Background: Art therapy is an experiential, non-threatening intervention, used especially with children. The current study aimed to explore the effect of integrative art therapy on the psychological well-being (mental health and self-perception) of pediatric cancer patients. Methods: Using a single-group pre-post research design, each therapy session was individually administered to participants for approximately 45 min. Fourteen participants (Boys = 9, Girls = 5) were recruited from the inpatient oncology unit at Shaukat Khanum Memorial Cancer Hospital & Research Centre over two months. The age range was from 5 years to 13 years (M = 7.95; SD = 1.65). Mental health, including physical and emotional symptoms associated with cancer, was assessed using the Edmonton Symptom Assessment Scale-Revised, while self-perception was measured with the House Tree Person projective drawing test. Results: The integrative art therapy model significantly improved positive self-image (F = 16.77, p < 0.01) and reduced negative self-image (F = 99.11, p < 0.01) and mental health problems from the baseline to the second and third phases (F = 19.50, p < 0.01). Conclusions: This integrative approach demonstrates its potential as an effective method to enhance self-perception, alleviate mental health challenges, and improve overall quality of life.
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that Fig. 6A on p. 320, showing the tumor volumes from the in vivo experiments, was lacking the units in the y‑axis, hence undermining the ability to usefully interpret the data in this figure part. In addition, after having performed an independent assessment of the data in this paper in the Editorial Office, it came to light that western blot data in Fig. 2D and flow cytometric plots in Fig. 3A appeared subsequently in different papers in different experimental contexts, one written by different authors in 2018 in the journal Journal of Experimental and Clinical Cancer Research, and the other featuring an author named Cong Long in the journal Oncology Letters. The authors have been contacted by the Editorial Office to offer an explanation for the concerns that have been identified in their paper, and we are awaiting their response. 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 these potential problems while the Editorial Office continues to investigate this matter further. [Oncology Reports 37: 313‑322, 2017; DOI: 10.3892/or.2016.5286].
Leptomeningeal metastasis (LM) is common in patients with lung adenocarcinoma, leading to high mortality rates. The predictors of systematic survival in patients with LM and lung adenocarcinoma remain poorly understood. The present study retrospectively analyzed 78 lung adenocarcinoma patients with or without LM treated at Ningbo Medical Center, Lihuili Hospital (Ningbo, China) between November 2016 and August 2024. Clinical characteristics and baseline hematological parameters obtained at LM diagnosis were evaluated for their associations with overall survival (OS). Median OS was 9.0 months (range: 0.2-48.9 months) in patients with LM. Univariate analysis identified age <60 years, Eastern Cooperative Oncology Group performance status (ECOG PS) 0-2, receipt of brain radiotherapy after a diagnosis of LM, no extracranial metastasis, epidermal growth factor receptor (EGFR) 19 mutation, receipt of third-generation EGFR tyrosine kinase inhibitor therapy before a diagnosis of LM, neutrophil-to-lymphocyte ratio <7.5755, platelet-to-lymphocyte ratio (PLR) <156.035 and a molecular graded prognostic assessment >1.5 to be significant predictors of superior OS. According to multivariate analysis, extracranial metastasis [hazard ratio (HR)=2.291; 95% CI, 1.074-4.888; P=0.032], PLR <156.035 (HR=0.233; 95% CI, 0.123-0.442; P<0.001) and ECOG PS 0-2 (HR=0.302; 95% CI, 0.152-0.599; P=0.001) remained predictive of OS. In conclusion, extracranial metastasis, PLR and ECOG PS were identified to be prospective independent clinical prognostic indicators of survival in patients with lung adenocarcinoma and LM. Overall, the present study highlighted the potential use of clinical characteristics and hematological variables before treatment to predict the outcomes of patients with lung adenocarcinoma complicated with LM.
