Cancer treatment and research communications最新文献

In oncology, glioblastoma multiforme (GBM) is considered a crucial challenge due to rapid drug resistance and the protective effects of the blood-brain barrier (BBB). Photodynamic therapy (PDT), photothermal therapy (PTT), and sonodynamic therapy (SDT) have emerged as promising approaches for GBM treatment, while limited energy penetration through the skull can restrict their effectiveness in intracranial tumors. The present systematic review aimed to evaluate studies on nanoparticle-based PDT, PTT, and SDT using online databases, including PubMed, Scopus, Web of Science, and Embase, from 2020 to 2025. Non-English studies, reviews, abstracts, book chapters, and retracted papers were excluded. A total of 663 records were initially identified, and 47 studies met the inclusion criteria. Based on the analysis of these studies, we observed a progressive shift in therapeutic strategies, categorized into four generations: (1) surface-limited ablation using near-infrared (NIR)-I thermal cytotoxicity; (2) multimodal synergistic therapies; (3) stimuli-responsive switch-on systems; and (4) deep-penetration modalities. The fourth generation is characterized by technologies, such as NIR-II lasers, X-ray-induced photodynamic therapy (X-PDT), low-intensity ultrasound (LIUS) and focused ultrasound, to overcome the depth barrier and promote immunogenic cell death. Nanoparticle-based GBM therapies are increasingly shifting toward multifunctional, BBB-targeted, and immune-engaging platforms. This trend highlights the need for multimodal, standardized, safe, and simpler designs.

Lung cancer mortality is driven largely by metastasis, which arises from tumor-intrinsic alterations and interactions within the tumor microenvironment (TME). Non-coding RNAs (ncRNAs), including miRNAs, lncRNAs, circRNAs, and extracellular vesicle-associated RNAs, regulate these interactions by modulating gene expression and intercellular signaling. This review examines ncRNA-mediated regulation of metastatic signaling in lung cancer, with particular emphasis on TGF-β signaling and its crosstalk with five additional pathways relevant to tumor dissemination: Wnt/β-catenin, hypoxia-inducible factor signaling, Notch, integrin/focal-adhesion signaling, and the CXCL12/CXCR4 axis. Particular attention is given to epithelial-mesenchymal transition, cancer stemness, extracellular matrix remodeling, angiogenesis, immune escape, and metastatic niche formation. The available evidence indicates that ncRNAs often act through interconnected regulatory circuits rather than isolated targets, and that their effects depend strongly on histological context, including LUAD, LUSC, other NSCLC subtypes, and SCLC, as well as on molecular background, cellular compartment, and experimental model. Findings derived from one histological or molecular setting should therefore not be assumed to apply uniformly across lung cancer. Hypoxia, cancer-associated fibroblasts, tumor-associated macrophages, and extracellular vesicles can alter ncRNA programs, while ncRNAs can reciprocally reshape these components. We also examine the potential translational relevance of ncRNA-based biomarkers and therapeutic strategies; however, most remain at the preclinical or exploratory stage and require further mechanistic, analytical, prospective, and clinical validation. Major barriers include delivery, target specificity, extracellular-vesicle standardization, reproducibility, and patient selection. A network-based interpretation may therefore provide a more realistic framework for understanding ncRNA contributions to lung cancer metastasis.

Background: Oxidative stress and redox dysregulation are important features of hepatocellular carcinoma (HCC), but their expression patterns in hepatitis B virus (HBV)- and hepatitis C virus (HCV)-associated HCC remain incompletely characterized. This study investigated redox-related gene expression and its potential functional and prognostic relevance.

Methods: A predefined 84-gene oxidative stress and redox-related quantitative real-time PCR array was used to profile 11 HCC samples (7 HCV-associated and 4 HBV-associated tumors) and 4 controls. Analyses included hierarchical clustering, gene-list overlap, functional enrichment, protein-protein interaction networks, gene-expression correlations, and exploratory survival analysis.

