目的探讨乳腺腺肌上皮瘤临床特点、诊断及治疗方法。方法回顾性分析乳腺腺肌上皮瘤6例。结果6例均表现为乳腺包块，直径在1.5～3 cm之间，对其均行乳腺包块切除术。术后随访6个月～6年，无复发。结论乳腺腺肌上皮瘤为良性肿瘤，首选治疗为包括肿瘤组织的局部扩大切除术。
【Abstract】ObjectiveTo investigate the expressions of hTERT mRNA and BRCA1 protein and to analyze the correlation between these two factors in breast cancer. MethodsThe expression of hTERT mRNA was examined by reverse transcription polymerase chain reaction (RT-PCR). The expression of BRCA1 protein was examined by immunohistochemistry. ResultsThe positive rates of hTERT mRNA and BRCA1 protein were 72.1%（31/43） and 34.9%（15/43） in breast cancer tissue, were 5.0%(2/40) and 77.5%(31/40) in paracancerous breast tissue respectively. Significant difference existed between breast cancer tissue and paracancerous breast tissue (P＜0.05). Significant negative correlation existed between the expression of BRCA1 protein and expression of hTERT mRNA （r=-0.995, P＜0.01）. ConclusionThe expression of hTERT mRNA is upregulated in breast cancer, and expression of BRCA1 protein is downregulated in breast cancer. BRCA1 protein expression may be associated with expression of hTERT mRNA in breast cancer, which may be involved in the carcinogenesis of breast cancer.
【摘要】目的 分析原发性乳腺恶性淋巴瘤（primary breast lymphoma,PBL)的临床特点、诊断和治疗。方法 回顾我院2001～2004年收治的3例PBL并复习有关文献，分析其临床特征、诊断情况和治疗方法。结果 3例均为非何杰金淋巴瘤（NHL），属B细胞源性。PBL分期均为Ⅱ期。结论 PBL早期正确诊断，行手术、放疗和化疗联合治疗，效果满意。
Objective To investigate the feasibility and operation effect of endoscopic sentinel lymph node biopsy （SLNB） in breast cancer. Methods The data of 410 breast cancer patients who underwent SLNB （including 107 patients with endoscopy and 303 with open operation） were analyzed in our hospital from January 2009 to March 2012. SLNB was performed by using methylene blue staining or the combination of methylene blue and 99Tcm-sulfur colloid tracing. Results The successful rate of SLN detection with methylene blue and 99Tcm-sulfur colloid tracing was 94.56% （139/147） in open operation group and 94.25% （82/87） in endoscopy group. The successful rate of SLN detection with methylene blue was 88.46% （138/156）in open operation group and 85.00% （17/20） in endoscopy group. The mean of detected SLN number with combined method or methylene blue was 1.90/1.98 in open operation group and 1.91/1.82 in endoscopy group respectively. SLN-positive rate was 22.30% （31/139） and 25.36% （35/138） in open operation group， and 19.51% （16/82） and 23.53% （4/17） in endoscopy group， respectively. The rate of subcutaneous effusion in endoscopy group was higher than that in open operation group （P=0.001）, but other postoperative complications presented no significant difference. Conclusions Endoscopic SLNB can obtain the similar safety and the clinical efficacy with traditional SLNB， but superior cosmetic effect. So it is worthy of clinical application in breast cancer.
ObjectiveTo explore the effects of exogenous estrogen receptor β1 (ERβ1) gene on the expression of human telomerase reverse transcriptase (hTERT) as well as the changes of proliferation ability in MDA-MB-231 cell line by transfecting recombinant eukaryotic expressing vector containing ERβ1 cDNA into human breast cancer MDA-MB-231 cell. MethodsRecombinant eukaryotic expressing vector containing ERβ1 cDNA was transfected into human breast cancer MDA-MB-231 cell by using cationic liposome as transfecting agent (acted as pcDNA3.1ERβ1 transfection group), empty vector group and non-transfection group acted as controls. The expression levels in both the mRNA and protein of both the ERβ1 and hTERT were tested by real-time PCR and Western blot, respectively. The change of proliferation ability in MDA-MB-231 cell was displayed by cell growth curve, and the change of cell apoptosis was detected by flow cytometry. ResultsThe expression level of ERβ1 mRNA in the pcDNA3.1-ERβ1 transfection group (0.449±0.077) significantly increased as compared with the nontransfection group (0.153±0.035) or the empty vector group (0.160±0.020), P=0.001 or P=0.000. The expression level of ERβ1 protein in the pcDNA3.1-ERβ1 transfection group (0.847±0.065) significantly increased as compared with the non-transfection group (0.356±0.050) or the empty vector group (0.390±0.030), P=0.001 or P=0.000. The expression level of hTERT mRNA in the pcDNA3.1-ERβ1 transfection group (0.127±0.020) significantly decreased as compared with the non-transfection group (0.283±0.025) or the empty vector group (0.283±0.049), P=0.001 or P=0.002. The expression level of hTERT protein in the pcDNA3.1-ERβ1 transfection group (0.147±0.023) significantly decreased as compared with the non-transfection group (0.783±0.025) or the empty vector group (0.802±0.019), P=0.001 or P=0.002. The rate of cell apoptosis in the pcDNA3.1-ERβ1 transfection group 〔(6.15±0.94)%〕 was higher than that in the non-transfection group 〔(1.41±0.42)%〕， P=0.001. Cell proliferation curve showed that proliferation ability significantly decreased in the pcDNA3.1-ERβ1 transfected groups as compared with the non-transfection group (Plt;0.05). ConclusionERβ1 could inhibit cell growth of human breast cancer MDA-MB-231 cell by down-regulating the expression of hTERT.
Objective To explore the effect of exogenous estrogen receptor β1 (ERβ1) gene on the expression of p53 as well as the changes of apoptosis in MDA-MB-231 cell line and to investigate the biological role of ERβ1 in breast cancer. Methods Recombinant eukaryotic expressing vector containing ERβ1 cDNA was transfected into human breast cancer cell MDA-MB-231 by using cationic liposome LipofectamineTM 2000. The expression levels of p53 and ERβ1 in mRNA and protein were evaluated by real-time PCR and Western blot, respectively. Cell growth curve was used to detect the changes of cell proliferation ability. Cell apoptosis was detected by flow cytometry. Results After transfected with vector containing ERβ1 cDNA, proliferation ability of MDA-MB-231 cell decreased and the expression levels of both ERβ1 and p53 in both mRNA and protein increased (Plt;0.01). Rate of cell apoptosis increased in ERβ1 upregulation groups （Plt;0.01）. Conclusion ERβ1 can induce apoptosis and inhibit the growth of MDA-MB-231 cells by upregulating p53 expression.