The extent of surgical management of thyroglossal duct-associated differentiated thyroid carcinoma remains controversial. This study aims to evaluate the role of total thyroidectomy in patients with thyroglossal duct-associated differentiated thyroid carcinoma and provide insights to support individualized, evidence-based care. A systematic literature search was conducted in MEDLINE, Embase, Web of Science, Cochrane CENTRAL, and Google Scholar from inception to January 2025. Screening was performed independently by two reviewers. Studies were included if they reported treatment details for patients with thyroglossal duct carcinoma, and excluded if they were letters, abstracts, reviews, or meta-analyses. The primary outcome consisted of recurrent disease. Secondary outcomes were presence of synchronous thyroid cancer, surgical treatments, and mortality. The study protocol was registered in PROSPERO (CRD-42023489730). Three hundred thirteen studies (243 case reports, 70 case series; range 1-26 patients per study) were included compromising 645 patients with differentiated thyroid carcinoma. Notably, no cohort studies were found. Recurrent disease occurred in 24/436 (5.5%) patients with reported follow-up (median, 35.5 months [12.0-80.0]). Among patients without preoperative suspicion for synchronous cancer in the thyroid, recurrence rates did not differ significantly between the Sistrunk-only group (n = 3/92 (3.3%), median follow-up 24 months [IQR, 12-48]) and the Sistrunk plus thyroidectomy group (n = 6/101 (5.9%), median follow-up 24 months [IQR, 12-69]; P = .502). The Sistrunk procedure alone may be sufficient in appropriately selected patients with thyroglossal duct carcinoma. The decision to perform total thyroidectomy should be individualized based on tumor characteristics and thorough thyroid assessment.
The Krüppel-like family (KLF) are important transcriptional regulators that have important, context-specific roles in gastrointestinal (GI) malignancies. Their roles are very heterogeneous; each of the KLF members may play tumor-suppressive or tumor-promoting roles, depending on the type of tumor, clinical stage and the cellular microenvironment, which fine-tunes the core biological processes of tumor cell proliferation, apoptosis, epithelial-mesenchymal transition and metabolism. This is a context-dependent functional heterogeneity that poses a big challenge in the translation of KLF family transcription factors from basic research into clinical applications. In addition to these classical regulatory functions, KLFs have a key role in the restructuring of the tumor immune microenvironment (TIME). KLFs have the potential to affect the effectiveness of cancer immunotherapy by modulating immune cell infiltration, immune cell functions and immune evasion by tumors. The present review is a systematic review that summarizes the molecular regulatory mechanisms of KLFs in the major GI malignancies, such as colorectal, gastric, liver, esophageal and pancreatic cancer. The present review points to their control of major signaling pathways, including Wnt/β-catenin and PI3K/AKT, and their new roles in the remodeling of TIME. Moreover, the present review assesses their translational utility as diagnostic and prognostic biomarkers and therapeutic targets, and confronts the clinical issues involved in targeting transcription factors, thus giving a theoretical basis for oncology approaches in different types of GI cancer.
Identifying malignant non-mass enhancement (NME) in contrast-enhanced breast magnetic resonance imaging (MRI) remains a notable diagnostic challenge due to overlapping imaging features between benign and malignant lesions. Although the delayed-phase kinetic patterns are well-established, the diagnostic value of the initial-phase kinetics has not been fully elucidated. The present study aimed to evaluate the dynamic and morphological characteristics of NME lesions, to determine whether incorporating initial-phase kinetics with delayed-phase analysis improves the discrimination between benign and malignant cases. A prospective study was conducted at the Oncology Teaching Hospital (Baghdad, Iraq) from April to December 2022, including patients referred for breast MRI. Only cases with pure NME (without associated mass lesions) were included. A core biopsy was performed for all cases, with excisional biopsy when indicated. Data collection followed the Breast Imaging Reporting and Data System 5th edition criteria. Among 38 enrolled patients (mean age, 45±11.45 years; range, 26-75 years; median, 44 years), 63.2% presented with a breast lump and 26.3% underwent screening. Histopathology confirmed malignancy in 26 cases (68.4%), comprising 12 cases of ductal carcinoma in situ and 14 of invasive ductal carcinoma. Segmental enhancement was the most common malignant pattern [positive predictive value (PPV), 83.3%], followed by regional enhancement (PPV, 64.3%). Benign lesions had slow (58.3%) or medium (41.7%) initial upslopes, whereas 50% of malignant tumors exhibited a rapid initial slope (P=0.001). Persistent delay was observed in 75% of benign cases but in only 26.9% of malignant cases (P=0.005). Integrating the initial upslope with the plateau-phase kinetics increased the PPV for malignancy from 75 to 81.8%. In conclusion, the integration of initial-phase kinetics with traditional delayed-phase and morphological assessment improves the diagnostic accuracy for malignant NME lesions. This multi-parametric approach could potentially serve as a valuable tool to reduce the rate of unnecessary biopsies in the future.
