Adenoid cystic carcinoma is a salivary gland cancer that grows slowly and has an unfavorable prognosis. The occurrence of adenoid cystic carcinoma in the parotid gland is extremely uncommon. It presents in three histopathological patterns: cribriform, tubular, and solid, and it is classified into three grades: grade i, grade ii, and grade III.

The combination of PD-1/PD-L1 inhibitors with chemotherapy (PC) has shown promise in treating advanced NSCLC. However, its added benefit over chemotherapy alone in Chinese patients remains unclear. We performed an updated synthesis of phase 3 randomized controlled trails (RCTs) to assess both therapeutic effectiveness and associated safety of PC therapy in this population.

To study the effect and predict the value of neoadjuvant treatment regimen for muscle invasive bladder cancer (MIBC) by construction of a columnar graphical model of patients by neutrophil-to-lymphocyte ratio (NLR), derived neutrophil-to-lymphocyte ratio (dNLR), and systemic immune-inflammatory index (SII) indexes.

Patients with human epidermal growth factor receptor 2 positive (HER2+) or triple-negative breast cancer are at higher risk than those with other breast cancer subtypes for developing brain metastases, including leptomeningeal metastases. Despite advances in the treatment of primary breast tumors, the prognosis of breast cancer patients with brain metastases remains poor. Frequent and sensitive monitoring of response to treatments is crucial to optimize treatments for brain metastases. Multimodal molecular analyses of cells in cerebrospinal fluid (CSF) may provide a less invasive approach than biopsy for monitoring disease in the central nervous system.

Breast cancer is the most prevalent malignancy worldwide, with approximately 50% of HER2-positive advanced breast cancer patients eventually developing brain metastases, significantly reducing survival. Current HER2-targeted therapies, such as trastuzumab, exhibit limited efficacy in patients with brain metastases due to poor blood-brain barrier penetration and drug resistance. This study aimed to develop a novel strategy for treating HER2-positive breast cancer brain metastases to improve overall survival. We engineered nanoparticles encapsulating circular RNA encoding the chemokine CXCL9 and an anti-PD-1 scFv, designed to target HER2-positive brain metastases. Our results demonstrate that these nanoparticles significantly enhance anti-tumor activity both in vitro and in vivo without exhibiting significant systemic toxicity. This approach improves the local tumor immune microenvironment while inducing lower systemic toxicity. In conclusion, we have established a platform of membrane-encapsulated circular RNA nanoparticles capable of targeting brain tumor lesions, showing potential for application in various brain disorders, including metastatic brain tumors. This novel approach offers a promising strategy for addressing the urgent need for effective treatments for HER2-positive breast cancer brain metastases.

Uncovering the mechanisms underlying tumor malignancy is extremely important for cancer treatment and management. In this study, using a pairwise cell model, LNCaP and its castration-resistant derivative C42B, we analyze the function of enhanced NASP protein in castration resistance. The data show that the expression of androgen receptor-targeted genes was obviously affected by NASP knockdown in C42B cells, and nearly 20% of the differential genes were AR dependent. ATAC-seq analysis revealed that NASP knockdown in C42B cells comprehensively increased chromatin accessibility, and disorders at AR occupancy regions were more prominent. Castration-induced genes, especially androgen-independent AR target genes, were enriched in the downregulated gene group. Further analysis of high-order chromatin interactions revealed that NASP knockdown in C42B led to frequent changes in multiple layers, including the compartment A/B transition, TAD boundary distance and chromatin loop, and AR-binding regions especially underwent more extensive reconstruction. Finally, we found that the recovery of the histone H3 pool in C42B can actually recall H3 back to the previous regions with both H3 and AR loss induced by NASP knockdown, but AR rebinding to the corresponding sites is obviously inhibited and lagging. These data indicate that NASP plays a fundamental role in guarding proper and fine mechanisms of AR in prostate cancer promotion and malignancy.

