血清CEA、CCR3、CXCL16与Ⅰ期非小细胞肺癌术后复发转移的关系

摘要 目的：探讨血清癌胚抗原（CEA）、C-C基序趋化因子受体3（CCR3）、C-X-C趋化因子配体16（CXCL16）与Ⅰ期非小细胞肺癌（NSCLC）术后复发转移的关系。方法：选取2015年1月～2017年6月南京医科大学附属南京医院收治的186例接受手术切除的Ⅰ期NSCLC患者为NSCLC组,根据术后是否发生复发转移分为复发转移组和未复发转移组,另选取60名健康体检者为对照组。采用酶联免疫吸附法检测血清CEA、CCR3和CXCL16水平,分析其与Ⅰ期NSCLC患者病理特征的关系。采用多因素Cox回归分析Ⅰ期NSCLC患者术后复发转移的影响因素,采用受试者工作特征（ROC）曲线分析血清CEA、CCR3和CXCL16对Ⅰ期NSCLC患者术后复发转移的预测价值。结果：与对照组比较,NSCLC组血清CEA、CCR3和CXCL16水平升高（P＜0.05）。血清CEA、CCR3和CXCL16水平与Ⅰ期NSCLC患者肿瘤直径、分化程度和TNM分期有关（P＜0.05）。随访5年,失访5例,181例Ⅰ期NSCLC患者术后复发转移为20.99%。多因素Cox回归分析显示,肿瘤直径≥2 cm、低分化、TNM分期ⅠB期和CEA、CCR3、CXCL16升高为Ⅰ期NSCLC患者术后复发转移的独立危险因素（P＜0.05）。ROC曲线分析显示,血清CEA、CCR3和CXCL16联合预测Ⅰ期NSCLC患者术后复发转移的曲线下面积（AUC）大于CEA、CCR3和CXCL16单独预测。结论：血清CEA、CCR3和CXCL16水平升高与Ⅰ期NSCLC患者术后复发转移独立相关,血清CEA、CCR3、CXCL16联合预测Ⅰ期NSCLC患者术后复发转移的价值较高。     

超声造影定量参数联合癌胚抗原、中性粒细胞/淋巴细胞比值对乳腺癌改良根治术后复发转移的预测价值

摘要 目的：探讨超声造影定量参数联合癌胚抗原（CEA）、中性粒细胞/淋巴细胞比值（NLR）对乳腺癌改良根治术后复发转移的预测价值。方法：选择2020年12月至2022年1月我院收治的120例行改良根治术治疗的乳腺癌患者,所有患者均行乳腺超声造影检查获得超声造影特征图像及超声造影定量参数,检测血清CEA水平和NLR,统计术后复发转移的发生情况。受试者工作特征（ROC）曲线分析超声造影定量参数联合CEA、NLR预测乳腺癌改良根治术后复发转移的价值。结果：两组术前超声造影特征比较,复发转移组增强强度略高,大部分为高增强或整体增强,造影剂分布尚均匀。18例术后发生复发转移（复发转移组）,复发转移组峰值强度（PI）大于未复发转移组,血清CEA水平和NLR高于未复发转移组,达峰时间（TTP）小于未复发转移组（P＜0.05）。PI、TTP、CEA、NLR预测乳腺癌改良根治术后复发转移的曲线下面积（AUC）为0.693、0.764、0.763、0.781,联合PI、TTP、CEA和NLR预测乳腺癌改良根治术后复发转移的AUC为0.909,大于各指标单独预测。结论：乳腺癌改良根治术后复发转移患者超声造影参数PI增大、TTP降低,血清CEA和NLR增高,联合检测TTP、PI、CEA和NLR在乳腺癌改良根治术后复发转移中具有较高的预测价值。     