The C-reactive protein-triglyceride-glucose index (CTI), integrating C-reactive protein and the triglyceride-glucose index, is a pragmatic biomarker reflecting systemic inflammation and metabolic stress in cancer. Although its prognostic value has been validated in heterogeneous cancer cohorts, data in homogeneous perioperative settings remain limited. The present study retrospectively evaluated 131 patients with locally advanced gastric or gastroesophageal junction adenocarcinoma who received perioperative fluorouracil, leucovorin, oxaliplatin and docetaxel (FLOT) chemotherapy between November 2018 and June 2024 (67 months). CTI was calculated at diagnosis, and patients were stratified using the 4.78 cut-off value previously validated in oncology populations. Associations between CTI and clinicopathological variables, pathological response, progression-free survival (PFS) and overall survival (OS) were analyzed. The results demonstrated that among the 131 patients who underwent curative-intent surgery after neoadjuvant FLOT, 113 (86.3%) had low CTI (<4.78) and 18 (13.7%) had high CTI (≥4.78). Patients with high CTI had significantly shorter PFS compared with those with low CTI (median, 12.2 vs. 25.5 months; P=0.006). OS was also markedly inferior in the high CTI group [median, 23.1 months vs. not reached (NR) in the low CTI group; P=0.001]. In the multivariable analysis, high CTI independently predicted poor PFS [hazard ratio (HR), 2.18; 95% confidence interval (CI), 1.21-3.95; P=0.010]. Regarding treatment response, the pathological complete response rate was 11.5% (13/113) in the low CTI group and 22.2% (4/18) in the high CTI group (P=0.221), indicating no significant association between CTI and pathological complete response. In conclusion, pretreatment CTI is an independent prognostic marker in patients with locally advanced gastric or gastroesophageal junction adenocarcinoma treated with perioperative FLOT, identifying individuals at higher risk of relapse and inferior survival. The simplicity, low cost and pretherapeutic availability of pretreatment CTI support its use as a promising tool for risk stratification that warrants prospective, multicenter validation.
Peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS) is the most common histological subtype of PTCL. PTCL-NOS has a relatively low incidence, and its pathogenesis and mechanisms of drug resistance remain unclear, leading to lagging research progress. The aim of the present study was to summarize the clinical features and outcomes of patients with PTCL-NOS. A total of 30 patients with treatment-naive PTCL-NOS who were admitted to The Second Hospital of Hebei Medical University (Shijiazhuang, China) between September 2013 and September 2023 were retrospectively analysed. The median age at diagnosis was 59 years (range, 17-70 years), and the male-to-female ratio was 2.75:1. The median follow-up duration was 59 months. The 3-year overall survival (OS) and progression-free survival (PFS) rates were 50.4 and 28.9%, respectively. Multivariate analysis showed that an Eastern Cooperative Oncology Group performance status >1, bone marrow involvement and a platelet count <150×109/l were independent risk factors for OS, whereas bone marrow involvement and albumin levels <35 g/l were independent risk factors for PFS. There was no significant difference between the cyclophosphamide, doxorubicin, vincristine, prednisone and etoposide regimen and the cyclophosphamide, vincristine, doxorubicin and prednisone regimen, whereas combinations with chidamide showed a trend toward an improved PFS. Within the cohort, 2 patients with relapsed and refractory CD30-positive PTCL-NOS received salvage chemotherapy with brentuximab vedotin (BV), a monoclonal antibody, and achieved complete metabolic remission, followed by sequential allogeneic haematopoietic stem-cell transplantation, resulting in long-term sustained remission. In conclusion, patients diagnosed with PTCL-NOS generally have a poor prognosis. Nevertheless, the use of innovative targeted therapies, such as chidamide and BV, shows potential to improve treatment outcomes in these patients.
Nobiletin, a polymethoxyflavone derived from Citrus peels, has emerged as a promising multi-target anticancer agent. The present review consolidates recent advances elucidating the efficacy of nobiletin in suppressing tumor growth across diverse cancer types, including breast, colon, lung and gastric cancer. Mechanisms for inducing cell cycle arrest and apoptosis, inhibiting metastasis and angiogenesis, and modulating key oncogenic pathways, such as phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin, mitogen-activated protein kinase and nuclear factor-κB are discussed. Crucially, the present review highlights the role of nobiletin in reversing chemoresistance and its synergistic potential with conventional therapeutics. Despite challenges in bioavailability, novel delivery strategies are paving the way for its clinical application. By reviewing current evidence, the present review underscores the notable potential of nobiletin as an integrative agent in oncology, offering a comprehensive perspective on its therapeutic prospects.