Unresectable hepatocellular carcinoma (uHCC) with portal vein tumor thrombosis (PVTT) has poor prognoses. This study evaluated the efficacy and safety of lenvatinib (LEN) combined with anti-PD-1 antibodies (PD-1) and locoregional therapy (LRT) in uHCC patients with PVTT.

For lung adenocarcinoma (LUAD), the competitive endogenous RNA (ceRNA) networks mediated by circular RNAs (circRNAs) have been partially constructed. However, a mass of networks still need to be thoroughly investigated to uncover novel regulatory axes in LUAD.

Accurate prediction of pathological complete response (pCR) to neoadjuvant chemotherapy has significant clinical utility in the management of breast cancer treatment. Although multimodal deep learning models have shown promise for predicting pCR from medical imaging and other clinical data, their adoption has been limited due to challenges with interpretability and generalizability across institutions.

Systemic chemotherapy may relieve symptoms and induce tumor downstaging in patients with unresectable gastric cancer. However, the survival benefit of primary tumor resection after chemotherapy remains unclear. This study aimed to determine the survival outcomes of conversion surgery in patients with unresectable gastric cancer.

Diabetes mellitus (DM) exhibits a strong association with tumorigenesis, yet its impact on tumor gene mutations remains poorly understood. Consequently, the present study was conducted to delve into the influence of DM on tumor gene mutations.

Non-small cell lung cancer (NSCLC) constitutes a substantial global health challenge, with surgical resection serving as a principal therapeutic approach. Nevertheless, the frequency of exploratory thoracotomy without en-bloc resection remains significant, particularly in advanced-stage cases, thereby adversely affecting prognosis. This study aims to predict risk scores for exploratory thoracotomy and analyze postoperative survival in patients with central NSCLC, utilizing CT (computed tomography) imaging subsequent to neoadjuvant therapy.

The purpose of this study was to explore the prognostic value of Immunoscore in patients with early-onset colorectal cancer.

Cancer has become a global health issue that demands transformative and advanced therapeutic approaches. Recent advancements in cancer research and therapeutics have shown that gold nanoparticles (AuNPs) possess potential anticancer, apoptotic, phagocytic, and immune modulation properties. Their unique physicochemical properties at the nanoscale make AuNPs effective candidate in various cancer therapeutics. This review uniquely highlights recent insights into the molecular mechanisms of AuNP-induced cancer cell death, cell cycle arrest, and immune modulation with multidimensional approach, an area often overlooked in earlier reviews. Also, it examines recent studies, exploring how AuNPs trigger their cancer-fighting properties such as cell death initiation, DNA destruction, and immune system modulation. AuNPs initiate cell death by targeting mitochondrial enzymes along with producing reactive oxygen species (ROS) and activating caspase proteins. AuNPs harm DNA, leading to cell cycle arrest, which in turn trigger apoptosis (programmed cell death) or other forms of cell death. Research study claims that AuNPs activate macrophages and regulate cytokine release which helps suppress tumor growth and metastasis. Moreover, this review compares chemical and green synthesis approaches, emphasizing green synthesis for its enhanced biocompatibility and alignment with targeted cancer therapy. Green synthesis methods are not only devoid of toxic chemicals but also superior in controlling particle size, shape, and surface functionality. Consequently, these green-synthesized AuNPs have been utilized in cancer research with improved therapeutic efficacy and enhanced cancer-targeting capabilities.

