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Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer [RRBS]

ABSTRACT: Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer [RRBS]

PROVIDER: PRJNA193503 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR787347_1.fastq.gz	Fastqsanger.gz
	SRR787347_2.fastq.gz	Fastqsanger.gz
	SRR787348_1.fastq.gz	Fastqsanger.gz
	SRR787348_2.fastq.gz	Fastqsanger.gz
	SRR787349_1.fastq.gz	Fastqsanger.gz

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Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer [RRBS]

Project description:Genetic and epigenetic alterations are essential for the initiation and progression of human cancer. We previously reported that primary human medulloblastomas showed extensive cancer-specific CpG island DNA hypermethylation in critical developmental pathways. To determine whether genetically engineered mouse models (GEMMs) of medulloblastoma have comparable epigenetic changes, we assessed genome-wide DNA methylation in three mouse models of medulloblastoma. In contrast to human samples, very few loci with cancer-specific DNA hypermethylation were detected, and in almost all cases the degree of methylation was relatively modest compared to the dense hypermethylation in the human cancers. To determine if this finding was common to other GEMMs, we examined a Burkitt lymphoma and breast cancer model and did not detect promoter CpG island DNA hypermethylation, suggesting that human cancers and at least some GEMMs are fundamentally different with respect to this epigenetic modification. These findings provide an opportunity to both better understand the mechanism of aberrant DNA methylation in human cancer and construct better GEMMs to serve as preclinical platforms for therapy development. Examination of DNA methylation in one representative human medulloblastoma patient sample and three different mouse models of medulloblastoma using RRBS

2013-10-10 | E-GEOD-45341 | biostudies-arrayexpress

Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer [RRBS]

2013-10-10 | GSE45341 | GEO

Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer [Methylation profiling by array]

2013-10-10 | GSE45240 | GEO

Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer [Methylation profiling by array]

Project description:Genetic and epigenetic alterations are essential for the initiation and progression of human cancer. We previously reported that primary human medulloblastomas showed extensive cancer-specific CpG island DNA hypermethylation in critical developmental pathways. To determine whether genetically engineered mouse models (GEMMs) of medulloblastoma have comparable epigenetic changes, we assessed genome-wide DNA methylation in three mouse models of medulloblastoma. In contrast to human samples, very few loci with cancer-specific DNA hypermethylation were detected, and in almost all cases the degree of methylation was relatively modest compared to the dense hypermethylation in the human cancers. To determine if this finding was common to other GEMMs, we examined a Burkitt lymphoma and breast cancer model and did not detect promoter CpG island DNA hypermethylation, suggesting that human cancers and at least some GEMMs are fundamentally different with respect to this epigenetic modification. These findings provide an opportunity to both better understand the mechanism of aberrant DNA methylation in human cancer and construct better GEMMs to serve as preclinical platforms for therapy development. Genome-wide DNA methylation profiles generated using the Denaturation Analysis of Methylation Differences (DAMD) assay of cancer versus normal samples.

2013-10-10 | E-GEOD-45240 | biostudies-arrayexpress

Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer.

Project description:Genetic and epigenetic alterations are essential for the initiation and progression of human cancer. We previously reported that primary human medulloblastomas showed extensive cancer-specific CpG island DNA hypermethylation in critical developmental pathways. To determine whether genetically engineered mouse models (GEMMs) of medulloblastoma have comparable epigenetic changes, we assessed genome-wide DNA methylation in three mouse models of medulloblastoma. In contrast to human samples, very few loci with cancer-specific DNA hypermethylation were detected, and in almost all cases the degree of methylation was relatively modest compared with the dense hypermethylation in the human cancers. To determine if this finding was common to other GEMMs, we examined a Burkitt lymphoma and breast cancer model and did not detect promoter CpG island DNA hypermethylation, suggesting that human cancers and at least some GEMMs are fundamentally different with respect to this epigenetic modification. These findings provide an opportunity to both better understand the mechanism of aberrant DNA methylation in human cancer and construct better GEMMs to serve as preclinical platforms for therapy development.

| S-EPMC3933486 | biostudies-literature

Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer [Methylation profiling by array]

Project description:Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer [Methylation profiling by array]

| PRJNA193489 | ENA

Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-10-10 | GSE45342 | GEO

Circular RNA CpG Island Hypermethylation-Associated Silencing in Human Cancer

Project description:Although less than 2% of the human genome code for proteins, most studies in cancer research has focused in this small portion of our DNA. However, it has been recognized in the last years that non-coding RNAs (ncRNAs) also participate in cellular transformation. In this context, microRNAs and long noncoding RNAs (lncRNAs) can act as oncogenes or tumor suppressor genes. Recent work have also demonstrated that ncRNAs with growth-inhibitory functions can undergo promoter CpG island hypermethylation-associated silencing in tumorigenesis. Herein, we wondered whether circular RNAs (circRNAs), a type of RNA transcripts lacking 5’-3´ends and forming closed loops that are gaining relevance in cancer biology, are also a target of epigenetic inactivation in tumors. To tackle this issue, we have used cancer cells genetically deficient for the DNA methyltransferase enzymes in conjuction with circRNA expression microarrays. We have found that the loss of DNA methylation provokes a release of circRNA silencing. We have particularly identified that promoter CpG island hypermethylation of the genes TUSC3 (tumor suppressor candidate 3), POMT1 (protein O-mannosyltransferase 1), ATRNL1 (attractin-like 1) and SAMD4A (sterile alpha motif domain containing 4A) is linked to the transcriptional downregulation of both linear mRNA and the hosted circRNA. Although a role in the control of the parental gene has been shown for some circRNAs, we did not observe changes in TUSC mRNA levels upon TUSC3 circ104557 overexpression. Most importantly, data mining for 5’-end CpG island methylation of TUSC3, ATRNL1, POMT1 and SAMD4A in a large collection of human cancer cell lines and primary tumors showed that the epigenetic defect was commonly observed among different tumor types, where it was also associated with the diminished expression of the corresponding transcript. Our findings support a role for circRNA DNA methylation-associated loss in human cancer.

2018-06-13 | GSE109676 | GEO

Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-10-10 | E-GEOD-45342 | biostudies-arrayexpress

Circular RNA CpG Island Hypermethylation-Associated Silencing in Human Cancer

Project description:Circular RNA CpG Island Hypermethylation-Associated Silencing in Human Cancer

| PRJNA431634 | ENA