血清OPN、CXCL13、CXCL16与宫颈癌根治术患者增殖基因表达及术后复发的关系

摘要 目的：探讨血清骨桥蛋白（OPN）、CXC亚家族趋化因子(CXCL)13、CXCL16水平与宫颈癌根治术患者增殖基因表达的相关性及与患者术后复发的关系。方法：选取2014年1月至2016年1月期间本院诊治的92例宫颈癌根治术患者(宫颈癌组),64例宫颈上皮内瘤变（CIN）患者作为CIN 组,48例健康查体志愿者作为对照组。采用酶联免疫吸附试验检测三组血清OPN、CXCL13、CXCL16水平。采用荧光定量PCR检测宫颈癌组和CIN组组织中增殖基因[血管生成素样蛋白4(ANGPTL4) mRNA、转录因子（FOXP3） mRNA]水平。Pearson相关分析血清OPN、CXCL13、CXCL16和增殖基因ANGPTL4 mRNA、FOXP3 mRNA的相关性。对宫颈癌组患者进行随访,根据随访期复发情况分为复发组39例、未复发组53例。单因素及多因素Logistic回归分析宫颈癌根治术后复发的危险因素。结果：宫颈癌组血清OPN、CXCL13、CXCL16水平显著高于CIN组和对照组 (P<0.05）。宫颈癌组病灶中增殖基因ANGPTL4 mRNA、FOXP3 mRNA表达明显高于CIN组（P<0.05）。宫颈癌组血清OPN、CXCL13、CXCL16水平与增殖基因ANGPTL4 mRNA、FOXP3 mRNA表达均呈显著正相关（P<0.05）。随访过程中,出现复发患者39例,复发率为42.39%（39/92）。复发与未复发组患者在FIGO分期、组织学分级、浸润深度、淋巴结转移,血清OPN、CXCL13、CXCL16水平之间,差异具有显著性(P<0.05)。FIGO分期Ⅱ期、组织学分级低分化、浸润深度＞1/2、有淋巴结转移、血清OPN≥3.65 ng/mL、血清CXCL13≥191.63 pg/mL、血清CXCL16≥119.46 pg/mL是宫颈癌患者根治术后复发的危险因素(P<0.05)。结论：血清OPN、CXCL13、CXCL16水平与宫颈癌增殖基因表达呈正相关,血清OPN、CXCL13、CXCL16高表达是宫颈癌根治术后复发的危险因素。     

术前CA125、OPN、CXCL8、NLR联合检测对乳腺癌改良根治术患者术后复发转移风险的评估价值

摘要 目的：探讨术前糖类抗原125（CA125）、骨桥蛋白（OPN）、趋化因子配体8（CXCL8）、中性粒细胞与淋巴细胞比值（NLR）联合检测对乳腺癌改良根治术患者术后复发转移风险的评估价值。方法：选取2015年4月-2016年4月期间我院收治的乳腺癌改良根治术患者384例按照术后有无复发转移分为未复发转移组（n=345）和复发转移组（n=39）,对比复发转移组、未复发转移组CA125、OPN、CXCL8、NLR,乳腺癌改良根治术患者术后复发转移的影响因素采用多因素Logistic回归分析。采用受试者工作特征（ROC）曲线来判断CA125、OPN、CXCL8、NLR检测对乳腺癌改良根治术患者术后复发转移风险的评估价值。结果：复发转移组的CA125、OPN、CXCL8、NLR高于未复发转移组,组间对比差异有统计学意义（P<0.05）。乳腺癌改良根治术患者术后复发转移与肿瘤最大直径、临床分期、术前新辅助化疗、人表皮生长因子受体2（HER2）、淋巴结转移、组织学类型、细胞增殖标志抗原（ki-67）、雌激素受体（ER）/孕激素受体（PR）、P53、术后放疗、术后内分泌治疗有关（P<0.05）。多因素Logistic回归分析结果显示：OPN偏高、CXCL8偏高、NLR偏高、肿瘤最大直径≥2 cm、淋巴结转移阳性、ER/PR双阴性、临床分期为III期、术前未接受新辅助化疗是乳腺癌改良根治术患者术后复发转移的危险因素（P<0.05）。术前CA125、OPN、CXCL8、NLR联合检测评估复发转移的曲线下面积（AUC）为0.855均高于各指标单独检测。结论：乳腺癌改良根治术后复发转移与OPN、CXCL8、NLR、肿瘤最大直径、淋巴结转移、ER/PR、临床分期、术前接受新辅助化疗均存在一定联系,临床需据此采取针对性干预措施加以防范。且术前CA125、OPN、CXCL8、NLR联合检测辅助评估术后复发转移的价值较高。     