Ovarian mucinous carcinoma (OMC) is a rare subtype of ovarian cancer characterized by frequent KRAS mutations and a poor response to platinum- and taxane-based chemotherapy, underscoring the need for novel therapeutic strategies. MRTX1133, a recently developed non-covalent and selective KRAS (G12D) inhibitor, has demonstrated potent antitumor activity in pancreatic and colorectal cancers; however, its efficacy in OMC remains unexplored. In the present study, the antitumor effects of MRTX1133 in the KRAS (G12D)-mutant OMC cell line MCAS and its interactions with conventional chemotherapeutic agents were evaluated. Cell viability was assessed using WST-1 assays, ERK phosphorylation was evaluated by western blotting and gene expression levels were analyzed by reverse transcription-quantitative PCR. Results indicated that MRTX1133 suppressed MCAS cell proliferation in a concentration-dependent manner, whereas proliferation of KRAS wild-type and KRAS (G12S)-mutant cells was not significantly inhibited. Treatment markedly inhibited ERK phosphorylation, suggesting suppression of the MAPK pathway. MRTX1133 reduced the mRNA expression of Ki-67 and numerous cyclins (D1, A2 and B1), suggesting attenuation of proliferative signaling. When combined with cytotoxic agents, including paclitaxel, SN38, gemcitabine and cisplatin, MRTX1133 reduced the sensitivity to cell cycle-dependent chemotherapeutic agents, namely paclitaxel, SN38 and gemcitabine, while not affecting the activity of the non-cell cycle-dependent agent cisplatin. The present study therefore provided preclinical evidence for the potential utility of KRAS (G12D)-targeted therapy in OMC and highlights the importance of sequential rather than concurrent scheduling of MRTX1133 with cell cycle-dependent chemotherapy to optimize therapeutic efficacy.
N6-methyladenosine (m6A) RNA methylation is implicated in cancer metabolism; however, to the best of our knowledge, the role of methyltransferase 5 (METTL5) in non-small cell lung cancer (NSCLC) progression remains unclear. Reprogrammed glycolytic metabolism (Warburg effect) supports tumor growth and immune evasion; however, the regulatory mechanisms of this process require further investigation. We hypothesized that METTL5 drives NSCLC progression by regulating glycolytic metabolism through m6A modification of phosphoglycerate mutase 1 (PGAM1) mRNA. The present study aimed to elucidate the molecular mechanisms, functional impacts and clinical relevance of the METTL5/PGAM1 axis. Integrated analyses of NSCLC cohorts from The Cancer Genome Atlas database were performed, and in vitro models (A549 and PC9 cell lines) and molecular techniques, including methylation inhibition, RNA stability assays and metabolic flux measurements (Seahorse XFe96 analyzer), were used. Key interactions were validated through western blotting, reverse transcription-quantitative PCR and correlation analyses. METTL5 was significantly upregulated in NSCLC tissues and in A549, PC9 and H520 cell lines, and high METTL5 expression was associated with poor patient survival (P<0.05). Silencing of METTL5 suppressed NSCLC cell proliferation and migration, while overexpression promoted proliferation and migration. METTL5 directly targeted PGAM1 mRNA through m6A modification, and the expression levels of METTL5 and PGAM1 exhibited a statistically significant but moderate positive correlation (R=0.45; P=5.4×10-56). YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) is an m6A reader that recognizes and binds to methylated PGAM1 mRNA, enhancing its stability and expression. PGAM1 knockdown reduced glycolysis (decreased extracellular acidification rate) and increased oxidative phosphorylation (increased oxygen consumption rate). Notably, the positive correlation between PGAM1 and GLUT1 expression (R=0.6; P=4.12×10-183) supports the role of the METTL5/PGAM1 axis in regulating GLUT1, thereby influencing glycolytic flux. Rescue experiments demonstrated that PGAM1 overexpression reversed GLUT1 downregulation in METTL5-knockdown cells. Overall, METTL5 may drive NSCLC progression by reprogramming glycolytic metabolism through m6A modification of PGAM1 mRNA. The METTL5/PGAM1/GLUT1 axis represents a novel therapeutic target for NSCLC.
