Abstract
Abstract Introduction: Estrogen receptor (ER) status in all breast cancer patients is recommended by immunohistochemistry (IHC) and is considered standard practice for selection of treatment options. However, the analytical sensitivity of IHC in detecting low levels of ER is often poor and likely due to methodological variation. Because biopsy is not often feasible in all patients presenting with recurrent and/or metastatic breast disease, circulating tumor cells (CTCs) offer an attractive alternative source of tumor tissue for determining ER status and can be monitored more readily to enable a more effective course of treatment. Experimental Design: Twenty ml of peripheral blood was collected prospectively from # patients diagnosed with late stage metastatic/recurrent breast cancer. CTCs were isolated using the microfluidic OncoCEE™ platform. A cocktail of antibodies was utilized for CTC capture and detection with an expanded anti-cytokeratin (CK) cocktail mixture and anti-CD45. ER protein expression was assessed by immunocytochemistry (ICC) on the cells captured within the microchannels and compared to IHC performed on the primary tumor. Results: CK+/CD45- cells were detected in 23 of 27 cases (85%). Among the 23 cases in which CK+ cells were detected, only moderate concordance (16/23; 70%) in ER status between primary tumor and CTCs was observed. Conclusions: There is significant heterogeneity between ER protein expression in CTCs and primary tumor. ER ICC on CTCs from peripheral blood using the OncoCEE™ platform is shown to be feasible but the comparison likely compromised by lack of tumor staging at the time of blood draw. Given that IHC was in some cases performed 5–10 years pre-blood draw and that tumors have the potential to convert, ER status only moderately correlates to the IHC status in the primary tumor. The significance of heterogeneity at the ER protein level in CTCs ascertaining to the prognosis and predictive response to anti-estrogen therapy needs further evaluation in larger prospective clinical trials. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P5-01-08.
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