Journal
CANCER DISCOVERY
Volume 1, Issue 7, Pages 580-586Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/2159-8290.CD-11-0215
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Funding
- NIH [CA016672, CA110793, CA109298, P50 CA083639, P50 CA098258, CA128797, RC2GM092599, U54 CA151668]
- Ovarian Cancer Research Fund, Inc.
- Department of Defense (DOD) [OC073399, W81XWH-10-1-0158, BC085265]
- Marcus Foundation
- Blanton-Davis Ovarian Cancer Research Program
- Betty Anne Asche Murray Distinguished Professorship
- National Cancer Institute [CA009666]
- NCI-DHHS-NIH [T32 CA101642]
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Metastasis is a complex, multistep process that begins with the epithelial-mesenchymal transition (EMT). Circulating tumor cells (CTC) are believed to have undergone EMT and thus lack or express low levels of epithelial markers commonly used for enrichment and/or detection of such cells. However, most current CTC detection methods target only EpCAM and/or cytokeratin (CK) to enrich epithelial CTCs, resulting in failure to recognize other, perhaps more important, CTC phenotypes that lack expression of these markers. Here, we describe a population of complex aneuploid CTCs that do not express CK or CD45 antigen in patients with breast, ovarian, or colorectal cancer. These cells were not observed in healthy subjects. We show that the primary epithelial tumors were characterized by similar complex aneuploidy, indicating conversion to an EMT phenotype in the captured cells. Collectively, our study provides a new method for highly efficient capture of previously unrecognized populations of CTCs. SIGNIFICANCE: Current assays for CTC capture likely miss populations of cells that have undergone EMT. Capture and study of CTCs that have undergone EMT would allow a better understanding of the mechanisms driving metastasis. Cancer Discovery; 1(7); 580-6. (C) 2011 AACR.
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