT were significantly lower in patients diagnosed with HCC than in healthy controls. When LRRC3-DT was assessed alongside AFP and PIVKA-II, the combination improved sensitivity for the detection of HCC. Despite earlier research indicating that LRRC3-DT is present primarily in the nucleus and is strongly associated with tumor proliferation, invasion, and apoptosis, the serum levels of LRRC3-DT were similar between patients with HCC and those with benign liver diseases in the present study. These findings indicate limited specificity in distinguishing between these two conditions.

Serum LRRC3-DT represents a potential auxiliary biomarker for early HCC screening; its combined use with other indicators improved diagnostic performance. However, it cannot individually discriminate HCC from benign liver disorders, and additional validation studies are warranted to confirm its differential diagnostic value.

Transmembrane protein 61 (TMEM61) has previously been reported in several malignancies. However, its function in ovarian cancer remains unclear. Here, we aimed to investigate the role and underlying mechanisms of TMEM61 in ovarian cancer cells.

Differentially expressed genes were identified by analyzing transcriptomic data of 426 ovarian cancer tissues from The Cancer Genome Atlas database and 88 normal ovarian tissues from the Genotype-Tissue Expression database using the web-based analytical tool GEPIA2. The effects of TMEM61 knockdown on ovarian cancer cell invasion, migration, and proliferation were evaluated using Transwell, wound healing, and Cell Counting Kit-8 assays. The effect of TMEM61 knockdown on DNA damage and cytosolic DNA accumulation was assessed using immunofluorescence and comet assays. TMEM61 and programmed death-ligand 1 (PD-L1) expression levels were assessed using immunoblotting and reverse transcription-quantitative polymerase chain reaction.

TMEM61 exhibited very low expression in normal ovarian tissues, but its expression was significantly upregulated in ovarian cancer tissues. TMEM61 knockdown significantly inhibited the proliferation, migration, and invasion of ovarian cancer cells; induced DNA damage and cytoplasmic DNA accumulation; and upregulated PD-L1 expression in ovarian cancer cells.

TMEM61 promotes malignant behavior and maintains genomic stability in ovarian cancer cells. TMEM61 may serve as a potential biomarker and molecular target for ovarian cancer.

To investigate the current status of sleep disorders in patients with oral and maxillofacial malignant tumors and analyze the influencing factors, so as to provide a basis for clinical intervention.

A convenience sampling method was used to recruit 487 patients with oral and maxillofacial malignant tumors in Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine from December 2023 to December 2024. The Pittsburgh Sleep Quality Index (PSQI), Hospital Anxiety and Depression Scale (HADS), and European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire Head and Neck 35 (EORTC QLQ-HN35) were used to evaluate sleep quality, psychological state, and symptom burden. Spearman rank correlation analysis and multivariate logistic regression analysis were used to explore the correlation.

84.6% of the patients had sleep disorders, and the use rate of hypnotic drugs in the recurrence group was significantly higher than that in the primary group (P＜0.05). The total PSQI score in the recurrence group was positively correlated with sensory perception and dry mouth (P＜0.05). The total PSQI scores of the two groups were positively correlated with pain, swallowing, speech, eating during social communication, dental problems, mouth opening, social interaction, disease perception, and the use of painkillers (P＜0.05), and negatively correlated with weight loss (P＜0.05). Multivariate logistic regression analysis showed that unemployment, smoking, anxiety, oral pain, speech disorders, dental problems, and disease perception were risk factors for sleep disorders in newly diagnosed patients; unemployment, swallowing disorders, and disease perception were risk factors for sleep disorders in recurrent patients.

The incidence of sleep disorders in patients with oral and maxillofacial malignant tumors is high, which is closely related to psychological state, oral dysfunction, and disease perception. Early intervention in symptom clusters is needed clinically to improve sleep quality and quality of life.