Results: Both HCC groups exhibited altered expression of genes associated with antioxidant defense, glutathione metabolism, mitochondrial redox regulation, and ferroptosis-related processes. In HCV-associated HCC versus controls, TXN, SPINK1, HSP90AA1, and DUSP1 showed increased expression. In HBV-associated HCC versus controls, GCLC, peroxiredoxins, CAT, and SOD1 showed increased expression. Eighteen genes were shared between comparison lists, including GPX4, GPX2, GPX3, PRDX1, PRDX5, TXN, GCLM, SOD2, and FTH1. Enrichment analyses implicated glutathione metabolism, oxidative stress, peroxisome function, and ferroptosis-associated processes. Network analysis identified GPX2, GPX3, GPX4, and SOD2 in a connected module. External exploratory survival analysis associated higher SPINK1 and HSP90AA1 expression with poorer overall survival.

Conclusions: These findings identify redox-related expression patterns warranting further investigation. Larger cohorts and functional studies are needed to establish etiological differences, ferroptosis susceptibility, and prognostic significance.

Background: Colposcopy-directed biopsy is widely used in the diagnosis of cervical dysplasia, but its accuracy is variable. Reliable detection of clinically significant lesions (CIN2+) is essential for appropriate treatment. This study assessed its diagnostic performance using histology after LEEP as the reference standard and explored factors associated with discrepancies.

Methods: 423 procedures were analyzed. Histological findings from colposcopy-directed biopsy were compared with the histology of the subsequent LEEP specimen. Diagnostic performance for CIN2+ was evaluated using sensitivity, specificity, predictive values, and accuracy; agreement was assessed using weighted Cohen's kappa. Subgroup analyses considered transformation zone (TZ) type, age, and menopausal status. Multivariable logistic regression assessed predictors of histopathological underestimation.

Results: Biopsy showed 97.0% sensitivity, 20.0% specificity, and 80.6% accuracy for CIN2+ detection. Exact histological agreement occured in 61.7% of procedures (κ = 0.31). Histopathological underestimation occurred in 12.3% and overestimation in 26.0%, indicating a tendency toward overestimation. Exact agreement decreased from 75.8% in TZ1 to 48.0% in TZ3 and from 65.2% in premenopausal to 48.4% in postmenopausal patients. Complete-case multivariable analysis included 227 procedures and 23 underestimation events. Compared with TZ1, TZ2 and TZ3 were independently associated with higher odds of underestimation other included covariates were not.

Conclusion: Colposcopy-directed biopsy shows high sensitivity but limited specificity for CIN2+ detection, with notable diagnostic discrepancies. Histological concordance was lower in patients with TZ 3 and in postmenopausal women, while TZ was independently associated with underestimation. These findings highlight the importance of considering anatomical and patient-related factors when interpreting biopsy results and planning clinical management.

Introduction: The gut microbiota may influence breast cancer risk through different biologic pathways. This analysis examined the association of the gut microbial composition with percent mammographic density (PMD), a strong predictor of breast cancer risk.

Methods: Postmenopausal women in the Adiposity Phenotype Study, a cross-sectional subset of the Multiethnic Cohort, from five racial/ethnic groups, provided a stool sample. Extracted bacterial DNA was sequenced for the V1-V3 region of the 16S rRNA gene. Bioinformatic analysis determined alpha-diversity and the abundance of 10 phyla and 152 genera. PMD was assessed in routine mammograms taken before stool collection with a quantitative computer-assisted method. Blood levels of estrogen metabolites were assessed using standard assays. General linear models regressed PMD on gut microbial diversity, phyla, and genera while adjusting for relevant covariates.

Results: Of 649 women (69.1 ± 2.7 years), 311 had low (<15%) and 338 had high (>=15%) PMD. Whereas alpha diversity or phyla were not associated with PMD, 10 genera were nominally related to PMD (p < 0.05) but not after adjusting for multiple comparisons: 7 positively (Bifidobacterium, Blautia, Dialister, Eubacterium_fissicatena_group, Lachnospira, Lachnospiraceae_UCG-008, Lachnospiraceae_uncultured) and 3 inversely (Alistipes, Senegalimassilia, Eubacterium_oxidoreducens_group), potentially implicating estrogen metabolism and short-chain fatty acid production. All blood steroid metabolites were significantly related to PMD, but only SHBG was associated with 2 genera after Bonferroni adjustment.

Conclusions: The nominal associations detected in this analysis suggest that certain gut microbiota may be associated with PMD, a marker of risk but not a measure of breast cancer incidence, due to their ability to affect circulating hormones or SCFA production.

Objectives: This study aims to evaluate the therapeutic efficacy and safety of tumor vaccine therapy in patients suffering from Hodgkin (HL) and Non-Hodgkin Lymphoma (NHL).

