Abstract P3-06-28: Use of the MiCK drug-induced apoptosis assay improves clinical outcomes in recurrent breast cancer (BRCA)

Abstract

Abstract Background: The microculture kinetic (MiCK) assay (Correct Chemo™) correlates with outcomes in acute myelocytic leukemia and ovarian cancer (Cancer Research, in press). A prior trial suggested that its use in breast cancer could improve clinical outcomes (Cancer, in press). This study was designed to correlate MiCK assay results with clinical outcomes in recurrent or metastatic BRCA. Methods: 30 patients with recurrent or metastatic breast cancer in 4 different institutions were evaluated. Each patient (pt) had a BRCA biopsy sent to a central laboratory, tumor cells were purified to over 90% homogeneity, and were then cultured with individual drugs or drug combinations. The induction of apoptosis was measured every five minutes continuously for 48 hours. The amount of apoptosis was expressed in kinetic units (KU), and results were sent to the attending oncologist within 72 hours of submission. Physicians were free to choose any treatment plan for the pts, and were free to add hormonal therapy or biotherapy. Clinical results were evaluated by oncologists using clinical criteria and the results of the MiCK assay were correlated with outcomes of complete (CR) or partial (PR) response, time-to-relapse (TTR), and overall survival (OS). Results: Median age was 57 years, and number of lines of prior therapy was a median of 2 (range 1–8). Median ECOG performance status was 1. The total number of drugs tested in the assay was a median of 12 (range 3–31). The MiCK assay was used to help select therapy in 22 pts (73%). There was change between drugs originally planned before MiCK assay and drugs used after MiCK in 15 pts (50%). The best therapy from the MiCK assay was used for treatment in 16 pts (53%). In five pts (17%), a single drug was used in place of a combination. Generic drugs were used in place of proprietary drugs in nine pts (30%). Hormonal therapy was added to drugs selected based on the MiCK assay in seven pts (23%), and bio-therapy drugs were added to chemotherapy drugs in eight pts (27%). If the MiCK results were used to help select therapy, eight pts had a CR or PR (27%), compared to 0 pts with CR or PR if MiCK was not used (p = 0.04). If the MiCK assay was used to determine therapy, 17 pts (59%) had a CR, PR or stable disease compared to only 2 pts (6.9%) in whom the MiCK assay was not used (p < 0.01). The TTR was significantly longer if the MiCK assay was used to select chemotherapy, 7.4 months, compared to only 2.2 months if the MiCK assay was not used (p < 0.01). There was a trend toward longer survival if the MiCK assay was used, 16.8 months, compared to 13.1 months if the MiCK assay was not used, but the difference was not statistically significant (p = 0.3). If the best chemotherapy from the MiCK assay was used, there were trends for increased TTR (7.3 vs 3.9 mo if best not used p = 0.13) and increased rate of CR or PR or stable (54% vs 17% p = 0.11). Conclusions: Use of the MiCK assay to determine chemotherapy was associated with a higher response rate and a longer time to relapse in pts with recurrent or metastatic BRCA. It is possible that OS is also improved, but longer follow up is needed. There was a trend for improved outcomes if the best chemotherapy based on the MiCK assay was used. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P3-06-28.