Ontology highlight
ABSTRACT:
PROVIDER: PRJNA590111 | ENA |
REPOSITORIES: ENA
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Project description:The cell of origin of hepatoblastoma in humans and mice (HB) is unknown; it has been hypothesized to be a transformed hepatocyte, an oval cell, or a multipotent hepatic progenitor cell. In mice, the current dogma is that HBs arise within hepatocellular neoplasms as a result of further transformation from a neoplastic hepatocyte. However, there is little evidence in the literature to support a direct relationship between these two cell types. Furthermore, due to differences in etiology and development of hepatoblastoma between mice and humans, many have questioned the relevance of these tumors in hazard identification and risk assessment. In order to better understand the relationship between hepatocellular carcinoma and hepatoblastoma, as well as better determine the molecular similarities between mouse and human hepatoblastoma, global gene expression analysis and targeted Hras and Ctnnb1 mutation analysis were performed using concurrent hepatoblastoma, hepatocellular carcinoma, and associated normal adjacent liver (in the context of vehicle control liver) samples from a recent National Toxicology Program chronic bioassay. The data from this study provides a better understanding of the origins of hepatoblastoma in the B6C3F1 mice and the relevance of mouse hepatoblastoma to humans when considering chemical exposures of potential human cancer risk. Compare mouse hepatoblastoma versus adjacent hepatocellular carcinomas versus adjacent non-tumor liver and vehicle control normal liver, 6 replicates each group.
2015-09-01 | E-GEOD-67316 | biostudies-arrayexpress
Project description:To explore the miRNA expression profiles between HBV-related Hepatocellular carcinoma and no HBV-related Hepatocellular carcinoma To performe microarray analysis to detect the miRNA expression profiles between HBV-related Hepatocellular carcinoma and no HBV-related Hepatocellular carcinoma
2021-05-29 | GSE151441 | GEO
Project description:Gene expression study in hepatocellular carcinoma
| PRJNA117467 | ENA
Project description:The cell of origin of hepatoblastoma in humans and mice (HB) is unknown; it has been hypothesized to be a transformed hepatocyte, an oval cell, or a multipotent hepatic progenitor cell. In mice, the current dogma is that HBs arise within hepatocellular neoplasms as a result of further transformation from a neoplastic hepatocyte. However, there is little evidence in the literature to support a direct relationship between these two cell types. Furthermore, due to differences in etiology and development of hepatoblastoma between mice and humans, many have questioned the relevance of these tumors in hazard identification and risk assessment. In order to better understand the relationship between hepatocellular carcinoma and hepatoblastoma, as well as better determine the molecular similarities between mouse and human hepatoblastoma, global gene expression analysis and targeted Hras and Ctnnb1 mutation analysis were performed using concurrent hepatoblastoma, hepatocellular carcinoma, and associated normal adjacent liver (in the context of vehicle control liver) samples from a recent National Toxicology Program chronic bioassay. The data from this study provides a better understanding of the origins of hepatoblastoma in the B6C3F1 mice and the relevance of mouse hepatoblastoma to humans when considering chemical exposures of potential human cancer risk.
2015-09-01 | GSE67316 | GEO
Project description:Recurrence and metastasis remain the major obstacles to prognosis of hepatocellular carcinoma (HCC), but the relationship between phosphoproteomics and drug targets need to be studied more systematically. In this study, we performed the phosphoproteomics data collected from 18 paired HCC patients to establish the phosphoproteomics profiles of HCC and provide an important resource to explore the relationships between protein phosphorylation and drug targets in HCC. Our data bring new insights on multi-omics data and have the potential to further understand the relationship between post-translational modification (PTM) levels of proteins and different molecular and clinical features of HCC patients. XAD1—XAD18 --- HCC adjacent normal tissues XC1—XC18--- HCC tumor tissues
2025-04-07 | PXD047213 | Pride
Project description:To investigate the relationship between MIF and SPP1, we induced THP-1 cells with lentivirus carrying SPP1 shRNA and negative control virus into HCC-TAMs and 4IPP-treated HCC-TAMs (tumor associated macrophages in hepatocellular carcinoma).
