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Exploring the Effect and Mechanisms of Telomerase Inhibition as A Novel Therapeutic Strategy for Glioma

ABSTRACT: Exploring the Effect and Mechanisms of Telomerase Inhibition as A Novel Therapeutic Strategy for Glioma

PROVIDER: PRJNA673806 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12964465_1.fastq.gz	Fastqsanger.gz
	SRR12964465_2.fastq.gz	Fastqsanger.gz
	SRR12964466_1.fastq.gz	Fastqsanger.gz
	SRR12964466_2.fastq.gz	Fastqsanger.gz
	SRR12964467_1.fastq.gz	Fastqsanger.gz

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Exploring the Effect and Mechanisms of Telomerase Inhibition as A Novel Therapeutic Strategy for Glioma

Project description:Exploring the Effect and Mechanisms of Telomerase Inhibition as A Novel Therapeutic Strategy for Glioma

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Exploring the Effect and Mechanisms of Telomerase Inhibition as A Novel Therapeutic Strategy for Glioma

Project description:The obejctive of this study is to establish the therapeutic role of 6-thio-dG for gliomas in vitro and in vivo and to elucidate the anti-tumor mechanisms of 6-thio-dG in glioma cells. And the ultimate goal of this proposal is to demonstrate the potential of 6-thio-dG as a novel strategy for primary and recurrent glioma.

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Exploring the Effect and Mechanisms of Telomerase Inhibition as A Novel Therapeutic Strategy for Glioma [2224, DBTGR-05MG, A172]

Project description:Exploring the Effect and Mechanisms of Telomerase Inhibition as A Novel Therapeutic Strategy for Glioma [2224, DBTGR-05MG, A172]

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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

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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.

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Therapeutic effects of telomerase in mice with pulmonary fibrosis induced by damage to the lungs and short telomeres

Project description:In our previous study, mice with pulmonary fibrosis induced by a bleomycin insult in the context of short telomeres develop pulmonary fibrosis. By using AAV9 vectors carrying the telomerase Tert gene to treat those mice, we explore the possibility of telomerase gene therapy as a possible treatment for IPF patients carrying short telomeres. To further understand gene expression changes undergoing in ATII cells upon telomerase activation, we isolated ATII cells from pulmonary fibrosis Tert-treated and empty vector-treated lungs at 1 week after AAV9 inoculation by FACS.

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Ablation of Telomerase and Ku86

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Project description:life strategy

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Telomerase-mediated Strategy for Overcoming Non-Small Cell Lung Cancer Targeted Therapy and Multi-drug Chemotherapy Resistance

Project description:Standard and targeted therapies almost universally fail due to tumor heterogeneity/plasticity leading to intrinsic or acquired drug resistance. We used the telomerase substrate precursor 6-thio-2’-deoxyguanosine (6-thio-dG) to target telomerase-expressing targeted therapy and platin-doublet chemotherapy resistant cells. We observed that erlotinib, paclitaxel/carboplatin and gemcitabine/cisplatin resistant cells are sensitive to 6-thio-dG in xenograft, syngeneic immunocompetent and genetically engineered mouse models. We also show sensitivity to 6-thio-dG on a large panel of non-small cell lung cancer cell lines (73 of 77). The 4 resistant NSCLC lines clustered together, providing a molecular signature for patients that may not respond to 6-thio-dG. We find SLC43A3 as a top candidate in this molecular signature. Thus, 6-thio-dG may prolong disease control of therapy-resistant lung cancer patients.

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