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61,005 resultsShowing papers similar to Endoplasmic Reticulum Stress-Related Signature for Predicting Prognosis and Immune Features in Hepatocellular Carcinoma
ClearEndoplasmic Reticulum Stress-related Classification for Prognosis Prediction in Hepatocellular Carcinoma
Researchers used gene expression data to create an endoplasmic reticulum stress-based classification system for predicting outcomes in liver cancer patients. The model identified patient subgroups with significantly different survival rates.
Identification and validation of novel signature associated with hepatocellular carcinoma prognosis using Single-cell and WGCNA analysis
This study identified a novel gene signature associated with hepatocellular carcinoma using TCGA datasets and validated key molecular targets with potential prognostic and therapeutic significance. The findings advance understanding of the molecular mechanisms driving liver cancer progression.
Acute Endoplasmic Reticulum Stress Induces Inflammation Reaction, Complement System Activation, and Lipid Metabolism Disorder of Piglet Livers: A Proteomic Approach
Researchers used piglet liver models to show that acute endoplasmic reticulum stress triggers a cascade of inflammation, complement system activation, and lipid metabolism disruption, providing proteomic insights relevant to understanding stress-related liver disease mechanisms.
Correlation Between Tumor Differentiation and Biomarkers in Hepatocellular Carcinoma: Implications for Early Diagnosis and Treatment
Researchers examined the correlation between tumor differentiation levels and biomarker expression in patients with hepatocellular carcinoma. The study found significant associations between tumor grade and certain biomarker levels, suggesting these markers may have potential value for early diagnosis and treatment planning in liver cancer.
Mitochondrial Quality Control and Metabolic Reprogramming in Hepatocellular Carcinoma: Implications for Immunotherapy and Treatment Resistance
Scientists reviewed research showing that liver cancer cells damage the tiny energy factories (mitochondria) inside immune cells, making it harder for the body's natural defenses to fight the cancer. When immune cells can't get enough energy, they become "exhausted" and stop working properly against tumors. The researchers suggest that targeting these energy problems in cells could help improve cancer treatments and make immunotherapy work better for liver cancer patients.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
Combining network toxicology, machine learning, and molecular docking, this study found that PET plastic degradation products ethylene glycol and terephthalic acid may influence colorectal cancer prognosis through 43 shared genes linked to TNF/IL-17 signaling and glucocorticoid-mediated metabolic pathways.
Exploration of biomarkers for predicting the prognosis of patients with diffuse large B-cell lymphoma by machine-learning analysis
Researchers used machine learning and weighted gene co-expression network analysis on three public genomic datasets to identify biomarkers for diffuse large B-cell lymphoma prognosis. They identified key hub genes and constructed a risk model that could predict patient survival, though this study is not directly related to microplastics.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
Researchers used network toxicology, machine learning, and molecular docking to investigate how PET degradation products—ethylene glycol and terephthalic acid—affect colorectal cancer prognosis through the glucocorticoid signaling pathway. The analysis identified 43 shared target genes, suggesting that PET breakdown products may worsen colorectal cancer outcomes by dysregulating glucocorticoid-mediated anti-inflammatory and cell survival signals.
Environmental PET-microplastic exposure and risk of non-alcoholic fatty liver disease: An integrated computational toxicology and multi-omics study
Researchers used computational toxicology and machine learning to identify six key genes linking PET microplastic exposure to non-alcoholic fatty liver disease (NAFLD), with the model achieving high diagnostic accuracy and molecular docking suggesting that PET-derived chemicals may directly bind to proteins controlling liver fat metabolism.
Early Predictor Tool of Disease Using Label-Free Liquid Biopsy-Based Platforms for Patient-Centric Healthcare
Algorithmic analysis of patient-derived cell clusters from liquid biopsy samples was combined with tumor models to develop an early disease prediction tool applicable across cancer types. The approach offers a label-free, non-invasive method for early cancer detection that could supplement or reduce reliance on conventional tissue biopsy.
A computational framework for multi-scale data fusion in assessing the associations between micro- and nanoplastics and human hepatotoxicity
Researchers developed a computational toxicology framework integrating multi-source data and network analysis to map associations between micro- and nanoplastics and hepatotoxicity, identifying key molecular pathways through which MNPs may damage the liver, offering a scalable alternative to traditional in vivo testing.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
This computational study investigated how PET microplastic degradation products affect colorectal cancer prognosis, identifying 43 genes linking ethylene glycol and terephthalic acid exposure to cancer pathogenesis via chronic inflammation mediated through TNF/IL-17 and glucocorticoid metabolic pathways.
