Chromosomal breakage-fusion-bridge events cause genetic intratumor heterogeneity
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Nondisjunction of a single chromosome leads to breakage and activation of DNA damage checkpoint in G2Centrosomal abnormalities, multipolar mitoses, and chromosomal instability in head and neck tumours with dysfunctional telomeresImaging genome abnormalities in cancer researchTherapeutic targeting of replicative immortalityPolo-like kinase 1 licenses CENP-A deposition at centromeresElevated tolerance to aneuploidy in cancer cells: estimating the fitness effects of chromosome number alterations by in silico modelling of somatic genome evolutionSeveral fusion genes identified by whole transcriptome sequencing in a spindle cell sarcoma with rearrangements of chromosome arm 12q and MDM2 amplificationWidespread genomic instability mediated by a pathway involving glycoprotein Ib alpha and Aurora B kinase.Mitotic catenation is monitored and resolved by a PKCĪµ-regulated pathwaySelective regain of egfr gene copies in CD44+/CD24-/low breast cancer cellular model MDA-MB-468.DNA repair pathway selection caused by defects in TEL1, SAE2, and de novo telomere addition generates specific chromosomal rearrangement signatures.Inverted duplication pattern in anaphase bridges confirms the breakage-fusion-bridge (BFB) cycle model for 11q13 amplification.Stabilization of dicentric translocations through secondary rearrangements mediated by multiple mechanisms in S. cerevisiae.Centromere-localized breaks indicate the generation of DNA damage by the mitotic spindle.A common copy-number breakpoint of ERBB2 amplification in breast cancer colocalizes with a complex block of segmental duplications.Expression of the HPV18/E6 oncoprotein induces DNA damage.Chromosomal instability confers intrinsic multidrug resistance.Low molecular weight cyclin E overexpression shortens mitosis, leading to chromosome missegregation and centrosome amplificationStructural and numerical chromosome changes in colon cancer develop through telomere-mediated anaphase bridges, not through mitotic multipolarity.How do tumors make ends meet?Telomere dysfunction triggers extensive DNA fragmentation and evolution of complex chromosome abnormalities in human malignant tumors.Escherichia coli induces DNA damage in vivo and triggers genomic instability in mammalian cellsThe absence of the dna-dependent protein kinase catalytic subunit in mice results in anaphase bridges and in increased telomeric fusions with normal telomere length and G-strand overhang.Increased sensitivity of subtelomeric regions to DNA double-strand breaks in a human cancer cell lineChromosome instability in human lung cancers: possible underlying mechanisms and potential consequences in the pathogenesis.The FEN1 E359K germline mutation disrupts the FEN1-WRN interaction and FEN1 GEN activity, causing aneuploidy-associated cancers.Telomere-based crisis: functional differences between telomerase activation and ALT in tumor progressionBayesian Hidden Markov Modeling of Array CGH DataCancer chromosomal instability: therapeutic and diagnostic challenges.Chromosome instability as a result of double-strand breaks near telomeres in mouse embryonic stem cellsCycles of chromosome instability are associated with a fragile site and are increased by defects in DNA replication and checkpoint controls in yeast.Ladder-like amplification of the type I interferon gene cluster in the human osteosarcoma cell line MG63Aneuploidy and malignancy: an unsolved equation.Checkpoint genes and Exo1 regulate nearby inverted repeat fusions that form dicentric chromosomes in Saccharomyces cerevisiaeHTLV-1 propels untransformed CD4 lymphocytes into the cell cycle while protecting CD8 cells from death.KLF4 Suppresses Tumor Formation in Genetic and Pharmacological Mouse Models of Colonic Tumorigenesis.Stable karyotypes in epithelial cancer cell lines despite high rates of ongoing structural and numerical chromosomal instability.DNA amplification by breakage/fusion/bridge cycles initiated by spontaneous telomere loss in a human cancer cell line.Breakage-fusion-bridge cycles and large insertions contribute to the rapid evolution of accessory chromosomes in a fungal pathogen.The relationship between spontaneous telomere loss and chromosome instability in a human tumor cell line.
P2860
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P2860
Chromosomal breakage-fusion-bridge events cause genetic intratumor heterogeneity
description
2000 nĆ® lÅ«n-bĆ»n
@nan
2000幓ć®č«ę
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2000幓č«ę
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2000幓č«ę
@zh-hant
2000幓č«ę
@zh-hk
2000幓č«ę
@zh-mo
2000幓č«ę
@zh-tw
2000幓č®ŗę
@wuu
2000幓č®ŗę
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@zh-cn
name
Chromosomal breakage-fusion-bridge events cause genetic intratumor heterogeneity
@en
type
label
Chromosomal breakage-fusion-bridge events cause genetic intratumor heterogeneity
@en
prefLabel
Chromosomal breakage-fusion-bridge events cause genetic intratumor heterogeneity
@en
P2093
P2860
P356
P1476
Chromosomal breakage-fusion-bridge events cause genetic intratumor heterogeneity
@en
P2093
D Gisselsson
F Mitelman
L Gorunova
L Pettersson
M Heidenblad
P2860
P304
P356
10.1073/PNAS.090013497
P407
P577
2000-05-01T00:00:00Z