Methods: a systematic search was done in PUBMED, WOS, Embase and Scopus in order to identify relevant studies from their inception to February 8th, 2026. At first, title and abstract of retrieved records were checked for eligibility and then, a full-text evaluations were conducted. Then relevant data were extracted from eligible studies. Risk of Bias of Included studies were assessed using Cochrane ROB-2 and ROBINS-I tool. Proportions were estimated using the metaprop function of the R meta package with logit transformation and back-transformation for presentation. Because of substantial clinical and methodological heterogeneity, results were not pooled; instead, individual study estimates with 95% confidence intervals were presented in forest plots for qualitative comparison.

Results: Across studies of non-Hodgkin lymphoma, objective response rates varied from 6% to 44%, with complete response rates ranging from 0% to 28% and partial response rates from 6% to 29%. Response estimates varied across treatment-naïve, relapsed/refractory, and mixed-treatment populations, without a consistent pattern according to previous treatment status; most studies evaluated patients with active disease and predominantly indolent NHL. Grade 3-5 adverse events ranged from 0% to 19%, with no severe events reported in most studies, although treatment strategies and concomitant therapies differed substantially across cohorts. Only one study evaluated Hodgkin lymphoma, reporting an ORR of 66.7% (2/3), consisting entirely of partial responses, with no grade 3-5 adverse events. Given the marked clinical and methodological heterogeneity, findings were synthesized descriptively without pooled effect estimates.

Conclusion: Therapeutic tumor vaccines showed variable but measurable antitumor activity in NHL, with generally low rates of grade 3-5 adverse events across most studies. However, substantial clinical and methodological heterogeneity, small sample sizes, non-randomized designs, and highly limited evidence in HL prevent firm conclusions regarding efficacy or comparative effectiveness. Stronger comparative evidence from multicenter cohorts and registries with longitudinal follow-up, appropriate control groups, and propensity-score methods is needed to clarify vaccine-associated clinical responses and identify settings suitable for subsequent randomized evaluation.

PIWI-interacting RNAs (piRNAs) and their associated proteins constitute an important regulatory system involved in genome stability, transposable-element repression, germ-cell development, and epigenetic regulation. Increasing evidence indicates that disruption of piRNA-associated proteins contributes to reproductive disorders and tumorigenesis through alterations in DNA methylation, histone modifications, RNA stability, and transposable-element activity. This review summarizes current evidence on the epigenetic functions of piRNA-associated proteins in infertility and cancer, with particular emphasis on TDRKH, PNLDC1, TDRD9, HENMT1, MORC1, MORC3, and other components of the piRNA pathway. Studies in mouse and zebrafish models demonstrate that defects in these proteins can impair piRNA biogenesis or stability, disrupt transposon silencing, alter germ-cell development, and result in male or female infertility. In human and cancer models, dysregulation of piRNA pathway components has been associated with ovarian, cervical, esophageal, breast, leukemia, and prostate cancers, with evidence implicating DNA and histone methylation as well as RNA modifications such as m⁶A and m⁵C. Collectively, these findings suggest that piRNA-associated proteins can act as important epigenetic regulators linking small-RNA-mediated mechanisms to genome integrity, reproductive function, and malignant transformation. Further characterization of these pathways may improve understanding of disease mechanisms and support the identification of potential diagnostic and therapeutic targets.

Introduction: Advanced esophageal cancer benefits from immunotherapy. For squamous cell carcinoma (SCC), allocation for immune checkpoint inhibitors (ICI) is based on PD-L1 positivity assessed by the tumor proportion score (TPS) and combined positive score (CPS). It is unclear whether patients without an indication for ICI based on TPS are eligible when CPS is considered, or vice versa.

Methods: A systematic literature search in Medline, Embase, Web of Science, and Cochrane was conducted to identify studies evaluating PD-L1 expression using TPS and CPS in esophageal SCC. PD-L1 discordant cases were defined as TPS<1 and CPS≥10, or TPS≥1% and CPS<10. When paired patient-level TPS/CPS classifications were unavailable, possible discordance ranges were estimated from marginal positivity rates.

Results: Eight studies comprising a total of 1,252 patients were selected. Two studies reported the percentage of discordant TPS/CPS cases, with 30.2% (16 out of 53) showing discordance. The minimum possible discordance among the six studies without paired patient-level data was estimated at 5.7% (69/1199), ranging from 2.4% to 14.4% across studies. The maximum possible discordance estimates ranged from 43.2% to 87.3%, reflecting the uncertainty introduced by the absence of paired patient-level data.