Autophagy affects hepatic fibrosis progression by regulating macrophage polarization and exosome secretion
This study found that autophagy regulates hepatic fibrosis progression by controlling macrophage polarization and exosome secretion, which in turn modulates hepatic stellate cell activation.
Exposure to microplastics and liver oncogenesis: A comprehensive review on molecular mechanisms and pathogenic pathways
Researchers reviewed mechanisms by which microplastic exposure may promote liver cancer, identifying oxidative stress, mitochondrial dysfunction, inflammatory signaling, and epigenetic disruption as key pathways, while noting that microplastics can also carry heavy metals and organic pollutants that synergistically amplify hepatotoxic and carcinogenic risk.
Phosphorus metabolism disorders in erythrocytes and lymphocytes among patients with inflammatory breast cancer, infiltrative stomach and colorectal cancer
Researchers examined phosphorus metabolism and energy dysfunction in erythrocytes and lymphocytes among 49 patients with inflammatory breast cancer, infiltrative stomach cancer, and colorectal cancer to identify prognostic markers. They found distinct phosphorus metabolism disorder patterns across cancer types, suggesting these metabolic disruptions as potential predictive factors for disease course and prognosis.
A comprehensive analysis of the hub genes for oxidative stress in ischemic stroke
Integrating three ischemic stroke genomic datasets identified nine hub genes involved in oxidative stress responses including TLR1, MMP9, and TLR4, which were highly expressed in stroke samples and associated with neutrophil and macrophage infiltration, with machine learning models confirming their predictive value.
BRCC36 Deubiquitinates HMGCR to Regulate the Interplay Between Ferroptosis and Pyroptosis
This study uncovered a molecular switch (an enzyme called BRCC36) that controls whether liver cancer cells die by ferroptosis or pyroptosis, two different forms of programmed cell death. While not directly about microplastics, ferroptosis has been identified as one of the ways nanoplastics damage cells in recent studies. Understanding how cells regulate ferroptosis could help explain why some tissues are more vulnerable to nanoplastic-induced damage than others.
Nanoplastic propels diet-induced NAFL to NASH via ER-mitochondrial tether-controlled redox switch
Researchers investigated how nanoplastic exposure may accelerate the progression of diet-induced fatty liver conditions in animal models. The study found that nanoplastics disrupted the connections between the endoplasmic reticulum and mitochondria, triggering oxidative stress responses that worsened liver inflammation and damage.
Identification of functional immune and neuronal tumour cells in glioma
Researchers developed the Single Cell Rule Association Mining (SCRAM) computational tool to integrate RNA-inferred genomic alterations with co-occurring cell type signatures at single-cell resolution, applying it to glioma to identify functional immune and neuronal tumour cells and distinguish tumour from non-tumour cells with greater precision than existing annotation algorithms.
Characterization of Microplastics in Human Gastric Cancer and Control Tissues and Analysis of Associated Genetic Features
Researchers detected and characterized microplastics in human gastric cancer tissue and adjacent healthy tissue, finding significantly higher microplastic concentrations in cancer tissue, and used transcriptome sequencing to explore potential molecular mechanisms linking microplastic exposure to gastric cancer development.
Immunotherapeutic strategy in the management of gastric cancer: molecular profiles, current practice, and ongoing trials
This review summarizes immunotherapy strategies for gastric cancer, focusing on PD-L1 expression and immune checkpoint inhibitors (ICIs). Accumulating evidence suggests that targeting the immune response, particularly through ICIs, may improve clinical outcomes in patients with gastric cancer.
Meta-analysis of H. pylori and the gut microbiome interactions and clinical outcomes
This meta-analysis identified specific gut microbial signatures associated with H. pylori infection and disease progression, offering predictive models for early diagnosis and risk stratification. The findings support microbiome-based approaches to personalized treatment of H. pylori-associated gastrointestinal disorders.
Metabolic disturbance and transcriptomic changes induced by methyl triclosan in human hepatocyte L02 cells
Exposure of human hepatocyte L02 cells to methyl triclosan demonstrated that oxidative stress and metabolic dysregulation are involved in its cytotoxicity, as shown by transcriptomic changes and metabolic disturbance. These findings suggest methyl triclosan poses a hepatotoxic risk at concentrations that may be encountered through environmental exposure.
Metabolomic and sphingolipidomic profiling of human hepatoma cells exposed to widely used pharmaceuticals
This study used metabolomic and sphingolipidomic profiling of human hepatoma cells exposed to wine bottle-associated microplastics, identifying disrupted lipid metabolism pathways and stress responses that may be relevant to human health risk assessment.