血清sCD105、Periostin、TK1在ⅢA-N2期非小细胞肺癌患者根治性切除术后复发中的临床应用价值研究

摘要 目的： 探讨血清可溶性CD105（sCD105）、骨膜蛋白（Periostin）、胸苷激酶1（TK1）对ⅢA-N2期非小细胞肺癌（NSCLC）患者根治性切除术后复发风险的预测价值。方法：选取2017年1月～2019年5月我院收治的127例接受根治性切除术的ⅢA-N2期NSCLC患者,根据术后3年是否复发分为复发组64例和无复发组63例,收集患者临床资料并采用酶联免疫吸附法检测血清sCD105、Periostin、TK1水平。通过多因素Logistic回归分析ⅢA-N2期NSCLC根治性切除术后复发的影响因素,受试者工作特征（ROC）曲线分析血清sCD105、Periostin、TK1水平对ⅢA-N2期NSCLC患者根治性切除术后复发的预测价值。结果：复发组血清sCD105、Periostin、TK1水平高于无复发组（P＜0.05）。复发组纵膈淋巴结转移数、隆突下淋巴结转移数、N2多站转移、N2多区域转移、N2跨区域转移比例高于无复发组（P＜0.05）。多因素Logistic回归分析显示,纵膈淋巴结转移数增加、N2跨区域转移和sCD105升高、Periostin升高、TK1升高为ⅢA-N2期NSCLC根治性切除术后复发的独立危险因素（P＜0.05）。ROC曲线分析显示,血清sCD105、Periostin、TK1单独与联合预测ⅢA-N2期NSCLC根治性切除术后复发的曲线下面积分别为0.788、0.771、0.787、0.917,三项联合预测的曲线下面积大于各指标单独预测。结论：血清sCD105、Periostin、TK1水平升高为ⅢA-N2期NSCLC患者根治性切除术后复发的独立危险因素,联合检测血清sCD105、Periostin、TK1对ⅢA-N2期NSCLC患者根治性切除术后复发的预测价值较高。     

血清CEA、G-17、MK、ProGRP与胃癌根治术患者术后复发风险的关系研究

摘要 目的：探讨血清癌胚抗原（CEA）、胃泌素17（G-17）、中期因子（MK）、胃泌素释放肽前体（ProGRP）与胃癌根治术（RG）患者术后复发风险的关系。方法：选取2018年1月～2020年8月新疆医科大学第一附属医院普外科收治的156例胃癌患者为胃癌组,根据RG后是否复发分为复发组和无复发组,另选取同期我院52名健康体检志愿者为对照组。收集胃癌患者临床资料,采用酶联免疫吸附法检测血清CEA、G-17、MK、ProGRP水平。通过单因素和多因素Logistic回归分析RG患者术后复发的影响因素,受试者工作特征（ROC）曲线分析血清CEA、G-17、MK、ProGRP水平对RG患者术后复发的预测价值。结果：与对照组比较,胃癌组血清CEA、G-17、MK、ProGRP水平升高（P＜0.05）。随访2年,失访2例,154例RG患者术后复发率为28.57%（44/154）。多因素Logistic回归分析显示,CEA、G-17、MK、ProGRP升高、TNM分期Ⅲ期、分化程度为低分化、淋巴结转移为RG患者术后复发的独立危险因素（P＜0.05）。ROC曲线分析显示,血清CEA、G-17、MK、ProGRP水平联合预测RG患者术后复发的曲线下面积（AUC）大于CEA、G-17、MK、ProGRP单独预测。结论：血清CEA、G-17、MK、ProGRP水平升高与RG患者术后复发密切相关,可能成为RG患者术后复发的辅助预测指标,且血清CEA、G-17、MK、ProGRP联合预测RG患者术后复发的价值较高。     

增强CT图像纹理参数联合血清CEA、CA724在食管癌术后复发转移中的临床应用价值

摘要 目的：研究增强计算机断层扫描（CT）图像纹理参数联合血清癌胚抗原（CEA）、糖类抗原724（CA724）在食管癌术后复发转移中的临床应用价值。方法：选取2019年6月-2021年7月于我院行手术治疗的86例食管癌患者,术前检测其血清CEA、CA724水平,并行增强CT扫描,将其动、静脉期图像数据行纹理分析,记录均值、中位数、标准差、不均匀度、偏度、峰度、熵值等参数。术后对86例食管癌患者进行12个月随访,根据其是否发生复发转移分为复发转移组（32例）与无复发转移组（54例）,比较两组增强CT图像纹理参数及血清CEA、CA724水平差异;采用受试者工作特征（ROC）曲线分析增强CT图像纹理参数联合血清CEA、CA724对食管癌患者术后复发转移的预测价值。结果：复发转移组动脉期熵值高于无复发转移组（P＜0.05）;复发转移组静脉期不均匀度、熵值均高于无复发转移组（P＜0.05）。复发转移组血清CEA、CA724水平高于无复发转移组（P＜0.05）。ROC曲线显示,血清CEA、CA724联合动脉期熵值及静脉期不均匀度、熵值的曲线下面积（AUC）、敏感度、特异度均较各指标单独应用有明显提升,联合应用的预测效能更高。结论：血清CEA、CA724水平和动脉期熵值及静脉期不均匀度、熵值升高与食管癌患者术后发生复发转移有关,动脉期熵值及静脉期不均匀度、熵值联合血清CEA、CA724在预测食管癌患者术后发生复发转移中的应用价值较高。     

