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Expression profiles of Telomerase+ vs. ALT+ G3 Atm-/-TERT-ER T-cell lymphomas

ABSTRACT: We used microarray profiling to document the difference between telomerase+ vs. ALT+ T-cell lymphomas developed on G3 Atm-/-TERT-ER genetic background.

ORGANISM(S): Mus musculus

PROVIDER: GSE35044 | GEO | 2012/01/17

SECONDARY ACCESSION(S): PRJNA155951

REPOSITORIES: GEO

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Expression profiles of Telomerase+ vs. ALT+ G3 Atm-/-TERT-ER T-cell lymphomas

Project description:We used microarray profiling to document the difference between telomerase+ vs. ALT+ T-cell lymphomas developed on G3 Atm-/-TERT-ER genetic background. T-cell lymphomas were developed in G3 Atm-/-TERT-ER mice with 4-OHT treatment. These cells were either maintained on SCID mice treated with 4-OHT or vehicle. Cells maintained on vehicle eventually developed ALT-dependent resistance. We used microarray to profile telomerase+ tumors vs. ALT+ tumors from the same parental lines.

2012-01-17 | E-GEOD-35044 | biostudies-arrayexpress

Genomic copy number profiling of different generations of Atm-/-TERT-ER T-cell lymphomas and associated resistant tumors following telomerase inhibition

Project description:Genomic copy numbers of various generations of Atm-/-TERT-ER mice treated with 4-OHT or vehicle were profiled. Genomic copy numbers of transplanted G3 Atm-/-TERT-ER T-cell lymphomas with telomerase or ALT T-cell lymphomas were developed in various generations of Atm-/-TERT-ER mice with 4-OHT or vehicle treatment. These tumors were profiled with aCGH. G3 Atm-/-TERT-ER tumors were transplanted into SCID mice treated with 4-OHT or vehicle. Cells maintained on vehicle eventually developed ALT-dependent resistance. We used aCGH to profile telomerase+ tumors vs. ALT+ tumors from the same parental lines.

2012-01-17 | E-GEOD-35045 | biostudies-arrayexpress

Genomic copy number profiling of different generations of Atm-/-TERT-ER T-cell lymphomas and associated resistant tumors following telomerase inhibition

2012-01-17 | GSE35045 | GEO

Anti-telomerase therapy provokes ALT and mitochondrial adaptive mechanisms

Project description:This SuperSeries is composed of the following subset Series: GSE35044: Expression profiles of Telomerase+ vs. ALT+ G3 Atm-/-TERT-ER T-cell lymphomas GSE35045: Genomic copy number profiling of different generations of Atm-/-TERT-ER T-cell lymphomas and associated resistant tumors following telomerase inhibition Refer to individual Series

2012-01-17 | E-GEOD-35046 | biostudies-arrayexpress

Expression of telomerase prevents ALT and maintains telomeric heterochromatin in juvenile brain tumors.

Project description:The up-regulation of a telomere maintenance mechanism (TMM) is an essential step in cancer progression to escape dysfunctional telomeres, senescence and apoptosis. Paediatric brain tumors frequently exhibit Alternative Lengthening of Telomere (ALT) as active TMM, but the mechanisms involved in the induction of ALT in brain tumor cells are not clear. Here, we report a model of juvenile zebrafish brain tumor that progressively develops ALT. We discovered that reduced expression of tert and increase in Terra expression precedes ALT development. Additionally, tumors show persistent telomeric DNA damage and loss of heterochromatin marks. Comparative analysis of gene expression after the rescue of ALT with telomerase and analysis of telomerase positive paediatric brain cancers showed normalization of telomeric heterochromatin and maintenance of telomere length, with reduced expression of genes of the pre-replicative complex as hallmark. Thus our study identifies telomere maintenance mechanisms as major drivers of DNA replication and chromatin status at telomeres in brain cancers.

