Ontology highlight
ABSTRACT:
PROVIDER: PRJDB20347 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR659426.fastq.gz | Fastqsanger.gz | |||
| DRR659427.fastq.gz | Fastqsanger.gz | |||
| DRR659428.fastq.gz | Fastqsanger.gz | |||
| DRR659429.fastq.gz | Fastqsanger.gz | |||
| DRR659430.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 193 |
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Project description:Tumor suppressors are mostly defined by inactivating somatic mutations in tumors, yet little is known about their epigenetic features in normal cells. Here, through integrative analysis of 1,134 genome-wide epigenetic profiles and mutations from >8,200 tumor-normal pairs, we discovered broad H3K4me3 (wider than 4 kb) as the first epigenetic signature for tumor suppressors in normal cells. Broad H3K4me3 is associated with increased transcription elongation and enhancer activity together leading to exceptionally high gene expression, and is distinct from other broad epigenetic features, such as super enhancers. Broad H3K4me3 conserved across normal cells represents core tumor suppressors, such as P53 and PTEN, whereas cell-type-specific broad H3K4me3 may indicate cell-identity genes and cell-type-specific tumor suppressors. Furthermore, widespread shortening of broad H3K4me3 in cancers is strongly associated with repression of tumor suppressors. Together, the broad H3K4me3 epigenetic signature we reported here may provide a new direction for the discovery and characterization of novel tumor suppressors. H3K4me3 ChIP-Seq was conducted in 1) liver tumor and matched tissue, 2) lung tumor and matched tissue, 3) cell line A549 grown under normal and flavopiridol treatment conditions.
2015-07-29 | E-GEOD-67471 | biostudies-arrayexpress
Project description:Tumor suppressors are mostly defined by inactivating somatic mutations in tumors, yet little is known about their epigenetic features in normal cells. Here, through integrative analysis of 1,134 genome-wide epigenetic profiles and mutations from >8,200 tumor-normal pairs, we discovered broad H3K4me3 (wider than 4 kb) as the first epigenetic signature for tumor suppressors in normal cells. Broad H3K4me3 is associated with increased transcription elongation and enhancer activity together leading to exceptionally high gene expression, and is distinct from other broad epigenetic features, such as super enhancers. Broad H3K4me3 conserved across normal cells represents core tumor suppressors, such as P53 and PTEN, whereas cell-type-specific broad H3K4me3 may indicate cell-identity genes and cell-type-specific tumor suppressors. Furthermore, widespread shortening of broad H3K4me3 in cancers is strongly associated with repression of tumor suppressors. Together, the broad H3K4me3 epigenetic signature we reported here may provide a new direction for the discovery and characterization of novel tumor suppressors.
2015-07-29 | GSE67471 | GEO
Project description:The analysis of roles of DROL1 and SUDL1 in defining intron-exon junctions
| PRJDB20390 | ENA
Project description:The analysis of roles of DROL1 and SUDL1 in defining intron-exon junctions
| PRJDB20389 | ENA
Project description:The paper describes a model on the Dynamics of Immune Checkpoints, Immune System, and BCG in the Treatment of Superficial Bladder Cancer.
Created by COPASI 4.25 (Build 207)
This model is described in the article:
Dynamics of Immune Checkpoints, Immune System, and BCG in the Treatment of Superficial Bladder Cancer
Farouk Tijjani Saad, Evren Hincal, and Bilgen Kaymakamzade
Computational and Mathematical Methods in Medicine, vol. 2017, no. 3573082
Abstract:
This paper aims to study the dynamics of immune suppressors/checkpoints, immune system, and BCG in the treatment of superficial bladder cancer. Programmed cell death protein-1 (PD-1), cytotoxic T-lymphocyte-associated antigen 4 (CTLA4), and transforming growth factor-beta (TGF-b) are some of the examples of immune suppressors/checkpoints. They are responsible for deactivating the immune system and enhancing immunological tolerance. Moreover, they categorically downregulate and suppress the immune system by preventing and blocking the activation of T-cells, which in turn decreases autoimmunity and enhances self- tolerance. In cancer immunotherapy, the immune checkpoints/suppressors prevent and block the immune cells from attacking, spreading, and killing the cancer cells, which leads to cancer growth and development. We formulate a mathematical model that studies three possible dynamics of the treatment and establish the effects of the immune checkpoints on the immune system and the treatment at large. Although the effect cannot be seen explicitly in the analysis of the model, we show it by numerical simulations.
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2024-09-02 | BIOMD0000000746 | BioModels