Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression profile of Hepatocellular Carcinoma

ABSTRACT: Expression profiling of tumor and adjacent non-tumorous tissues of Hepatocellular Carcinoma (HCC) patients. Illumina HumanHT-12 V4.0 expression beadchip was used to obtain expression profiles across more than 31,000 annotated genes. Samples included 59 tumors and 59 adjacent non-tumorous samples. Total RNA obtained from the 39 tumors and 39 adjacent non-tumorous samples

ORGANISM(S): Homo sapiens

SUBMITTER: Lee Caroline

PROVIDER: E-GEOD-57957 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Methylation profiles reveal distinct subgroup of hepatocellular carcinoma patients with poor prognosis.

Mah Way-Champ WC Thurnherr Thomas T Chow Pierce K H PK Chung Alexander Y F AY Ooi London L P J LL Toh Han Chong HC Teh Bin Tean BT Saunthararajah Yogen Y Lee Caroline G L CG

PloS one 20140805 8

Hepatocellular Carcinoma (HCC) is one of the leading causes of cancer-associated mortality worldwide. However, the role of epigenetic changes such as aberrant DNA methylation in hepatocarcinogenesis remains largely unclear. In this study, we examined the methylation profiles of 59 HCC patients. Using consensus hierarchical clustering with feature selection, we identified three tumor subgroups based on their methylation profiles and correlated these subgroups with clinicopathological parameters. ...[more]

PMID: 25093504

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Project description:Disease relapse and resistance to chemotherapy represent challenging issues in a subset of Hodgkin Lymphoma (HL) patients. Activity and mechanism(s) of action of a novel PI3K/ERK dual inhibitor AEZS-136 (Ãterna Zentaris GmbH, Germany, EU) were examined in L-540, SUP-HD1, KM-H2 and L-428 cell lines. Despite exposure to AEZS-136 induced a significant cell growth inhibition (range, 30-80%), levels of caspase-independent cell death and mitochondrial dysfunction, were only observed in L-540 (62 Â±9 vs 14 Â±3%, P â¤.0001) and SUP-HD1 (46 Â±2% vs 15 Â±2%, P â¤.0001) cells. Gene expression profiling indicated that the effects of AEZS-136 treatment are associated with the modulation of cell cycle and cell death pathways. Exposure to AEZS-136 resulted in sustained production of reactive oxygen species (ROS) and activation of necroptotic cell death. The necroptosis inhibitor Necrostatin-1 prevented AEZS-136-induced ROS production, mitochondrial injury, activation of JNK and cell death. Knockdown experiments identified the immediate early response 3 (IER3) as a key signaling molecule that mediates AEZS-136-resistance to oxidative death of HL cells. Furthermore, in vivo xenograft studies demonstrated a 40-70% reduction in tumor burden (P < 0.0001) and a 10-fold increase in tumor necrosis in AEZS-136-treated animals compared to control mice. These data support further clinical evaluation of AEZS-136 in refractory/relapsed HL. The Hodgkin lymphoma cell lines were obtained from the DSMZ (Braunschweig, Germany, EU). Cells were routinely maintained in RPMI medium 1640 (Lonza, Basel, Switzerland) supplemented with 20% FBS (Lonza) and 2 mM glutamine (Lonza). Cells were maintained at 37Â°C in a water-saturated atmosphere of 5% CO2 in air. 4x106 HL cells were seeded in 75 cm2 flask and, after 24 hrs, cells were treated with 10 ÂµM AEZS-136 (Aeterna Zentaris, Frankfurt, Germany, EU) in culture medium for 24 hours. At the end of treatment, cells were collected and RNA extracted.

Dataset Information

Expression profile of Hepatocellular Carcinoma

Publications

Methylation profiles reveal distinct subgroup of hepatocellular carcinoma patients with poor prognosis.

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