Replication stress induces tumor-like microdeletions in FHIT/FRA3B - Wikidata - awgldk - TriplyDB

Replication stress induces tumor-like microdeletions in FHIT/FRA3B

Replication stress induces tumor-like microdeletions in FHIT/FRA3B

http://www.wikidata.org/entity/Q36423451

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Mechanisms of change in gene copy number Inhibition of topoisomerase I prevents chromosome breakage at common fragile sites Adaptive evolution of pelvic reduction in sticklebacks by recurrent deletion of a Pitx1 enhancer The replication fork: understanding the eukaryotic replication machinery and the challenges to genome duplication Comparative genomics and molecular dynamics of DNA repeats in eukaryotes 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 The FHIT gene product: tumor suppressor and genome "caretaker"Environmental and chemotherapeutic agents induce breakage at genes involved in leukemia-causing gene rearrangements in human hematopoietic stem/progenitor cells.Reduced FHIT expression is associated with mismatch repair deficient and high CpG island methylator phenotype colorectal cancer.DNA double-strand break repair and the evolution of intron density.Over half of breakpoints in gene pairs involved in cancer-specific recurrent translocations are mapped to human chromosomal fragile sites.ATR preferentially interacts with common fragile site FRA3B and the binding requires its kinase activity in response to aphidicolin treatment.Fhit loss in lung preneoplasia: relation to DNA damage response checkpoint activation.DNA breaks at fragile sites generate oncogenic RET/PTC rearrangements in human thyroid cells.Copy number variants are produced in response to low-dose ionizing radiation in cultured cells.Analysis of the t(3;8) of hereditary renal cell carcinoma: a palindrome-mediated translocation.Mechanisms of genomic instabilities underlying two common fragile-site-associated loci, PARK2 and DMD, in germ cell and cancer cell lines Break-induced DNA replication Genome-wide mapping of nuclear mitochondrial DNA sequences links DNA replication origins to chromosomal double-strand break formation in Schizosaccharomyces pombe.DNA instability at chromosomal fragile sites in cancer An oncogenomics-based in vivo RNAi screen identifies tumor suppressors in liver cancer De novo CNV formation in mouse embryonic stem cells occurs in the absence of Xrcc4-dependent nonhomologous end joining.Recovery of arrested replication forks by homologous recombination is error-prone.Pericentromeric regions are refractory to prompt repair after replication stress-induced breakage in HPV16 E6E7-expressing epithelial cells.Hits, Fhits and Nits: beyond enzymatic function.Cell-type-specific replication initiation programs set fragility of the FRA3B fragile site.Genomic instability in induced stem cells DNA topoisomerases participate in fragility of the oncogene RET.Deletion at fragile sites is a common and early event in Barrett's esophagus.Large transcription units unify copy number variants and common fragile sites arising under replication stress Hydroxyurea induces de novo copy number variants in human cells.Aberrant firing of replication origins potentially explains intragenic nonrecurrent rearrangements within genes, including the human DMD gene.The breast cancer susceptibility gene BRCA2 is required for the maintenance of telomere homeostasis.A genome-wide analysis of common fragile sites: what features determine chromosomal instability in the human genome?The role of fragile sites in sporadic papillary thyroid carcinoma Characterization of the role of Fhit in suppression of DNA damage.Role of DNA secondary structures in fragile site breakage along human chromosome 10 Aberrant expression of DNA damage response proteins is associated with breast cancer subtype and clinical features Replication stress induces genome-wide copy number changes in human cells that resemble polymorphic and pathogenic variants.

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Replication stress induces tumor-like microdeletions in FHIT/FRA3B

http://www.wikidata.org/entity/Q36423451

description

2007 nî lūn-bûn

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2007年の論文

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年學術文章

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2007年學術文章

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2007年學術文章

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Replication stress induces tumor-like microdeletions in FHIT/FRA3B

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Replication stress induces tumor-like microdeletions in FHIT/FRA3B

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Replication stress induces tumor-like microdeletions in FHIT/FRA3B

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Replication stress induces tumor-like microdeletions in FHIT/FRA3B

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Replication stress induces tumor-like microdeletions in FHIT/FRA3B

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Replication stress induces tumor-like microdeletions in FHIT/FRA3B

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Proceedings of the National Academy of Sciences of the United States of America

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Replication stress induces tumor-like microdeletions in FHIT/FRA3B

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Jennifer G Mulle

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Martin F Arlt

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Ryan L Ragland

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Sandra G Durkin

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Stephen T Warren

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Thomas W Glover

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P2860

WWOX, a novel WW domain-containing protein mapping to human chromosome 16q23.3-24.1, a region frequently affected in breast cancer

Common chromosomal fragile site FRA16D sequence: identification of the FOR gene spanning FRA16D and homozygous deletions and translocation breakpoints in cancer cells

The FHIT gene, spanning the chromosome 3p14.2 fragile site and renal carcinoma-associated t(3;8) breakpoint, is abnormal in digestive tract cancers

Genetic applications of an inverse polymerase chain reaction

Molecular basis for expression of common and rare fragile sites

High-resolution profiling of histone methylations in the human genome

Modulation of DNA end joining by nuclear proteins

DNA polymerase alpha inhibition by aphidicolin induces gaps and breaks at common fragile sites in human chromosomes

FRA3B extends over a broad region and contains a spontaneous HPV16 integration site: direct evidence for the coincidence of viral integration sites and fragile sites

BRCA1 is required for common-fragile-site stability via its G2/M checkpoint function

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5686108

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18162546

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2224195

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