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Objective To observe the levels of serum VEGF in different molecular subtypes of breast cancer and explore its relationship with response to neoadjuvant chemotherapy. Methods Levels of serum VEGF in 110 cases with breast cancer underwent neoadjuvant chemotherapy were detected by ELISA prior to and after 3 cycles of neoadjuvant chemotherapy. Clinical response to neoadjuvant chemotherapy was evaluated by physical examination and ultrasonography. Results Levels of serum VEGF were significantly increased in breast cancer patients with≥4 lymph node metastasis than those with < 4 lymph node[(307.31 ± 101.42) pg/mL vs. (170.16 ± 73.07) pg/mL,P = 0.017]. Patients with positive HER-2 status had significantly higher levels of serum VEGF than those with HER-2 negative status [(235.15 ± 88.42 ) pg/mL vs. (179.82 ± 69.90) pg/mL, P = 0.024]. No significant difference was observed among age , menopausal status and hormone status. In patients with neoadjuvant chemotherapy of cCR and Cpr,the mean levels of serum VEGF were (205.75 ± 78.12) pg/mL and (226.04 ± 89.04) pg/mL, respectively. After 3 cycles of chemotherapy, levels of serum VEGF decreased to (145.15 ± 67.08) pg/mL and (161.27 ± 93.57) pg/mL. There was significant difference between two groups (P=0.009,0.014). In patients with SD or PD response, no significant difference was observed between levels of serum VEGF before and after chemotherapy (P = 0.577). Conclusions Levels of serum VEGF in breast cancer correlate with lymph nodes metastasis and HER-2 status and may decrease after neoadjuvant chemotherapy. However,whether or not the levels of serum VEGF can be used as a biomarker for response to neoadjuvant chemotherapy needs more further studies.
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Objective To study the dissociation of EDTA-dependent pseudo platelet aggregation by amikacin and to clarify the potential mechanism.Methods At different time points,two concentrations of amikacin (6.5 mg/ml and 10.0 mg/ml) were respectively added to EDTA-K2 anti-coagulated whole blood samples collected from two subjects with EDTA-dependent pseudothrombocytopenia.The aggregated-platelet dissociation was investigated by platelet count and microscopical examination.CD41,CD61,CD62p,PAC-1,and IgG on the platelets of the two patients and of a normal control were determined by the FCS under various conditions.Results When amikacin (6.5 mg/ml) was added within 1 hour after blood collection,it dissociated the EDTA induced platelet aggregation and the platelet counts returned to the normal level. The expression of CD62p,PAC-1,and PA-IgG on the platelets was decreased,yet the expression of CD41 and CD61 had no change.Conclusion Amikacin supplementation (6.5 mg/ml) within 1 hour after blood sampling may dissociate the aggregated platelets caused by EDTA. The mechanism may be associated that amikacin might inhibit the expression of CD62p,PAC-1,and PA-IgG on platelets. The amikacin supplementation would be an inexpensive,effective,and practical method to solve the platelet aggregation induced by EDTA.