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Lung cancer remains the primary cause of cancer-related mortality worldwide. BUD23, also known as Williams-Beuren syndrome critical region 22, is an rRNA methyltransferase involved in ribosome maturation and RNA methylation. It has been reported to promote tumor progression in several malignancies. Although BUD23 has been implicated in drug resistance in lung cancer cells, its role in non-small cell lung cancer (NSCLC) remains incompletely understood. In the present study, transcriptomic and proteomic datasets were analyzed to evaluate the expression of BUD23 in NSCLC and normal tissues, and Kaplan-Meier survival analysis was performed to assess its prognostic significance. Immune infiltration algorithms were used to examine the correlation between BUD23 expression and tumor immune cell infiltration in NSCLC. Gene set enrichment analysis (GSEA), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and single-cell enrichment analysis were conducted to explore the biological pathways associated with BUD23 expression. In vitro, the effect of BUD23 knockdown on the viability, motility and apoptosis of NSCLC cell lines was evaluated by Cell Counting Kit-8, wound healing and Annexin V/PI flow cytometry assays, respectively, and the mRNA expression levels of potential downstream genes were quantified by reverse transcription-quantitative PCR. BUD23 was found to be significantly upregulated in NSCLC and associated with poor patient survival. Immunogenomic analyses indicated that high BUD23 levels are correlated with reduced immune cell infiltration. GSEA, KEGG and single-cell pathway enrichment analyses consistently implicated BUD23 in 'DNA repair' and 'cell cycle' pathways. In vitro, BUD23 knockdown suppressed the proliferation and migration of NSCLC cells, and reduced RNA polymerase II subunit J expression. Collectively, these findings suggest that BUD23 may contribute to the development and progression of NSCLC, and provide a strong basis for future mechanistic and clinical investigations.
Metastatic gastric cancer is an aggressive malignancy characterized by poor survival rates and heterogeneous treatment outcomes. Reliable prognostic tools to identify patients who may benefit from systemic therapy remain limited. Therefore, there is a need for easily accessible and clinically applicable prognostic tools. The present single-center retrospective study included 70 patients with microsatellite-stable, HER2-negative metastatic gastric cancer who were treated with first-line fluoropyrimidine-based chemotherapy between 2020 and 2024. The present study aimed to develop and evaluate a novel composite prognostic score integrating systemic inflammation and tumor burden. The neutrophil-C-reactive protein (CRP)-CA19-9 (NCC) score was constructed based on baseline neutrophil-to-lymphocyte ratio (NLR ≥5), CRP >20 mg/l and CA19-9 levels (>90 U/ml). Patients were classified into low-risk (0-1) and high-risk (2-3) groups. Overall survival (OS) and progression-free survival (PFS) were analyzed using Kaplan-Meier and Cox regression methods, with internal validation performed by bootstrap resampling. The median OS for the entire cohort was 13.4 months. A high NCC score was associated with significantly shorter OS compared with a low NCC score (9.6 vs. 15.2 months; P=0.00065) and an increased risk of mortality (hazard ratio=2.59; 95% CI: 1.47-4.56). The median PFS was also shorter in the high-risk NCC group (9.2 vs. 10.1 months; P=0.04). The optimism-corrected C-index for OS was 0.60, indicating that the NCC score is a simple and practical prognostic tool for survival stratification with favorable discriminative performance compared with established prognostic indices in metastatic gastric cancer.
The liver is the most common metastatic target organ of pancreatic cancer (PC). Currently, imaging examination is effective for detecting liver metastases (LM) of PC, but some small metastases are difficult to detect, making it necessary to establish a comprehensive diagnostic model with which to predict LM. A total of 59 patients with PC were enrolled as the training cohort and 16 patients with PC were included as the external validation cohort. The 59 patients in the training cohort were divided into LM and No-LM groups. Univariate and multivariate logistic regression analyses were performed to identify independent risk factors for synchronous liver metastasis (SLM) in PC. Based on these findings, a diagnostic model was constructed and a nomogram was developed to facilitate practical application. The accuracy and reliability of this diagnostic model were then evaluated using the area under the receiver operating characteristic curve (AUC), Hosmer-Lemeshow (HL) curves and decision curve analysis (DCA). Multivariate analysis identified CEA [odds ratio (OR)=1.05, 95% CI: 1.01-1.08], CA153 (OR=1.18, 95% CI: 1.06-1.31), white blood cells (WBC; OR=1.71, 95% CI: 1.08-2.72) and platelets (PLT; OR=1.01, 95% CI: 1.00-1.03) as independent risk factors. In the training and external validation cohorts, the diagnostic efficacy of the model's AUC was 0.92 and 0.90, respectively, with sensitivities of 0.96 and 0.83, and specificities of 0.86 and 0.75, respectively. The HL and DCA curves indicate the excellent calibration and clinical net benefit of the model. In conclusion, the diagnostic model integrating CEA, CA153, WBC and PLTs shows high predictive performance for identifying SLM in patients with PC.
