Your browser doesn't support javascript.
loading
Single-chromosome Gains Commonly Function as Tumor Suppressors.
Sheltzer, Jason M; Ko, Julie H; Replogle, John M; Habibe Burgos, Nicole C; Chung, Erica S; Meehl, Colleen M; Sayles, Nicole M; Passerini, Verena; Storchova, Zuzana; Amon, Angelika.
Afiliación
  • Sheltzer JM; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA; David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Electronic address: sheltzer@cshl.edu.
  • Ko JH; David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Replogle JM; David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Habibe Burgos NC; David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Chung ES; Albert Einstein College of Medicine, Bronx, NY 10461, USA.
  • Meehl CM; David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Sayles NM; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
  • Passerini V; Group Maintenance of Genome Stability, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
  • Storchova Z; Group Maintenance of Genome Stability, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany; Department of Molecular Genetics, University of Kaiserslautern, 67663 Kaiserslautern, Germany.
  • Amon A; David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Electronic address: angelika@mit.edu.
Cancer Cell ; 31(2): 240-255, 2017 02 13.
Article en En | MEDLINE | ID: mdl-28089890
Aneuploidy is a hallmark of cancer, although its effects on tumorigenesis are unclear. Here, we investigated the relationship between aneuploidy and cancer development using cells engineered to harbor single extra chromosomes. We found that nearly all trisomic cell lines grew poorly in vitro and as xenografts, relative to genetically matched euploid cells. Moreover, the activation of several oncogenic pathways failed to alleviate the fitness defect induced by aneuploidy. However, following prolonged growth, trisomic cells acquired additional chromosomal alterations that were largely absent from their euploid counterparts and that correlated with improved fitness. Thus, while single-chromosome gains can suppress transformation, the genome-destabilizing effects of aneuploidy confer an evolutionary flexibility that may contribute to the aggressive growth of advanced malignancies with complex karyotypes.
Asunto(s)
Palabras clave

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Aberraciones Cromosómicas / Aneuploidia / Neoplasias Límite: Animals / Humans Idioma: En Revista: Cancer Cell Asunto de la revista: NEOPLASIAS Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Aberraciones Cromosómicas / Aneuploidia / Neoplasias Límite: Animals / Humans Idioma: En Revista: Cancer Cell Asunto de la revista: NEOPLASIAS Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos