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Título

Centromere fission, not telomere erosion, triggers chromosomal instability in human carcinomas

AutorMartínez-Alonso, Carlos; Van Wely, Karel H. M.
Palabras claveCancer
Chromosomal instability
Mitosis
Spindle defect
Breakage-fusion-bridge
Fecha de publicación2011
EditorOxford University Press
CitaciónCarcinogenesis 32(6): 796-803 (2011)
ResumenThe majority of sporadic carcinomas suffer from a kind of genetic instability in which chromosome number changes occur together with segmental defects. This means that changes involving intact chromosomes accompany breakage-induced alterations. Whereas the causes of aneuploidy are described in detail, the origins of chromosome breakage in sporadic carcinomas remain disputed. The three main pathways of chromosomal instability proposed until now (random breakage, telomere fusion, and centromere fission) are largely based on animal models and in vitro experiments, and recent studies revealed several discrepancies between animal models and human cancer. Here, we discuss how the experimental systems translate to human carcinomas and compare the theoretical breakage products to data from patient material and cancer cell lines. The majority of chromosomal defects in human carcinomas comprise pericentromeric breaks that are captured by healthy telomeres, and only a minor proportion of chromosome fusions can be attributed to telomere erosion or random breakage. Centromere fission, not telomere erosion, is therefore the most likely trigger of chromosomal instability and early carcinogenesis. Similar centromere-telomere fusions might drive a subset of congenital defects and evolutionary chromosome changes.
Descripción8 páginas, 6 figuras.-- El PDF del artículo esta en pre-print.
Versión del editorhttp://dx.doi.org/10.1093/carcin/bgr069
URIhttp://hdl.handle.net/10261/34691
DOI10.1093/carcin/bgr069
ISSN0143-3334
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