Microsatellite stable (MSS) metastatic colorectal cancer (mCRC) hardly benefits from immune-monotherapy. Immune checkpoint inhibitor (ICI)-based combinations have been explored with mixed results. To evaluate the treatment patterns and outcomes across lines of immunotherapy in MSS mCRC, a retrospective real-world data analysis was performed in the present study. A total of 202 patients treated at Renmin Hospital of Wuhan University from June 2019 to December 2023 were included in the analysis, encompassing 38, 41 and 123 cases that received first-(1L), second-(2L) and third-line or above (3L+) ICI-based therapies, respectively. ICI combined with chemotherapy, ICI combined with chemotherapy and anti-VEGF(R)/EGFR/HER2 monoclonal antibody, and ICI combined with tyrosine kinase inhibitor (TKI) were the main options for the 1L, 2L and 3L+ cohorts, respectively. The objective response rates of the 1L, 2L and 3L+ treatment cohorts were 63.2, 22.0 and 11.4%, respectively, and the disease control rates of these three cohorts were 94.7, 75.6 and 70.7%, respectively. The median progression-free survival of the 1L, 2L and 3L+ cohorts was 11.1, 6.5 and 4.7 months, respectively, and overall survival (OS) was not reached, 16.0 and 11.9 months, respectively. After propensity score matching, patients who received ICI cross-line therapy at least once in the 3L+ cohort showed directional OS improvement (14.3 vs. 11.3 months; hazard ratio, 0.66; 95% confidence interval, 0.39-1.14; P=0.123) compared with those who did not receive ICI cross-line therapy. Grade ≥3 adverse events (AEs) occurred in 43.6% of patients, with thrombocytopenia, leukopenia and abnormal hepatic function being the most common. The incidence of immune-related AEs (irAEs) was 38.6% and that of grade ≥3 irAEs was 15.3%. These findings suggest that chemotherapy remains the cornerstone of 1L and 2L treatment for MSS mCRC, while the combination of ICI and TKI has developed into a major trend at the 3L+ setting with improved survival and controllable safety.
The infiltration of regulatory T cells (Tregs) in lung adenocarcinoma (LUAD) is associated with a poor prognosis. The present study aimed to explore the potential function of Treg marker genes in prognosis and immunotherapy using the transcriptome profiles of five LUAD cohorts sourced from public databases. Among them, the single-cell dataset GSE131907 was employed to identify cell types in lung cancer tissues and to identify Treg markers. The prognostic Treg markers were screened using univariate Cox and Least Absolute Shrinkage and Selection Operator regression analyses. Subsequently, a prognostic model was constructed and assessed using Kaplan-Meier and receiver operating characteristic curves. Furthermore, the effect of prognostic Treg markers on clinical characteristics, the immune microenvironment and tumor mutation burden (TMB) were evaluated. In addition, the function of genes strongly correlated with the prognostic risk score were investigated using Spearman and functional enrichment analysis. Finally, the genes expression levels were assessed using reverse transcription-quantitative PCR (RT-qPCR) and western blotting. By analyzing the single-cell data, 13 Treg markers [centromere protein M (CENPM), pituitary tumor-transforming gene 1 protein, interleukin 1 receptor type 2, baculoviral IAP repeat containing 3, glucocorticoid induced 1 (GLCCI1), melanoma-associated antigen H1 (MAGEH1), CD5, cytokine inducible SH2 containing protein, zinc finger protein 101 (ZNF101), Ikaros family zinc finger protein 4 (IKZF4), ankyrin repeat and SOCS box protein 2, zinc finger CCCH-type containing 12D and C-C motif chemokine receptor 6] were identified as prognostic features. The prognostic model constructed using these 13 genes revealed that the high-risk group had a poorer prognosis than the low-risk group. Moreover, it was demonstrated that the risk score could be an independent prognostic factor affecting the prognosis of patients with LUAD. Additionally, the high-risk group had a lower ESTIMATE score, higher TMB score and lower T cell receptor richness than the low-risk group. Finally, RT-qPCR and western blotting showed that the expression levels of CENPM, ZNF101, MAGEH1 and IKZF4 were significantly altered in cancer tissues compared with the adjacent normal tissues. In conclusion, a reliable prognostic model based on 13 Treg markers was developed. The comprehensive characterization of the Treg markers of LUAD may help to monitor the prognosis and provide new strategies for LUAD treatment.
