To evaluate the cardioprotective effects of dexrazoxane (DEX) on breast cancer patients who received anthracycline-containing chemotherapy.A total of 122 breast cancer patients after operation were randomly divided into two groups: The experimental group of 61 cases treated with EPI plus DEX (DEX:EPI = 10:1) as adjuvant chemotherapy regimen, and the control group of 61 cases treated with EPI but without DEX. All patients received four cycles of adjuvant chemotherapy and their changes of specific cardiac functional status and hematology status before and after chemotherapy, as well as non-cardiac toxicity were observed and analyzed.Brain natriuretic peptide (BNP) before chemotherapy and after four cycles of chemotherapy in the control group was (106.78 ± 4.52)×10(-6) µg/ml and (187.19 ± 8.71)×10(-6) µg/ml, respectively, with a significant difference between them (P < 0.05). It in the experimental group was (102.34 ± 8.76)×10(-6) µg/ml and (105.29 ± 7.21)×10(-6) µg/ml, respectively, without a significant difference (P > 0.05). Cardiac troponin T (cTnT) before chemotherapy and after four cycles of chemotherapy in the control group was (12.55 ± 2.73)×10(-3) µg/ml and ( 31.05 ± 7.10 )×10(-3) µg/ml, respectively, with a significant difference between them (P < 0.05). It in the experimental group was (12.70 ± 2.15)×10(-3) µg/ml and (13.65 ± 7.82)×10(-3) µg/ml, respectively, without a significant difference (P > 0.05). The hart rate (HR) before chemotherapy and after four cycles of chemotherapy in the control group, was 75.32 ± 7.14 bpm and 89.60 ± 9.21 bpm, respectively, with a significant difference (P < 0.05). It in the experimental group was 78.60 ± 6.29 bpm and 83.10 ± 7.56 bpm, respectively, without a significant difference (P > 0.05). The left ventricular ejection fraction (LVEF) before chemotherapy and after four cycles of chemotherapy in the control group was (65.23 ± 7.82)% and (55.21 ± 7.23)%, respectively, with a significant difference between them (P < 0.05). It in the experimental group was (64.12 ± 6.25)% and (59.6 ± 4.72)%, respectively, without a significant difference (P > 0.05). The absolute neutrophil count before chemotherapy and after four cycles of chemotherapy in the control group was (3.95 ± 1.36)×10(9)/L and (3.50 ± 1.52)×10(9)/L, respectively, without a significant difference (P > 0.05). It in the experimental group, was (4.96 ± 1.41)×10(9)/L and (3.10 ± 1.26)×10(9)/L, respectively, with a significant difference (P < 0.05). The incidence of grade I-IV bone marrow suppression in the experimental group was 21.3%, 16.4%, 24.6%, and 4.9%, respectively. It in the control group was 16.4%, 11.5%, 9.8%, and 5.5%, respectively, with a significant difference (P < 0.05).Cardiac toxicity after anthracycline treatment in breast cancer patients may be significantly reduced by DEX, without increase of non-cardiac and and non-hematologic toxicity. DEX combined with anthracycline increases the risk of bone marrow suppression, therefore, peripheral blood picture should be monitored or routine bone marrow support may be needed.