2022-07-01 | GSE134135 | GEO

Telomerase is a prognostic marker of poor outcome and a therapeutic target in neuroblastoma

Project description:The aim of this study is to determine the clinical relevance of telomerase activation versus ALT as biomarkers in pre-treatment neuroblastoma, and to assess the potential value of telomerase as a therapeutic target. Therefore, the genomic status of TERT and MYCN was assessed in 457 pretreatment neuroblastomas by fluorescence-in-situ-hybridization. ALT was examined in 273/457 tumors by detection of ALT-associated promyelocytic leukemia nuclear bodies, and TERT expression was determined by 4x44k microarrays in 223 of these. The presence of activated telomerase, i.e., TERT rearrangements, MYCN amplification, or high TERT expression without these alterations, was associated with poorest overall survival, and was an independent prognostic marker in multivariable analyses.

2019-09-16 | E-MTAB-8248 | biostudies-arrayexpress

Evolutionarily conserved role of Telomerase reverse transcriptase (TERT) in programming the microenvironment via regulation of cGAS/STING pathway

Project description:Telomerase holoenzyme plays a critical role in maintaining telomere length, and thus in regulating inflammation caused by telomeric DNA damage. However, beyond its role in telomere maintenance, the molecular function of telomerase in directly regulating inflammation remains unclear. Here, we show that the reverse transcriptase component of telomerase, TERT, has a cell-type-specific role in directly regulating inflammation via the cytoplasmic cGAS-STING nucleic acid-sensing pathway. Analyses of murine and zebrafish models of gut inflammation and human colitis/Crohn’s patients document that this function of TERT is evolutionarily conserved. Using our novel knock-in TERTVAA mouse model where reverse-transcriptase-inactive TERT is driven by its endogenous loci, and molecular, pharmacological and single-cell approaches we identify the myeloid subpopulation, termed T-MAC, wherein TERT enhances STING activation and initiates type-1 interferon responses independent of reverse transcriptase activity or telomere length. We highlight a hitherto unappreciated role of TERT in directly regulating inflammation and provide a therapeutic rationale for targeting TERT beyond cancers.

2024-07-22 | GSE241725 | GEO

A gene expression signature classifying telomerase and ALT immortalization I

Project description:A gene expression signature classifying telomerase and ALT immortalisation reveals an hTERT regulatory network and suggests a mesenchymal stem cell origin for ALT Telomere length is maintained by 2 known mechanisms, activation of telomerase or alternative lengthening of telomeres (ALT). The molecular mechanisms regulating the ALT phenotype are poorly understood and it is unknown how the decision of which pathway to activate is made at the cellular level. We have shown previously that active repression of telomerase gene expression by chromatin remodelling of the promoters is one mechanism of regulation, however other genes and signalling networks are likely to be required to regulate telomerase and maintain the ALT phenotype. Using gene expression profiling we have uncovered a signature of 1305 genes to distinguish telomerase positive and ALT cell lines. By combining this with gene expression profiles of liposarcoma tissue samples we refined this signature to 297 genes significantly associated with telomere maintenance mechanism. Network analysis of known direct interactions between genes within this signature revealed a regulatory signalling network consistent with a model of hTERT repression in ALT cell lines and liposarcomas. This network expands on our existing knowledge of hTERT regulation and provides a platform to understand differential regulation of hTERT in different tumour types and normal tissues. In addition we show evidence to suggest a novel mesenchymal stem cell origin for ALT immortalisation in cell lines and mesenchymal tissues. Keywords: cell type comparison, gene expression

2009-11-02 | GSE14487 | GEO

A gene expression signature classifying telomerase and ALT immortalization II

2009-11-02 | GSE14529 | GEO

Functional loss of ATRX and telomerase activates Alternative Lengthening of Telomeres (ALT)

Project description:The presence of ALT is strongly associated with recurrent cancer-specific somatic inactivating mutations in the ATRX-DAXX chromatin remodeling complex. Here, we generate an ALT-positive adenocarcinoma cell line following functional inactivation of ATRX and telomerase in a telomerase-positive carcinoma cell line.

2019-09-25 | GSE129448 | GEO

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