983e99e9-5c32-41cb-9203-2e9d678e5b99 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001008216 | EGA |
REPOSITORIES: EGA
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Project description:RNA-seq dataset (BAM files) of 28 HCCs and 19 non-tumor livers derived from 8 patients undergoing sorafenib treatment.
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Project description:Due to the global obesity epidemic the incidences of nonalcoholic steatohepatitis (NASH) and NASH-related hepatocellular carcinoma (HCC) are on the rise. Non-invasive treatment options for HCC are scarce and innovative therapy regimes are urgently needed. The mechanistic target of rapamycin (mTOR) is of fundamental importance for the regulation of cellular metabolism and mTOR pathway activation is frequently observed in HCCs. However, mTOR inhibition failed to benefit the clinical course of HCC patients, demonstrating the need for a better understanding of the molecular and functional consequences of blocking mTOR signaling in primary liver cancer. To address this, we established a tumor cell-specific inactivation of mTOR in a murine model of non-alcoholic steatohepatitis (NASH)-driven HCC. After 30 weeks of diet, tumor, and liver volumes as well as whole body fat percentage were evaluated by non-invasive in vivo micro-computed tomography (µCT), and livers were collected for subsequent analyses. Unexpectedly, the tumor load exploded in mTORLEC livers and knock-out mice showed improved glucose tolerance among other signs of major metabolic alterations. Detailed proteome analysis indicated extensive changes in arachidonic and bile acid metabolism in the liver. The simulation of metformin intervention via kinetic modeling predicted the existence of a therapeutic window, in which the drug selectively targets mTORLEC HCC tissue.
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Project description:Hepatocellular carcinoma (HCC) affects millions of people worldwide and is a lethal malignancy for which there are no effective therapies. To identify prognostic gene markers for liver cancer, we conducted transcriptome profiling of frozen tissues (tumor and non-tumor) from 300 early-to-advanced stage HCCs plus 40 cirrhotic and 6 normal livers. We have profiles 268 HCC tumor, 243 adjacent non-tumor, 40 cirrhotic and 6 healthy liver samples.
2011-07-05 | E-GEOD-25097 | biostudies-arrayexpress
Project description:Hepatocellular carcinoma (HCC) affects millions of people worldwide and is a lethal malignancy for which there are no effective therapies. To identify prognostic gene markers for liver cancer, we conducted transcriptome profiling of frozen tissues (tumor and non-tumor) from 300 early-to-advanced stage HCCs plus 40 cirrhotic and 6 normal livers.
2011-07-05 | GSE25097 | GEO
Project description:Hepatocellular carcinoma (HCC) remains a major health problem worldwide, and HCC patients have a poor prognostic outcome. In this study, we systematically disclose mechanisms of hepatocarcinogenesis, and also effectively identify and validate novel anticancer targets in HCCs. Keywords: disease state analysis total 58 cDNA microarrays, all experiment samples are hepatocellular carcinoma. RNAs from 33 corresponding noncancerous livers and 5 normal livers were used as the reference, respectively. The tumor samples were labeled with Cy5-dUTP.The nontumor samples were labeled with Cy3-dUTP.
2009-01-06 | E-GEOD-4108 | biostudies-arrayexpress
Project description:Hepatocellular carcinoma (HCC) is one of the most common and lethal cancers worldwide and has a poor prognosis. Promoters represent an essential regulatory element of gene transcription in the human genome. In order to understand the promoter methylation in relation with gene transcription in HCCs, we applied a liquid hybridization capture-based bisulfite sequencing (LHC-BS) approach to examine the promoter methylome of HCCs, for which we customized 150,407 capture probes and enabled coverage of 91.8% of the RefSeq gene promoters within the human genome. We found the differential promoter DNA methylation between HCCs and peripheral normal tissues. Then we integrated promoter methylomic and transcriptomic profiling and described gene expression and regulation in HCCs. Lastly, we validated the key genes in a larger number of samples and screened candidate genes aberrantly regulated by DNA methylation in human HCCs. Capture-based whole genome promoter bisulfite-seq for 8 pairs of HCC tumor and non-tumor liver (NTL) samples.
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Project description:Generation of a new library of targeted mass spectrometry assays for accurate protein quantification in malignant and normal kidney tissue. Aliquots of primary tumor tissue lysates from 86 patients with initially localized renal cell carcinoma (RCC), 75 patients with metastatic RCC treated with sunitinib or pazopanib in the first line and 17 adjacent normal tissues treated at Masaryk Memorial Cancer Institute (MMCI) in Brno, Czech Republic, or University Hospital Pilsen (UHP), Czech Republic, were used to generate the spectral library. Two previously published datasets (dataset A and B) and two newly generated RCC datasets (dataset C and D) were analyzed using the newly generated library showing increased number of quantified peptides and proteins, depending on the size of the library and LC-MS/MS instrumentation. This PRIDE project also includes quantitative analysis results for all four datasets and raw files for dataset C and D. Dataset A is characterized in DOI: 10.1038/nm.3807. It consists of 18 samples from 9 RCC patients involving one cancer and non-cancerous sample per patient. Dataset B is characterized in DOI: 10.3390/biomedicines9091145. It consists of 16 tumor samples and 16 adjacent normal tissues from 16 mRCC patients treated at Masaryk Memorial Cancer Institute (MMCI) in Brno, Czech Republic. Dataset C involves only tumor tissues from dataset B. Half of them responded to sunitinib treatment in the first line three months after treatment initiation and half did not. Dataset D involves 16 RCC patients treated at University Hospital Pilsen (UHP), Czech Republic. All were localized at the time of initial diagnosis, half of the tumors developed distant metastasis in five years after the diagnosis.
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