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Integrated analysis of ovarian juvenile granulosa cell tumors reveals distinct epigenetic signatures and recurrent TERT rearrangements

ABSTRACT: Integrated analysis of ovarian juvenile granulosa cell tumors reveals distinct epigenetic signatures and recurrent TERT rearrangements

PROVIDER: PRJNA793908 | ENA |

REPOSITORIES: ENA

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Integrated analysis of ovarian juvenile granulosa cell tumors reveals distinct epigenetic signatures and recurrent TERT rearrangements

Project description:Genome wide DNA methylation profiling of ovarian granulosa cell tumors. The Illumina Infinium EPIC Human DNA methylation Beadchips were used to obtain DNA methylation profiles across 32 samples. JGCTs show a distinct methylation signature compared to AGCTs

2022-12-28 | GSE192967 | GEO

TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors

Project description:Whole genome sequencing detected structural rearrangements of TERT in 17/75 high stage neuroblastoma with 5 cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted immediate up- and down-stream regions of TERT, placing in 7 cases a super-enhancer close to the breakpoints. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high stage neuroblastoma, each associated with very poor prognosis

2015-10-21 | GSE73537 | GEO

HDAC inhibition suppresses telomerase activity in neuroblastoma cells harboring TERT rearrangements

Project description:HDAC inhibition suppresses telomerase activity in neuroblastoma cells harboring TERT rearrangements

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Chromosomal rearrangements juxtapose the TERT coding sequence to strong enhancer elements

Project description:Chromosomal rearrangements juxtapose the TERT coding sequence to strong enhancer elements

| PRJNA613274 | ENA

TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors

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HDAC inhibition suppresses telomerase activity in neuroblastoma cells harboring TERT rearrangements [array]

Project description:HDAC inhibition suppresses telomerase activity in neuroblastoma cells harboring TERT rearrangements [array]

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Chromosomal rearrangements juxtapose the TERT coding sequence to strong enhancer elements

Project description:Chromatin immunoprecipitation (ChIP) sequencing with an anti-acetyl-H3K27 antibody showed an enhancer region rearranged to the TERT gene, and ChIP sequencing with an anti-BRD4 antibody showed BRD4 protein binding to the enhancer in TERT-rarranged neuroblasstoma PDX CCI-NB07-RMT cells

2021-03-01 | GSE147181 | GEO

E4F1 and ZNF148 are transcriptional activators of the A57C and wildtype TERT promoter

Project description:Point mutations within the TERT promoter are the most common recurrent somatic non-coding mutation identified across different cancer types, including glioblastoma, melanoma, hepatocellular carcinoma and bladder cancer. They are most abundant at C146T and C124T and more rare at A57C, with the latter originally described as a familial case but subsequently shown also to occur somatically. All three mutations create de novo ETS (E-twenty-six specific) binding sites and result in the reactivation of the TERT gene, allowing cancer cells to achieve replicative immortality. Here, we employed a systematic proteomics screen to identify transcription factors preferentially binding to the C146T, C124T and A57C mutations. While we confirmed binding of multiple ETS factors to the mutant C146T and C124T sequences, we identified E4F1 a an A57C-specific binder and ZNF148 as a TERT WT binder that is excluded from the TERT promoter by the C124T allele. Both proteins are activating transcription factors that bind specifically to the A57C and wildtype (at position 124) TERT promoter sequence in corresponding cell lines and upregulate TERT transcription and telomerase activity.

2023-11-04 | PXD037776 | Pride

HDAC inhibition suppresses telomerase activity in neuroblastoma cells harboring TERT rearrangements [ChIP-Seq]

Project description:HDAC inhibition suppresses telomerase activity in neuroblastoma cells harboring TERT rearrangements [ChIP-Seq]

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Identification of recurrent chromosome breaks underlying structural rearrangements in mammary cancer cell lines [Break-seq]

Project description:Cancer genomes are characterized by accumulation of small-scale somatic mutations as well as large-scale chromosomal deletions, amplifications, and complex structural rearrangements. This characteristic is at least partially dependent on the ability of cancer cells to undergo recurrent chromosome breakage. In order to address to what extent chromosomal structural rearrangement breakpoints correlate with recurrent DNA double strand breaks (DSBs), we simultaneously mapped chromosome structural variation breakpoints by whole genome DNA-seq and spontaneous DSB formation by Break-seq in the breast cancer cell line MCF-7 and a non-cancer control cell line MCF-10A. We identified concurrent DSBs and structural variation breakpoints almost exclusively in the pericentromeric region of chromosome 16q in MCF-7 cells. We fine-tuned the identification of copy number variation breakpoints on 16q. In addition, we detected recurrent DSBs that occurred in both MCF-7 and MCF-10A. We propose a model for DSB-driven chromosome rearrangements that led to the translocation of 16q, likely with 10q, and the eventual 16q loss that does not involve the pericentromere of 16q. We present evidence from RNA-seq data that select genes, including SHCBP1, ORC6 and MYLK3, which are immediately downstream from the 16q pericentromere show heightened expression in MCF-7 cell line compared to the control. Data published by The Cancer Genome Atlas showed that all three genes have increased expression in breast tumor samples. We suggest that these genes are potential oncogenes for breast cancer progression. The search for tumor suppressor loss that accompanies the 16q loss ought to be augmented by the identification of potential oncogenes that gained expression during chromosomal rearrangements.

2022-07-12 | GSE207714 | GEO

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