Similar Datasets
Project description:lncRNAs and mRNAs profiling of tissues from HCC patients comparing tumor tissues with non-tumor tissues. Two-condition experiment, tumors vs. non-tumors. Biological replicates: 7 tumor replicates, 7 non-tumor replicates.
2014-05-29 | E-GEOD-58043 | biostudies-arrayexpress
Project description:There are significant differences in the expression of genes that regulate metabolic pathways in HCC as compared to Cirrhosis or non-tumor liver tissues. These charcteristic pathways can be exploited for metabolic imaging biomarkers of HCC. We used microarrays to perform genome-wide association study expression in human Grade III hepatocellular carcinoma and surrounding tissues.
2017-08-25 | GSE45050 | GEO
Project description:Hepatic cirrhosis or advanced fibrosis caused by chronic hepatitis may be the main risk factor contributing to the occurrence of HCC. Growing clinical evidence show that patients with hepatic cirrhosis or advanced fibrosis may have a 7-fold higher incidence rate of HCC than those without, suggesting a crucial role of inflammation-carcinogenesis malignant transformation in HCC development and progression. We used microarrays to detail the global programme of gene expression underlying inflammation-carcinogenesis malignant transformation in HCC and identified distinct classes of up-regulated and down-regulated genes during this process
2021-02-12 | GSE166163 | GEO
Project description:lncRNAs and mRNAs profiling of tissues from HCC patients comparing tumor tissues with non-tumor tissues.
2014-05-29 | GSE58043 | GEO
Project description:Hepatocellular carcinoma (HCC) is one of the main subtypes of primary liver cancer, which accounts for 75-85% of all cases [1]. Despite increasing availability of treatments for liver cancer, HCC clinical trials are not promising since most HCC patients are in an advanced stage of HCC at the time of diagnosis. Additionally, highly metastatic and recurrent phenotype aggravate poor prognosis of liver cancer [2]. Therefore, there is an urgent need to explore the underlying molecular mechanism in HCC progression.
2023-09-18 | PXD036831 | JPOST Repository
Project description:Hepatocellular carcinoma (HCC) is a rapidly increasing and highly lethal cancer worldwide, with many patients diagnosed at advanced stages and early-stage patients often experiencing high recurrence rates. The combination of atezolizumab plus bevacizumab emerged as a groundbreaking immunotherapy, establishing a new standard of care for advanced HCC. There's an urgent need for reliable biomarkers to predict patient responses and personalize treatment. We collected tumor samples from advanced HCC patients wirth atezolizumab plus bevacizumab therapy and performed comprehensive analyses of the tumor microenvironment using bulk RNA sequencing to identify key features influencing the effectiveness of atezolizumab plus bevacizumab.
2025-10-02 | GSE285963 | GEO
Project description:We report the application of RNA sequencing technology for high-throughput profiling in HCC tissues. In the present study, to explore novel biomarkers of HCC, we firstly explored the expression profiles of mRNAs and miRNAs in three pairs of HCC patients (tumor tissues and non-tumorous tissues) by high-throughput RNA sequencing. A total of 1024 mRNAs were found to be significantly dysregulated (636 up-regulated and 388 down-regulated), 50 miRNAs were found to be significantly dysregulated (27 up-regulated and 23 down-regulated) in the HCC tissues compared with the non-tumorous tissues.Then validae the differentially expressed miRNAs by qRT-PCR in HCC tissues and serum. This study provides a framework for the application of miRNAs to be ideal biomarkers for HCC.
2023-02-28 | GSE146719 | GEO
Project description:Past studies have identified hepatic tumors with mixed hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC) characteristics which have a more aggressive behavior and a poorer prognosis than classic HCC. Whether this pathological heterogeneity is due to a cell of origin of bipotent liver progenitors or the plasticity of cellular constituents comprising these tumors remains debated. In this study, we investigated the potential acquisition of CC-like traits during advanced development of HCC in mice. We first characterized the primary and rare high-grade HCC developed in a genetic mouse model. We further developed a mouse model of highly efficient HCC invasion and metastasis via orthotopic transplantation of liver cancer organoids (LCOs) propagated from primary tumors in the genetic model. We found invasive/metastatic tumors developed in both models closely recapitulated advanced human HCC, and displayed a striking acquisition of CC-related pathological and molecular features which was absent in the primary HCC tumors. Our study directly demonstrates the pathological evolution of HCC during advanced tumor development, providing the first evidence that tumors with mixed HCC and CC features, or at least a subset of these tumors, represent a more advanced developmental stage of HCC. Lastly, we found LCO-generated high-grade tumors exhibited significantly increased extracellular vesicle (EV) secretion, suggesting that identifying tumor-specific EV proteins in plasma may be a promising tool for liver cancer detection.
2017-11-28 | GSE94583 | GEO
Project description:Hepatocellular carcinoma (HCC) is a highly lethal cancer for which current available treatment options have limited efficacy. Immunotherapy has emerged as a promising therapeutic option for HCC, yet resistance to immunotherapy is a major challenge. Here, we uncover protein arginine methyltransferase 3 (PRMT3) as a novel driver of immunotherapy resistance in HCC. We show that PRMT3 expression is induced by activated T cells in response to immune checkpoint blockade (ICB) via an interferon-gamma (IFN)STAT1 signaling pathway, and that high PRMT3 expression inversely correlates with tumor-infiltrating CD8+ T cells and predicts poor response to ICB in HCC patients. We demonstrate that genetic depletion and pharmacological inhibition of PRMT3 induce a profound influx of T cells into tumors and activate anti-tumor immunity to suppress HCC progression. Mechanistically, we demonstrate that PRMT3 methylates HSP60, a mitochondrial chaperone protein, at R446, and that this novel post-translational modification is required for HSP60 oligomerization and maintaining mitochondrial homeostasis. We reveal that targeting PRMT3-dependent HSP60-R446 methylation boosts anti-tumor immunity by disrupting mitochondrial function, increasing mitochondrial DNA (mtDNA) leakage, and activating the cGAS/STING pathway, a key innate immune sensor of cytosolic DNA. Importantly, we provide genetic and pharmacologic evidence that targeting PRMT3 enhances anti-PD1 efficacy and anti-tumor immunity in HCC mouse models. Our study identifies PRMT3 as a potential biomarker and therapeutic target to overcome immunotherapy resistance in HCC.
2024-05-29 | GSE249999 | GEO
Project description:Hepatocellular carcinoma (HCC) is a complex and deadly disease lacking druggable genetic mutations. The limited efficacy of systemic treatments for advanced HCC implies that novel predictive biomarkers and drug targets are urgently needed. Most HCC drugs target protein kinases and their kinase-dependent signaling networks to drive HCC progression. To identify HCC signaling networks that determine responses to kinase inhibitors (KIs), we apply a pharmacoproteomics approach integrating kinome activity in 17 HCC cell lines with their responses to 299 KIs, resulting in a comprehensive dataset of pathway-based drug response signatures. By profiling patient HCC samples, we identify signatures of clinical HCC drug responses in individual tumors. Our analyses reveal kinase networks promoting the epithelial-mesenchymal transition (EMT) and drug resistance, including a FZD2-AXL-NUAK1/2 signaling module, whose inhibition reverses the EMT and sensitizes HCC cells to drugs. Our approach identifies cancer drug targets and molecular signatures of drug response for personalized oncology.
2018-12-15 | MSV000083236 | MassIVE