Splenomegaly has been linked to a poor prognosis in certain cancer types, possibly due to a weakened immune system. The present study evaluated the association between splenic volume (SV) and oncological outcomes in patients with upper tract urothelial carcinoma (UTUC) after radical nephroureterectomy (RNU). A total of 465 patients with non-metastatic UTUC who underwent RNU between 2009 and 2020, with available preoperative abdominal computed tomography scans and hemogram data collected within 1 month before the operation, were retrospectively analyzed. SV (cm3) was calculated using the cross-sectional area summation method and standardized by body surface area (m2). A receiver operating characteristic curve identified 79 cm3/m2 as the optimal SV cut-off. Patients were stratified by SV and lymphocyte percentage (lym%) values. Survival outcomes were evaluated using Kaplan-Meier analysis and multivariate Cox regression analysis. Among the 465 patients, those with high SV (n=206; 44.3%) demonstrated significantly shorter overall survival (OS) and cancer-specific survival (CSS) times. Stratified analysis showed that patients with both elevated SV and low lym% had the poorest outcomes, including significantly shorter metastasis-free survival (MFS) time. Multivariate analysis confirmed that the combined high SV/low lym% phenotype was an independent predictor of OS, CSS and MFS. In conclusion, the combination of high standardized SV and low lym% was independently associated with an unfavorable prognosis following RNU in UTUC. This dual biomarker approach may enhance risk stratification and inform tailored postoperative management.
Alternating electric fields (AEF), also known as tumor treating fields (TTFields), have emerged as a non-invasive anticancer modality; however, their clinical benefit in non-small cell lung cancer (NSCLC) still depends heavily on prolonged daily wear time, which often limits patient adherence due to discomfort and skin irritation. Despite recent Food and Drug Administration approval of TTFields for metastatic NSCLC, the relative contributions of field intensity and exposure duration, particularly from a quantitative and dosimetric perspective, have not been systematically evaluated. In the present study, H460 and A549 NSCLC cell lines were exposed to three TTFields regimens combining different intensity-duration configurations (0.4 V/cm for 24 h, 0.8 V/cm for 6 h and 1.6 V/cm for 3 h), and short-(48 h) and long-term (7-day) responses were assessed. TTFields significantly reduced cell viability, clonogenic survival and migratory capacity while increasing apoptotic susceptibility. Notably, treatment conditions with different intensity-duration combinations produced partially overlapping inhibitory effects, suggesting that overall exposure may contribute to the observed responses. These findings indicated that NSCLC cells respond to TTFields in a dosimetry-dependent manner and support the existence of an intensity-duration trade-off. The present study provided preliminary evidence for flexible TTFields exposure strategies while underscoring the need for energy-matched and in vivo validation in future research to refine treatment scheduling in NSCLC.
Endocrine therapy remains one of the primary treatment modalities for estrogen receptor (ER) positive breast cancer, serving a pivotal role in improving patient outcomes and extending survival. Nevertheless, the gradual emergence of endocrine resistance continues to limit its clinical efficacy. In recent years, advances in molecular biology and genomics have driven the development of innovative technologies and therapeutic strategies in this field. The present review highlights the latest progress in endocrine therapy for breast cancer, including the introduction of next-generation selective ER degraders (SERDs), ER antagonists/degraders and selective ER modulators (SERMs). In addition, combination strategies integrating endocrine therapy with small-molecule inhibitors of critical signaling pathways, such as PI3K/AKT/mTOR and CDK4/6, have demonstrated promising potential in overcoming resistance. Cutting-edge technologies, such as single-cell sequencing and organoid models, are providing novel insights into treatment monitoring and the implementation of personalized therapy. Looking ahead, precision medicine platforms powered by artificial intelligence and big data are expected to further refine therapeutic strategies and ultimately improve patient prognosis. Collectively, endocrine therapy for breast cancer is evolving toward a more diversified, precise and individualized approach, offering patients broader treatment options and enhanced survival benefits.