CTCs from patients with CRPC have specialized markers

A team of researchers at Duke University have shown that most men with castration-resistant prostate cancer (mCRPC) express multiple epithelial proteins in their circulating T cells (CTCs).

In a new paper by Armstrong et al. in Molecular Cancer Research, the Duke team has been able to build on an earlier, pre-clinical model of prostate cancer to demonstrate the following:

  • Epithelial to mesenchymal transitions (EMTs) can be identified in the CTCs of men with castration-resistant prostate cancer (as well as in women with metastatic breast cancer).
  • >80 percent of the CTCs in men with metastatic CRPC co-express
    • Epithelial proteins (e.g., epithelial cell adhesion molecule [EpCAM], cytokeratin, and E-cadherin)
    • Mesenchymal proteins (e.g., vimentin, N-cadherin, and O-cadherin)
    • The stem cell marker CD133
  • > 75 percent of the CTCs from women with metastatic breast cancer co-express
    • Cytokeratin
    • Vimentin
    • N-Cadherin
  • These findings have potential implications for the application and interpretation of approved methods to detect CTCs.

The blood tests currently approved by the U.S. Food & Drug Administration for detection of CTCs already “flag” molecules associated with epithelial transitions. What the Duke team has now been able to do is to add new targets that can potentially enhance the usefulness and sensitivity of the currently available tests.

In a media release from the Duke Cancer Institute, Dr. Armstrong is quoted as stating that “Cancer is a hijacking of [the] normal embryonic stem cell process. It reactivates this silent program that is turned off in adult cells, allowing tumor cells to move throughout the body and become resistant to therapy.”

What is very important to appreciate in the potential of this research finding is that it may offer new opportunities that go way beyond the short-term possibility to improve the identification of CTCs. It may also make possible novel therapies for prostate cancer (and for breast cancer) that target these “morphing” mechanisms.

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