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The genesis and evolution of high-grade serous ovarian cancer

Nature Reviews Cancer volume 10, pages 803–808 (2010)Cite this article

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Abstract

Germline mutation in either BRCA1 or BRCA2 is associated with an increased risk of ovarian cancer, particularly the most common invasive histotype — serous carcinoma. In addition, serous ovarian cancers have an unusually high frequency of other molecular events involving BRCA pathway dysfunction. Recent findings show a high frequency of TP53 mutation, chromosomal instability, distinct molecular subtypes and DNA copy number-driven changes in gene expression. These findings suggest a model in which homologous recombination repair deficiency initiates a cascade of molecular events that sculpt the evolution of high-grade serous ovarian cancer and dictate its response to therapy.

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Figure 1: Comparison of Type I and Type II serous ovarian cancers.
Figure 2: Model outlining the stages of the initiation and progression of high-grade serous ovarian cancer.

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Acknowledgements

Critical feedback during the drafting of this article by the following colleagues was much appreciated: A. Ahmed, K. Alsop, P. Cowin, D. Etemadmoghadam, A. DeFazio, D. Huntsman, J. Sambrook and C. Stewart.

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  1. Department of Biochemistry, David D. L. Bowtell is at the Peter MacCallum Cancer Centre, University of Melbourne, Melbourne 3002, Australia. d.bowtell@petermac.org,

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Bowtell, D. The genesis and evolution of high-grade serous ovarian cancer. Nat Rev Cancer 10, 803–808 (2010). https://doi.org/10.1038/nrc2946

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