Discussion: This review suggests that the current TPS≥1 and CPS≥10 thresholds are not interchangeable for determining treatment eligibility in ESCC. These discrepancies may significantly impact treatment eligibility, although the clinical benefit of ICI in TPS/CPS-discordant patients remains unknown.

Conclusion: Understanding TPS/CPS concordance is crucial for optimizing patient selection for ICI in esophageal SCC. Sequential assessment, starting with TPS and followed by CPS when TPS is negative, may represent a pragmatic eligibility-based testing strategy to reduce the risk of overlooking potentially eligible patients.

Breast cancer survivors frequently experience persistent pain, cancer-related fatigue, and interconnected symptom clusters that impair quality of life, functional status, and treatment adherence. Psychological factors, including pain catastrophizing, anxiety, depression, fear-avoidance behaviors, and maladaptive cognitive appraisals, are associated with the amplification and maintenance of these symptoms through proposed mechanisms involving central sensitization, HPA axis dysregulation, inflammatory signaling, and behavioral deconditioning. This narrative overview, rather than a systematic review, examines these determinants primarily in post-treatment survivorship, defined as the period following completion of surgery, chemotherapy, and radiotherapy and including patients continuing adjuvant endocrine therapy; evidence from active treatment and metastatic disease is identified by treatment phase where drawn upon. Persistent pain is reported by an estimated 25-60% of survivors, and pooled severe post-treatment fatigue by 26.9%, with estimates varying substantially by case definition. Persistent pain has multiple clinically distinct causes, including post-mastectomy pain syndrome, shoulder and myofascial disorders, lymphedema, radiation fibrosis, chemotherapy-induced neuropathy, and endocrine therapy-associated musculoskeletal pain; several of these are correctable, and their evaluation should precede psychological attribution. Psychological predictors are consistently identified but modest in magnitude and operate alongside rather than in place of surgical and disease-stage determinants. Cognitive behavioral therapy for insomnia shows large effects on insomnia severity with concurrent fatigue and mood benefit; mindfulness-based interventions show small pooled effects on distress. Symptom burden and access to intervention remain disproportionately worse among younger patients, those with metastatic disease, and underserved populations.

Purpose: To evaluate biomarker-targeted therapy utilization, healthcare costs, and overall survival (OS) with comprehensive genomic profiling (CGP), small panel, or no molecular testing for patients with metastatic non-small cell lung cancer (mNSCLC).

Patients and methods: This retrospective claims analysis identified patients with newly diagnosed mNSCLC (index date) from 08/01/2020-12/31/2022, using the Optum Labs Data Warehouse. Patients were grouped by first molecular testing approach: 1) CGP (>50 genes); 2) small panel (individual gene or ≤50 gene panel); or 3) no molecular testing. Post-diagnosis outcomes assessed during variable follow-up included biomarker-targeted therapy use, healthcare costs per patient per month (PPPM) during the first 180 days, and OS.

Results: Among 8783 patients identified, the molecular testing approach consisted of 41.4% CGP, 30.3% small panel, 23.4% no testing, and 4.9% unassigned. For CGP, the specimen type was 40.6% blood, 37.2% tissue, 2.8% blood and tissue, and 19.4% undefined. Use of biomarker-targeted therapy was higher with CGP than small panel testing (12.4%vs. 7.7%, P < 0.001). In an exploratory analysis, biomarker-targeted therapy use was higher with blood vs. tissue CGP (14.3%vs. 11.2%, P = 0.01). Among treated patients, adjusted OS did not differ significantly for CGP and small panel testing (HR 1.03, 95% CL 0.94 to 1.12, P = 0.58). Among treated patients, mean total healthcare costs PPPM were similar between CGP and small panel testing across both Medicare Advantage ($17,974 vs. $17,593, P = 0.31) and commercial ($40,655 vs. $39,802, P = 0.68) insurance and remained consistent after adjusting for baseline characteristics.

Conclusion: In mNSCLC, patients with CGP received biomarker-targeted therapy at higher rates than patients with small panel testing. Among treated patients, adjusted analyses showed no statistically significant difference in OS between CGP and small panel testing, and total healthcare costs were comparable between testing approaches.