STAT3在艾滋病相关弥漫性大B细胞淋巴瘤中的表达及意义
作者: |
1高波,
2孙晶晶,
3段月勋,
1邓刚,
4杨倩,
5王霖,
1潘云
1 大理大学附属医院病理科,云南 大理 671000 2 云南省第一人民医院超声科,昆明 650100 3 云南省传染病专科医院外科,昆明 650301 4 昆明市第一人民医院病理科,昆明 650000 5 昆明市传染病医院病理科,昆明 650200 |
通讯: |
潘云
Email: panyun09@163.com |
DOI: | 10.3978/j.issn.2095-6959.2016.11.011 |
基金: | 云南省高校病理学科技创新团队计划支持项目, 云教科[2014]22号 云南省临床重点专科建设项目, 云财社[2012]311号 |
摘要
目的:探讨STAT3在艾滋病相关弥漫性大B细胞淋巴瘤(ADIS/HIV-related diffuse large B-cell lymphoma,HIV-DLBCL)中的表达及意义。方法:收集21例HIV-DLBCL组织标本作为实验组。对照组15例标本,分别为6例HIV阴性的DLBCL(non-HIV-DLBCL)、4例HIV阳性淋巴结反应性增生(HIV-reactive hyperplasia,HIV-RH)、5例HIV阴性淋巴结反应性增生(non-HIV-RH)。采用免疫组化检测各样本中STAT3的表达情况,并结合患者的临床病理因素分析。结果:HIV-DLBCL中STAT3总阳性表达率为76.19%,以胞核表达为主占81.25%;non-HIV-DLBCL中STAT3总阳性表达率为66.67%,以胞核表达为主占50%;两组总阳性率及核阳性率差异无统计学意义(P>0.05)。HIV-RH和non-HIV-RH中,STAT3仅表达于淋巴滤泡细胞;HIV-DLBCL中STAT3表达率与良性病变组具有显著性差异(P<0.05)。STAT3在non-GCB型HIV-DLBCL中的表达明显高于GCB型HIV-DLBCL(P<0.01),与性别、年龄、发病部位及临床分期等因素无关(P>0.05)。结论:STAT3在HIV-DLBCL和non-HIV-DLBCL中均呈高表达,且以核表达为主,提示STAT3过表达与DLBCL的发生有关;STAT3表达与HIV-DLBCL的免疫表型有关,因不同免疫表型DLBCL的预后存在差异,提示STAT3可能是HIV-DLBCL的潜在预后标志物。
关键词:
艾滋病相关弥漫性大B细胞淋巴瘤
信号传导与转录激活因子3
免疫表型
Expression and significance of STAT3 in AIDS-related diffuse large B-cell lymphoma
CorrespondingAuthor: PAN Yun Email: panyun09@163.com
DOI: 10.3978/j.issn.2095-6959.2016.11.011
Abstract
Objective: To investigate the expression and significance of STAT3 in AIDS/HIV-related diffuse large B-cell lymphomas (HIV-DLBCL). Methods: The 21 cases of HIV-DLBCL were collected as the experiment group. The control group consisted of 5 cases of non-HIV-DLBCL, 4 cases of HIV-reactive hyperplasia (HIV-RH) and 5 cases of non-HIV-RH. The expression of STAT3 was detected by immunohistochemistry and analyzed in combination with clinicopathologic characteristics. Results: The total positive rate of STAT3 was 76.19% in HIV-DLBCL and 66.67% in non-HIV-DLBCL. Most DLBCL cells showed nuclear staining pattern and the nuclear positive rate was 81.25% in HIV-DLBCL and 50% in non-HIV-DLBCL. The difference of STAT3 expression between HIV-DLBCL and non-HIV-DLBCL was not statistically significant (P>0.05). STAT3 was expressed in lymphoid follicle cells in HIV-RH and non-HIV-RH tissues. There was significant difference of STAT3 expression between HIV-DLBCL and benign lesion (P<0.05). STAT3 expression in non-GCB HIV-DLBCL was significantly higher than that in GCB HIV-DLBCL (P<0.01). However, STAT3 expression had no correlation with sex, age, location of tumor and clinical stage (P>0.05). Conclusion: STAT3 was mainly located in nuclear and overexpressed in HIV-DLBCL and non-HIV-DLBCL, suggesting that STAT3 overexpression was involved in tumorigenesis of DLBCL. STAT3 expression was correlated with immunophenotype of DLBCL. As the prognosis was different in different immunophenotype subgroups, STAT3 may be the potential marker of prognosis for HIV-DLBCL.