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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Cyclin E dysregulation and chromosomal instability in endometrial cancer.

Deregulation of cyclin E, an activator of cyclin-dependent kinase 2 (Cdk2), has been associated with a broad spectrum of human malignancies. Yet the mechanism linking abnormal cyclin E expression to carcinogenesis is largely unknown. The gene encoding the F-box protein hCdc4, a key component of the molecular machinery that targets cyclin E for degradation, is frequently mutated in endometrial cancer, leading to deregulation of cyclin E expression. Here we show that hCDC4 gene mutation and hyperphosphorylation of cyclin E, a parameter that usually correlates with hCDC4 mutation, have a strong statistically significant association with polypoidy and aneuploidy in endometrial cancer. On the contrary, elevated expression of cyclin E by itself was not significantly correlated with polyploidy or aneuploidy when tumors of similar grade are evaluated. These data suggest that impairment of cell cycle regulated proteolysis of cyclin E may be linked to carcinogenesis by promoting genomic instability.[1]

References

  1. Cyclin E dysregulation and chromosomal instability in endometrial cancer. Hubalek, M.M., Widschwendter, A., Erdel, M., Gschwendtner, A., Fiegl, H.M., Müller, H.M., Goebel, G., Mueller-Holzner, E., Marth, C., Spruck, C.H., Reed, S.I., Widschwendter, M. Oncogene (2004) [Pubmed]
 
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