目的 研究乳腺癌患者雌激素受体（ER）、孕激素受体（PR）、人表皮生长因子受体2（HER-2）表达情况及免疫组织化学分子亚型分布。 方法 对2003年1月－2008年9月四川大学华西医院病理科3 365例乳腺癌病理报告存档资料进行激素受体（ER/PR）、HER-2表达情况及免疫组织化学分子亚型分布进行分析。 结果 3 365例确诊的乳腺癌患者中，ER阳性1 824例（54.2%），PR阳性1 841例（54.7%），HER-2过表达284例（8.4%）。相关分析显示ER与PR表达呈正相关（P＜0.001），HER-2与ER、PR表达均呈负相关（P＜0.001）。免疫组织化学分子亚型结果显示luminal A型最常见，为1 993例（59.2%）；basal-like型为623例（18.5%）；HER-2过表达型为169例（5.0%）；luminal B型最少，为115例（3.4%）；未分类的为465例（13.8%）。 结论 乳腺癌患者激素受体及HER-2表达有特殊性，激素受体阳性率＞50%，HER-2阳性率在不同研究中显示出不同的结果，尚需进一步研究；ER、PR与HER-2具有良好的相关性；免疫组织化学分子亚型中luminal A型最常见。
ObjectiveTo analyze the influencing factors for hepatitis B virus (HBV) infection screening in lymphoma patients prior to chemotherapy with a focus on HBV reactivation after chemotherapy. MethodsThe HBV infection screening data of 449 patients with lymphoma treated by chemotherapy between June 2010 and July 2012 were analyzed retrospectively. ResultsAmong the 449 patients, 387 (86.2%) were screened for HBV before initiation of chemotherapy, and patients with elevated aminotransferase levels were more likely to receive pre-chemotherapy HBV testing (OR=2.509, P=0.040). HBV reactivation was observed in 16.1% (9/56) of the HBsAg-positive patients after chemotherapy, and it was more likely to occur in patients with the use of rituximab (29.2% vs. 6.3%; P=0.030). Prophylactic antiviral therapy can significantly reduce the incidence of chemotherapy-induced HBV reactivation (12.0% vs. 50.0%; P=0.046). Two cases of reactivation occurred in patients who were HBsAg negative and hepatitis B core antibody positive. ConclusionHBV reactivation, especially for people with the use of rituximab, is a common complication in patients with HBV infection. HBV infection testing should be considered for lymphoma patients who were planned for chemotherapy. Prophylactic antiviral therapy can greatly decrease the incidence of HBV reactivation.
This research aims to construct a lentiviral expression vector carrying the extracelluar domain (ED) of human hepatocyte growth factor receptor (C-Met), and to express it in transfected 293T cells. The extracellular domain of C-Met was amplified by RT-PCR, ligated with lentiviral expression vector p RRL-CMV-ED, and then expressed in 293T cell line. The expressed protein was purified and identified by RT-PCR and Western blot. The enzyme digestion and sequence analysis showed that the lentiviral expression vector p RRL-CMV-ED was constructed correctly. The size of amplified genes was about 2 700 bp. The purified protein with Ni-affinity column was about 105 kD analyzed by SDS-PAGE. The Western blot and ELISA results showed that the expressed protein which could bind to HGF specifically was the extracelluar domain of human hepatocyte growth factor receptor. This research may lay a foundation for further study of anti-C-MET monoclonal antibody and neutralizing antibody.