ObjectiveTo evaluate the significance of CK19 mRNA monitoring in peripheral blood of breast cancer patients.MethodsPeripheral blood samples were collected from 137 breast cancer patients preoperatively,one day post-operation,7 days,1,3,6,12,18,and 24 months after operation.RTPCR was used to detect CK19 mRNA expression.The relationships were analyzed between CK19 mRNA expression and treatment result, between CK19 mRNA expression and clinicopathological parameters.ResultsThere was no significant difference between the level of CK19 mRNA as tested preoperatively,and 1,7 days postoperatively(P ＞ 0.05 ).From one month and thereafter,CK 19 mRNA decreased significantly when compared with that immediate perioperatives ( P ＜ 0.05 ). Postoperative peripheral CK19 mRNA expression increased in those found with recurrent or metastasized tumors ( P ＜ 0.01 ). CK19 mRNA expression does not correlate with patient's menstrual status,estrogen receptor expression,progesterone receptor expression,HER-2 expression and Ki67 proliferation expression (P ＞ 0.05 ). But there was statistically significant correlation between CK19 mRNA expression and tumour size,histology grading,pathological type,lymph node metastasis ( P ＜ 0.01 ).ConclusionsIn breast cancer patients peripheral blood CK19 mRNA expression is correlated with risk clinicopathological parameters, and increases in patients with postoperative recurrence and tumor metastasis.

Background and purpose: Multidrug resistance of tumor cells is the main factor for the failure of chemotherapy. It is found that the apigenin has the anti-tumor effect, but its role in multidrug resistant cells was rarely reported. This study aimed to investigate the effect of apigenin on multidrug resistant breast cancer cell line MCF-7/ADR, and to explore the role of apigenin in reversing multidrug resistance. Methods: The MCF-7/ADR cells were cultured with different concentrations of apigenin, and the same cells were cultured with ADR in the control group. Thecell proliferation was detected by MTT, the cell cycle distribution was detected by PI, and the cell apoptosis was detect-ed by Annexin V/PI. The drug sensitivity in vitro was detected by the method of MTT, and the drug retention rate was detected by rhodamine 123 accumulation. The expression of P-gp protein was measured by Western blot, the RT-PCR method was used to detect the transcription of multidrug resistance gene MDR1. Results: The MCF-7/ADR cell prolif-eration was inhibited by the apigenin, the cell cycle progression was blocked by the apigenin, and the cell apoptosis was induced by the apigenin. There were significant differences between the apigenin group and the ADR group (P<0.05). The IC50 of ADR on MCF-7/ADR cell was (12.37±0.18) μg/mL with the apigenin effect, while the IC50 of ADR on MCF-7/ADR cell was (39.83±0.29) μg/mL without the apigenin effect (P<0.05). The reversal index was 3.22. The retention rate of rhodamine 123 in MCF-7/ADR cells in the apigenin group was higher than that in the ADR group. The MDR1 gene transcription level in MCF-7/ADR cells was higher than that in the MCF-7 cells, and the P-gp expression in MCF-7/ADR cells was higher than that in the MCF-7 cells. However, the level of MDR1 gene transcription and P-gp expression were down-regulated by the apigenin in the MCF-7/ADR cells. Conclusion: The apigenin had anti-MCF-7/ADR effect, and played the role of reversing multidrug resistance in the MCF-7/ADR cells. The mechanism may be related to down-regulation of the MDR1 gene transcription and the P-gp mediated drug e?ux function.