Aneuploidy and cancer

@article{Sen2000AneuploidyAC,
  title={Aneuploidy and cancer},
  author={Subrata Sen},
  journal={Current Opinion in Oncology},
  year={2000},
  volume={12},
  pages={82-88}
}
  • Subrata Sen
  • Published 2000
  • Medicine
  • Current Opinion in Oncology
Numeric aberrations in chromosomes, referred to as aneuploidy, is commonly observed in human cancer. Whether aneuploidy is a cause or consequence of cancer has long been debated. Three lines of evidence now make a compelling case for aneuploidy being a discrete chromosome mutation event that contributes to malignant transformation and progression process. First, precise assay of chromosome aneuploidy in several primary tumors with in situ hybridization and comparative genomic hybridization… Expand
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  • Biology, Medicine
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References

SHOWING 1-10 OF 43 REFERENCES
Aneuploidy correlated 100% with chemical transformation of Chinese hamster cells.
  • R. Li, G. Yerganian, +4 authors R. Hehlmann
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 1997
TLDR
It is concluded that aneuploidy is the cause rather than a consequence of transformation of cancer, which can explain the numerous unique properties of cancer cells, such as invasiveness, dedifferentiation, distinct morphology, and specific surface antigens. Expand
Genetic instability of cancer cells is proportional to their degree of aneuploidy.
TLDR
It is concluded that aneuploidy is sufficient to explain genetic instability and the resulting karyotypic and phenotypic heterogeneity of cancer cells, independent of gene mutation. Expand
Centrosome defects and genetic instability in malignant tumors.
TLDR
Centrosomes in nearly all tumors and tumor-derived cell lines were atypical in shape, size, and composition and were often present in multiple copies, suggesting they may contribute to genetic instability in cancer. Expand
Mutations of mitotic checkpoint genes in human cancers
TLDR
It is shown that CIN is consistently associated with the loss of function of a mitotic checkpoint in cancers displaying CIN, and in some cancersThe loss of this checkpoint wasassociated with the mutational inactivation of a human homologue of the yeast BUB1 gene; BUB 1 controls mitotic checkpoints and chromosome segregation in yeast. Expand
Molecular karyotype (amplotype) of metastatic colorectal cancer by unbiased arbitrarily primed PCR DNA fingerprinting.
TLDR
Overrepresentation of these chromosomal regions is a critical step for metastatic colorectal cancer, and Comparative amplotype analysis from primary and metastatic tumors suggest the existence in chromosome 4 of gene(s) whose loss is specifically selected in cells that reach the metastatic stage. Expand
Tumour amplified kinase STK15/BTAK induces centrosome amplification, aneuploidy and transformation
TLDR
It is reported that STK15 (also known as BTAK and aurora2), encoding a centrosome-associated kinase, is amplified and overexpressed in multiple human tumour cell types, and is involved in the induction of centrosomes duplication-distribution abnormalities and aneuploidy in mammalian cells. Expand
Genetic instability in colorectal cancers
TLDR
It is shown that colorectal tumours without microsatellite instability exhibit a striking defect in chromosome segregation, resulting in gains or losses in excess of 10 –2 per chromosome per generation, and that such instability can arise through two distinct pathways. Expand
The mitotic machinery as a source of genetic instability in cancer.
TLDR
This review will discuss mitotic defects that cause chromosome missegregation, examine components and regulatory mechanisms of the mitotic machine implicated in cancer, and explore mechanisms by which chromosomeMissegregation could lead to cancer. Expand
Evolution of neoplastic cell lineages in Barrett oesophagus
TLDR
The evolutionary relationships of non-random LOH, TP53 and CD KN2A mutations, CDKN2A CpG-island methylation and ploidy during neoplastic progression are determined and indicate that clonal evolution is more complex than predicted by linear models. Expand
17p (p53) allelic losses, 4N (G2/tetraploid) populations, and progression to aneuploidy in Barrett's esophagus.
  • P. Galipeau, D. Cowan, +5 authors B. Reid
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 1996
TLDR
The results indicate that increased 4N (G2/tetraploid) populations predict progression to aneuploidy and that the development of 4N abnormalities is interdependent with inactivation of the p53 gene in Barrett's esophagus in vivo. Expand
...
1
2
3
4
5
...