Metastasis remains the leading cause of cancer-related mortality, yet shared molecular mechanisms across cancer types are poorly understood. Identifying conserved metastatic pathways could offer new therapeutic targets. We performed an integrative cancer analysis across five cancer types (breast, lung, endometrial, prostate, colorectal) using RNA-Seq datasets from the GEO database. Differentially expressed genes (DEGs) between primary and metastatic tumors were identified using limma. Overlapping DEGs across cancers underwent pathway enrichment and protein-protein interaction (PPI) network analysis to identify hub genes. Key pathways and hub genes were validated for prognostic relevance across 15 cancer types using independent TCGA datasets and Cox regression models. We analyzed six publicly available datasets comprising primary and metastatic tumors across five cancer types: breast, lung, endometrial, prostate, and colorectal. We identified 10 overlapping DEGs, with ITGAX and CXCL12 emerging as hub genes connected to critical pathways, such as ERBB4 signaling, integrin-mediated adhesion, glycosphingolipid metabolism, and platelet function. Validation in TCGA confirmed the prognostic significance of hub genes across multiple cancers, with ITGAX significant in 6, while CXCL12 was significant in 2 out of 15 cancers tested. Our approach identified conserved genes and pathways involved in metastasis across cancers, with ERBB4 signaling and hub genes ITGAX and CXCL12 emerging as key regulators. These findings provide a framework for understanding metastatic processes. Future studies should explore targeting the common metastatic process across cancer types.

Synaptotagmin 12 (SYT12), a protein found to be upregulated in papillary thyroid cancer (PTC), has emerged as a potential biomarker for this malignancy. However, the mechanisms governing its expression remain poorly understood. In this study, we identify SYT12 as a novel substrate of SPOP, an adaptor of the Cullin 3 E3 ubiquitin ligase complex. SPOP binds to SYT12 and mediates SYT12's K48-linked polyubiquitination and subsequent proteasomal degradation. This interaction is dependent on the degron motif within SYT12, and deletion or mutation of the degron significantly impairs SPOP binding and stabilizes SYT12. We further demonstrate that GSK-3β-mediated phosphorylation of the degron is essential for SPOP recognition. Pharmacological inhibition of GSK-3β disrupts the SPOP-SYT12 interaction and increases SYT12 protein levels. Functionally, the SPOP-SYT12 axis modulates PTC cell viability and proliferation. Collectively, these findings uncover a novel regulatory mechanism of SYT12 expression and suggest that targeting the SPOP-SYT12 pathway may represent a promising therapeutic strategy for PTC.

Hepatocellular carcinoma (HCC) progression and prognosis are influenced by various molecular markers. This study aimed to identify the hub gene associated with HCC clinical characteristics and its role in HCC progression. Differentially expressed genes (DEGs) between HCC tumor and normal tissues, as well as between stage I/II and stage III/IV, were analyzed. Machine learning algorithms were used to pinpoint three critical hub genes (SPP1, ADH4, and ANXA10). A prognostic risk model was constructed and evaluated using Kaplan-Meier curves, COX regression, and decision curve analysis, which could effectively predict HCC survival. Among the three hub genes, SPP1 was significantly associated with the overall survival (OS) of HCC patients and effectively predicted prognosis. More importantly, SPP1 was upregulated in HCC tumor tissues and cells, and its overexpression enhanced HCC cell proliferation, migration, invasion, and drug resistance. It also promoted fatty acid metabolism in HCC cells, with malignant characteristics and drug resistance induced by SPP1 being mitigated by fatty acid oxidation inhibition. In vivo experiments showed that SPP1 knockdown inhibited tumor growth and fatty acid metabolism of HCC mice. In conclusion, SPP1 is a pivotal gene that influences HCC prognosis by enhancing malignancy and drug resistance through fatty acid metabolism.

