Oncogene-induced replication stress preferentially targets common fragile sites in preneoplastic lesions. A genome-wide study. - Wikidata - awgldk - TriplyDB

Oncogene-induced replication stress preferentially targets common fragile sites in preneoplastic lesions. A genome-wide study.

Oncogene-induced replication stress preferentially targets common fragile sites in preneoplastic lesions. A genome-wide study.

http://www.wikidata.org/entity/Q40034793

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Telomere dysfunction and chromosome instability Fragile histidine triad protein, WW domain-containing oxidoreductase protein Wwox, and activator protein 2gamma expression levels correlate with basal phenotype in breast cancer Common fragile sites: genomic hotspots of DNA damage and carcinogenesis Ataxia-telangiectasia: future prospects Tumor Suppressor Genes within Common Fragile Sites Are Active Players in the DNA Damage Response Snaps and mends: DNA breaks and chromosomal translocations Initiation of genome instability and preneoplastic processes through loss of Fhit expression Fhit loss in lung preneoplasia: relation to DNA damage response checkpoint activation.Identification of the elementary structural units of the DNA damage response.PTEN C-terminal deletion causes genomic instability and tumor development.Telomere loss as a mechanism for chromosome instability in human cancer WWOX, the common fragile site FRA16D gene product, regulates ATM activation and the DNA damage response.Genome stability control by checkpoint regulation of tRNA gene transcription.Are common fragile sites merely structural domains or highly organized "functional" units susceptible to oncogenic stress?Rescue from replication stress during mitosis.Cell-type-specific replication initiation programs set fragility of the FRA3B fragile site.Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.Fragile site instability in Saccharomyces cerevisiae causes loss of heterozygosity by mitotic crossovers and break-induced replication.The replicometer is broken: telomeres activate cellular senescence in response to genotoxic stresses.High level of chromosomal aberration in ovarian cancer genome correlates with poor clinical outcome Lac operator repeats generate a traceable fragile site in mammalian cells Stress-induced DNA damage biomarkers: applications and limitations.A genome-wide analysis of common fragile sites: what features determine chromosomal instability in the human genome?Folate levels modulate oncogene-induced replication stress and tumorigenicity Urothelial tumor initiation requires deregulation of multiple signaling pathways: implications in target-based therapies.Genome-wide profiles of H2AX and γ-H2AX differentiate endogenous and exogenous DNA damage hotspots in human cells.Evidence for chromosome fragility at the frataxin locus in Friedreich ataxia.Mechanisms of telomere loss and their consequences for chromosome instability.Characterization of the role of Fhit in suppression of DNA damage.A TRF1-controlled common fragile site containing interstitial telomeric sequences.Role of DNA secondary structures in fragile site breakage along human chromosome 10 The ATM signaling network in development and disease.Aberrant expression of DNA damage response proteins is associated with breast cancer subtype and clinical features Global organization of replication time zones of the mouse genome Nucleotide deficiency promotes genomic instability in early stages of cancer development Alternative lengthening of telomeres: recurrent cytogenetic aberrations and chromosome stability under extreme telomere dysfunction.The ubiquitin-proteasome system in cancer, a major player in DNA repair. Part 1: post-translational regulation.Genome-wide reorganization of histone H2AX toward particular fragile sites on cell activation.Studies of genomic copy number changes in human cancers reveal signatures of DNA replication stress Early replication fragile sites: where replication-transcription collisions cause genetic instability.

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Oncogene-induced replication stress preferentially targets common fragile sites in preneoplastic lesions. A genome-wide study.

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Initial sequencing and analysis of the human genome

The Hallmarks of Cancer

The tumor spectrum in FHIT-deficient mice

Molecular basis for expression of common and rare fragile sites

Targeted deletion of Wwox reveals a tumor suppressor function

Genetic instabilities in human cancers

Initiation of the breakage-fusion-bridge mechanism through common fragile site activation in human breast cancer cells: the model of PIP gene duplication from a break at FRA7I

Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions

DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis

Circular binary segmentation for the analysis of array-based DNA copy number data

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