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Molecular profiling supports the role of epithelial-to-mesenchymal transition (EMT) in ovarian cancer metastasis

Loukia N Lili1, Lilya V Matyunina1, L DeEtte Walker1, Stephen L Wells2, Benedict B Benigno23 and John F McDonald13*

Author Affiliations

1 Integrated Cancer Research Center, School of Biology, and Parker H. Petit Institute of Bioengineering and Biosciences, Georgia Institute of Technology, 315 Ferst Dr., Atlanta, GA 30332, USA

2 Northside Hospital, 1000 Johnson Ferry Rd, Atlanta, GA 30342, USA

3 Ovarian Cancer Institute, 960 Johnson Ferry Rd, Suite 130, Atlanta GA 30342, USA

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Journal of Ovarian Research 2013, 6:49  doi:10.1186/1757-2215-6-49

Published: 10 July 2013



While metastasis ranks among the most lethal of all cancer-associated processes, on the molecular level, it remains one of the least well understood. One model that has gained credibility in recent years is that metastasizing cells at least partially recapitulate the developmental process of epithelial-to-mesenchymal transition (EMT) in their transit from primary to metastatic sites. While experimentally supported by cell culture and animal model studies, the lack of unambiguous confirmatory evidence in cancer patients has led to persistent challenges to the model’s relevance in humans.


Gene expression profiling (Affymetrix, U133) was carried out on 14 matched sets of primary (ovary) and metastatic (omentum) ovarian cancer (serous adenocarcinoma) patient samples. Hierarchical clustering and functional pathway algorithms were used in the data analysis.


While histological examination reveled no morphological distinction between the matched sets of primary and metastatic samples, gene expression profiling clearly distinguished two classes of metastatic samples. One class displayed expression patterns statistically indistinguishable from primary samples isolated from the same patients while a second class displayed expression patterns significantly different from primary samples. Further analyses focusing on genes previously associated with EMT clearly distinguished the primary from metastatic samples in all but one patient.


Our results are consistent with a role of EMT in most if not all ovarian cancer metastases and demonstrate that identical morphologies between primary and metastatic cancer samples is insufficient evidence to negate a role of EMT in the metastatic process.

Metastasis; Epithelial-to-mesenchymal transition; EMT; Ovarian cancer