Glioma is a highly heterogeneous and aggressive brain tumour that demands an integrated understanding of its molecular and immunological landscape. We collected multi-omics data from 575 TCGA diffuse-glioma patients (156 IDH-wild-type WHO-grade 4 glioblastomas and 419 IDH-mutant WHO-grade 2/3 diffuse gliomas) together with two validation cohorts (CGGA n = 970; GEO n = 110). Using the MOVICS framework, we derived three integrative molecular subtypes-CS1, CS2 and CS3. Ten machine-learning algorithms in MIME were benchmarked, and the Lasso + SuperPC combination yielded an eight-gene GloMICS (Glioma Multi-Omics Consensus Signature) prognostic score. The subtypes display discrete biology: CS1 (astrocyte-like) is characterized by glial lineage features, immune-regulatory signaling, and relatively favorable prognosis; CS2 (basal-like/mesenchymal) shows epithelial-mesenchymal transition, stromal activation, and high immune infiltration, including PD-L1 expression; CS3 (proneural-like/IDH-mut metabolic) exhibits metabolic reprogramming (OXPHOS, hypoxia) and an immunologically cold tumour microenvironment (TME). CS2 is associated with the worst overall survival, whereas CS1 confers the most favourable outcome. Dual checkpoint blockade or T-cell-rejuvenation strategies may benefit CS2 tumours, while metabolic inhibitors could prove effective in CS3. The eight-gene GloMICS score outperformed 95 published prognostic models (C-index 0.74-0.66 across TCGA, CGGA and GEO). TME deconvolution, immune checkpoint profiling and TIDE analysis indicate that high-risk GloMICS tumours harbour immunosuppressive fibroblast-rich niches and exhausted CD8⁺ T cells. Connectivity-map screening nominated dabrafenib, irinotecan and three additional CTRP/PRISM compounds as candidate agents for the high-risk group. Our study establishes robust glioma subtypes and a transferable prognostic signature, offering a blueprint for biomarker-guided therapy. Future work should include single-cell and immunohistochemical validation of subtype hallmarks and prospective trials stratified by GloMICS score.

This study aims to investigate the role of MSH6 in the diagnosis and prognosis of bladder cancer and its association with immunity. Various analyses were conducted on The Cancer Genome Atlas (TCGA) data, and the results were validated using the Gene Expression Omnibus (GEO) database. The potential mechanism of MSH6 in bladder cancer was revealed using R tools, Gene Set Enrichment Analysis (GSEA), and Gene Ontology (GO) analysis. Bladder cancer patients admitted to the Affiliated Hospital of Inner Mongolia Medical University from June 2023 to December 2023 were enrolled. Pathological specimens of bladder cancer and adjacent tissues were obtained. Immunohistochemical results showed the expression of MSH6 in bladder cancer tissues was higher than in adjacent tissues. High expression of MSH6 was identified as an independent prognostic factor for bladder cancer. The occurrence of bladder cancer was also influenced by age, pathological T stage, and pathological stage. According to the Kaplan-Meier survival curve, the overall survival rate of the MSH6 high-expression group was lower (P = 0.004). After MSH6 was knocked down in cell experiments, the proliferation, colony formation, and migration abilities of bladder cancer cells were significantly inhibited. MSH6 is significantly associated with the diagnosis and prognosis of bladder cancer, suggesting its potential utility as a biomarker for these purposes. MSH6 is closely related to the tumor immune microenvironment, implying a significant role in immunotherapy.

The mechanisms underlying mitophagy and mitochondrial dynamics (MD) in cervical cancer (CC), a disease with a high mortality rate, remain poorly understood. This study aimed to assess the prognostic significance of these processes in CC. Mendelian randomization (MR) and 101 machine learning models were employed to identify mitophagy- and MD-associated prognostic genes in CC. A subsequent risk model was developed to stratify patients by risk. Further analyses included functional pathway enrichment, immune infiltration, and single-cell RNA sequencing (scRNA-seq) analysis. The results identified PLOD3, SBK1, and SLC39A10 as prognostic genes for CC. Among these, PLOD3 and SLC39A10 were associated with poor prognosis, while SBK1 was protective. The risk model demonstrated high accuracy, with area under the curve (AUC) values exceeding 0.6. Following this, a prognostic nomogram was constructed incorporating risk score and pathological T stage, achieving high predictive accuracy. Gene Set Enrichment Analysis (GSEA) revealed significant enrichment in pathways such as ECM receptor interaction and olfactory transduction in high-risk groups. Additionally, SBK1 showed the strongest correlation with neutrophil infiltration. Expression pattern alterations of prognostic genes were observed in endothelial cells, T cells, and epithelial cells. In conclusion, a risk model based on mitophagy- and MD-related prognostic genes was established, offering a promising approach for the personalized management of patients with CC.