2023-07-10 | GSE230666 | GEO
Project description:Purpose: Renal medullary carcinoma (RMC) is a highly aggressive malignancy defined by the loss of the SMARCB1 tumor suppressor. It mainly affects young individuals of African descent with sickle cell trait, and it is resistant to conventional therapies used for other renal cell carcinomas. This study aimed to identify potential biomarkers for early detection and disease monitoring of RMC. Experimental Design: Integrated profiling of primary untreated RMC tumor tissues and paired adjacent kidney controls was performed using RNA-sequencing (RNA-seq) and histone Chromatin Immunoprecipitation Sequencing (ChIP-seq). The expression of serum cancer antigen 125 (CA-125), was prospectively evaluated in 47 patients with RMC. Functional studies were conducted in RMC cell lines to assess the effects of SMARCB1 re-expression and MUC16 knockdown. Results: MUC16, encoding for CA-125, was identified as one of the top upregulated genes in RMC tissues, with concomitant enrichment of active histone marks H3K4me3 and H3K27ac at its promoter. Elevated serum CA-125 levels were found in 31 of 47 (66%) RMC patients and correlated significantly with metastatic tumor burden (p = 0.03). SMARCB1 re-expression significantly reduced MUC16 expression in RMC cell lines. Functional studies in RMC cell lines demonstrated that SMARCB1 re-expression significantly reduced MUC16 expression, and that MUC16 knockdown induced apoptosis and reduced cell proliferation. Conclusions: The correlation between serum CA-125 levels and metastatic burden suggests that CA-125 is a clinically relevant biomarker for RMC. These findings support further exploration of CA-125 for disease monitoring and targeted therapeutics in RMC.
2025-01-07 | GSE284394 | GEO
Project description:Purpose: Renal medullary carcinoma (RMC) is a highly aggressive malignancy defined by the loss of the SMARCB1 tumor suppressor. It mainly affects young individuals of African descent with sickle cell trait, and it is resistant to conventional therapies used for other renal cell carcinomas. This study aimed to identify potential biomarkers for early detection and disease monitoring of RMC. Experimental Design: Integrated profiling of primary untreated RMC tumor tissues and paired adjacent kidney controls was performed using RNA-sequencing (RNA-seq) and histone Chromatin Immunoprecipitation Sequencing (ChIP-seq). The expression of serum cancer antigen 125 (CA-125), was prospectively evaluated in 47 patients with RMC. Functional studies were conducted in RMC cell lines to assess the effects of SMARCB1 re-expression and MUC16 knockdown. Results: MUC16, encoding for CA-125, was identified as one of the top upregulated genes in RMC tissues, with concomitant enrichment of active histone marks H3K4me3 and H3K27ac at its promoter. Elevated serum CA-125 levels were found in 31 of 47 (66%) RMC patients and correlated significantly with metastatic tumor burden (p = 0.03). SMARCB1 re-expression significantly reduced MUC16 expression in RMC cell lines. Functional studies in RMC cell lines demonstrated that SMARCB1 re-expression significantly reduced MUC16 expression, and that MUC16 knockdown induced apoptosis and reduced cell proliferation. Conclusions: The correlation between serum CA-125 levels and metastatic burden suggests that CA-125 is a clinically relevant biomarker for RMC. These findings support further exploration of CA-125 for disease monitoring and targeted therapeutics in RMC.
2025-01-07 | GSE284319 | GEO
Project description:Recurrence and metastasis remain the major obstacles to prognosis of hepatocellular carcinoma (HCC), but the relationship between proteomics and poor prognosis need to be studied more systematically. In this study, we performed the proteomics data collected from 85 HCC tumors and 18 adjacent normal tissues (ANTs) to establish the proteomics profiles of HCC and reveal the correlation between poteomics and ubiquitomics features of tumor tissues in HCC. Our data bring new insights on multi-omics data and have the potential to further understand the relationship between post-translational modification (PTM) levels of proteins and different molecular and clinical features of HCC patients. XAD1—XAD18 --- HCC adjacent normal tissues XC1—XC85--- HCC tumor tissues
2025-04-07 | PXD047168 | Pride