Abstract P3-02-04: QM-FISH analysis of the genes involved in the G1/S checkpoint signaling pathway in triple-negative breast cancer

Abstract

Abstract OBJECTIVES: To analyze copy number alterations(CNAs) of the genes involved in the G1/S checkpoint signaling pathway of triple-negative breast cancer (TNBC) and non- triple-negative breast cancer(non-TNBC) and in order to find specific CNAs associated with overall survive for TNBC.In all,to provide an effective target for future treatment. METHODS: We selected the samples randomly form Tianjin Cancer Hospital between August, 2006 and August, 2007,which contained one hundred TNBC cases and one hundred non-TNBC cases. Quantitative mμlti-gene fluorescence in situ hybridization (QM-FISH) was used to study CNAs of the genes involved in the G1/S checkpoint signaling pathway, including CCND1,c-Myc,p21, CHEK2, p16, Rb1, Mdm2and p53. RESULTS: The amplification rates of c-Myc and the deletion rates of p53 in TNBC tended to be higher than those in non-TNBC, whereas the amplification rates of CCND1 and Mdm2 in non-TNBC tended to be higher than those in TNBC. In Kaplan-Meier analysis, the amplification of CCND1 (P = 0.02) and c-Myc (P = 0.02) as well as the deletion of p53 (P = 0.01) predicted worse survival in the TNBC group. While in the non-TNBC group, the amplification of CCND1 (P = 0.01) and Mdm2 (P = 0.04) as well as the deletion of p53 (P = 0.049) were associated with worse survival. The amplification of c-Myc and the deletion of p53 in TNBC were associated with higher mortality risk (HR,2.87;95%CI,1.14-7.21[P = 0.03]; HR, 3.34;95%CI, 1.22-9.09 [P = 0.02]), whereas the mortality risk tended to be higher in the patients with amplification of CCND1 (HR, 4.35;95%CI,1.23-15.39 [P = 0.02])in non-TNBC. CONCLUSIONS: The amplification rates of c-Myc and deletion rates of p53 in TNBC tended to be higher than those in non-TNBC, whereas the amplification rate of CCND1 and Mdm2 tended to be higher in non-TNBC. c-Myc and p53 were independent prognostic factors for TNBC, while CCND1 was the independent prognostic factors for non-TNBC. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P3-02-04.