Abstract: A purpose of this study was to establish a novel molecular diagnostic model and provide new insight into the intraoperative evaluation of the sentinel lymph node (SLN) metastasis in breast cancer. A total of 124 breast cancer patients who met the criteria of sentinel lymph node biopsy (SLNB) and underwent intraoperative biopsy were consecutively enrolled in this study. After the SLNs obtained from each patient were labeled, MOC-31 monoclonal antibody-mediated immunomagnetic separation (IMS) and flow cytometry were used to determine the expressions of breast cancer metastasis-related markers, including Mucin 1 (MUC1), CD44v6, and HER2. Alternatively, conventional intraoperative hematoxylin and eosin (HE) staining and cytokeratin immunohistochemistry (CK-IHC) were performed to detect potential SLN metastasis. The sensitivity, specificity, and false-negative rate of the three intraoperative diagnostic methods were compared and analyzed. A total of 55 positive-SLNs were found in 38 breast cancer patients using IMS, yielding a sensitivity of 86.4% (38/44), specificity of 94.7% (36/38), accuracy of 93.5% (116/124), false-positive rate of 2.5% (2/80), false-negative rate of 13.6% (6/44), positive predictive value of 95.5% (42/44), and negative predictive value of 93.0% (80/86). Patients with high expressions of CD44v6, MUC1, and HER2 in SLNs tended to have higher number of positive lymph nodes, among which the MUC1 and HER2 showed significant differences ( P <0.05). Therefore, compared with conventional HE staining and CK-IHC, IMS technology has remarkably higher sensitivity and specificity and relative lower false-negative rate, thus making it an effective and feasible intraoperative detection method of SLN for breast cancer diagnosis to some extent. Keywords: immunomagnetic separation, breast cancer, sentinel lymph node, MUC1, CD44v6, HER2
To determine the clinical, pathological and prognostic features associated with triple-negative breast cancer (TNBC).Clinical and histologic data of 21,749 breast cancer patients who were treated at Tianjin Medical University Cancer Institute and Hospital between July 2002 and December 2011 were collected. Patients were divided into two groups: those with TNBC and those with other types of breast cancer. Patients and tumor characteristics were compared between the two groups using the Chi-square test. The prognostic results of 9,823 patients in the study population were also analyzed to determine long-term survival rates in the two groups of breast cancer patients.Among the breast cancer patients treated in our hospital between 2003 and 2011, 10.4%-13.5% of them had triple-negative breast cancers. Data analyses revealed significant differences in disease onset age, family history of breast cancer, tumor size, tumor histologic grade, lymph note positivity and metastatic status between TNBC and non-TNBC patients. There were also significant differences in 5-year, 7-year and 9-year disease-free and 7-year and 9-year overall survival probability between the groups.TNBC are associated with younger disease onset age, larger tumor size, higher rate of axillary lymph node positivity, and higher tumor histologic grade. TNBC is also related to family history of breast cancer, increased metastatic risk and poor prognosis.
Introduction: Previous studies have found that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was involved in the progression of pulmonary hypertension (PH), and TRAIL knocking (KO) has an inhibitory effect on PH, but its mechanism is not completely clear. Methods: The effects of TRAIL on the accumulation of extracelluar matrix (ECM), which is one of the most important processes of vascular remodeling, were observed in mice and isolated pulmonary artery smooth muscle cells (PASMCs). In vivo, mice were divided into four groups: Control group (n = 5), hypoxia-induced PH mice group (n = 8), anti-TRAIL antibody (TRAIL-Ab) treatment group (n = 8) and IgG antibody (IgG) group (n = 8). The effects of TRAIL-Ab on ECM expression in hypoxic induced PH were researched; in vivo, PASMCs were divided into three groups: Control group, hypoxia-induced group, TRAIL-Ab group. Expressions of p-Smad2/3 and p-Smad1/5/8 were compared among the three groups. Results: Hypoxia-induced PH mice had significant increases in right ventricle systolic pressure (RVSP) (P < 0.001), right ventricular hypertrophy (RVH) (P = 0.007), vascular stenosis (P < 0.001) compared with controls. Mice with anti-TRAIL antibody had lower levels in RVSP (P < 0.001), RVH (P < 0.001), vascular stenosis (P < 0.001) than PH mice. Besides, the TRAIL-Ab significantly inhibited the phosphorylation of Smad2/3 compared with hypoxia-induced group. Conclusion: TRAIL regulates the accumulation of ECM in pulmonary artery by activating pSmad2/3.
Objective: Propofol is a common intravenous anesthetic in cancer resection surgery, which is considered to exhibit anti-tumor effect in various cancer types. This study was aimed at investigating the role and mechanism of propofol in breast cancer stemness and proliferation. Methods: The breast cancer cells with propofol treatment were sequenced. The expression of FOXO3 in propofol treated cells was detected by RT-qPCR and Western blot. The CSC properties were analyzed by screen cells with ESA+CD44+CD24-/low through flow cytometry and the proliferation capacity were also detected. The expression correlation of FOXO3 and target genes were detected by western blot. The potential binding site of FOXO3 on SOX2 was predicted by JASPAR and verified by dual-luciferase reporter assay and ChIP assay. Results: FOXO3 was found to be upregulated in propofol 24h-treated cells. Propofol could inhibit the capacity of breast cancer cell stemness and proliferation by upregulation FOXO3, which inhibited SOX2 expression transcriptionally. Conclusion: In this study, we uncovered the role of propofol-FOXO3-SOX2 in breast cancer cell stemness and proliferation, which might serve as potential targets for breast cancer therapy.
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