CD64指数、sCD14、sCD163与胸腔镜肺癌根治术后并发重症肺部感染的关系研究

摘要 目的：探讨CD64指数、可溶性白细胞分化抗原14（sCD14）、可溶性白细胞分化抗原163（sCD163）与胸腔镜肺癌根治术后并发重症肺部感染的关系。方法：选择2020年1月至2023年1月南通市肿瘤医院收治的行胸腔镜肺癌根治术治疗的非小细胞肺癌（NSCLC）患者共415例。根据术后是否并发重症肺部感染将患者分为感染组（21例）和未感染组（394例）。检测外周血CD64指数和血清sCD14、sCD163水平。多因素Logistic回归分析影响胸腔镜肺癌根治术后并发重症肺部感染的因素。受试者工作特征（ROC）曲线分析CD64指数、sCD14、sCD163预测胸腔镜肺癌根治术后并发重症肺部感染的价值。结果：感染组外周血CD64指数、血清sCD14、sCD163水平高于未感染组（P＜0.05）。多因素Logistic回归分析显示高CD64指数、sCD14、sCD163、降钙素原（PCT）是胸腔镜肺癌根治术后并发重症肺部感染的危险因素（P＜0.05）,高呼气峰值流量（PEF）是保护因素（P＜0.05）。CD64指数、sCD14、sCD163、PCT预测胸腔镜肺癌根治术后并发重症肺部感染的曲线下面积为0.834、0.815、0.842、0.784,联合预测曲线下面积为0.928,高于单独预测。结论：血清CD64指数、sCD14、sCD163、PCT水平升高是胸腔镜肺癌根治术后并发重症肺部感染的危险因素。联合CD64指数、sCD14、sCD163、PCT可较好地预测术后重症肺部感染的风险。     

乳腺癌改良根治术患者术后复发转移的危险因素及血清CA125、COX-2、sTNFR-P55的预测价值研究

摘要 目的：探讨乳腺癌改良根治术患者术后复发转移的危险因素及血清糖类抗原125（CA125）、环加氧酶-2（COX-2）、可溶性肿瘤坏死因子受体P55（sTNFR-P55）的预测价值。方法：对2014年1月至2016年12月新疆医科大学第一附属医院收治的109例行乳腺癌改良根治术的乳腺癌患者进行前瞻性研究,所有患者术后均随访5年,其中2例失访,107例完成随访。根据5年内患者复发转移情况将其分为复发转移组（n=31）和未复发转移组（n=76）。收集患者入院时的临床病理资料,采用电化学发光法检测术前血清CA125,采用酶联免疫吸附法检测术前血清COX-2、sTNFR-P55。采用logistic回归模型分析患者术后复发转移的影响因素,绘制受试者工作特征（ROC）曲线评估血清CA125、COX-2、sTNFR-P55对术后复发转移的预测价值。结果：复发转移组肿瘤直径＞5 cm、浸润性非特殊癌、脉管癌栓、雌激素受体（ER）/孕激素受体（PR）阴性、无内分泌治疗构成比、TNM分期IIIA期、腋窝淋巴结转移数量4~9个构成比高于未复发转移组（P<0.05）。复发转移组血清CA125、COX-2、sTNFR-P55水平高于未复发转移组（P<0.05）。多因素logistic回归分析结果显示,肿瘤直径＞5 cm、浸润性非特殊癌、TNM分期IIIA期、脉管癌栓、腋窝淋巴结转移数量4~9个、CA125升高、COX-2升高、sTNFR-P55升高是乳腺癌改良根治术患者术后5年内复发转移的独立危险因素（OR=1.318、1.213、1.223、1.137、1.257、1.241、1.313、1.351,P<0.05）。血清CA125、COX-2、sTNFR-P55均可有效预测乳腺癌术后复发转移,曲线下面积（AUC）分别为0.803、0.749、0.761,三指标联合预测术后复发转移的AUC为0.915,灵敏度和特异度分别为0.94、0.83。结论：肿瘤直径、浸润性非特殊癌、TNM分期、脉管癌栓、腋窝淋巴结转移数量以及术前血清CA125、COX-2、sTNFR-P55异常升高是乳腺癌改良根治术患者术后5年内复发转移的危险因素,术前血清CA125、COX-2、sTNFR-P55联合检测可预测乳腺癌改良根治术后的复发转移风险。     

非小细胞肺癌患者外周血循环肿瘤细胞与临床病理特征和血清CEA、NSE、Cyfra21-1、pro-GRP的关系分析

摘要 目的：研究非小细胞肺癌（NSCLC）患者外周血循环肿瘤细胞（CTC）与临床病理特征及血清癌胚抗原（CEA）、神经元特异性烯醇化酶（NSE）、细胞角蛋白21-1（Cyfra21-1）、胃泌素释放肽前体（pro-GRP）的关系。方法：将中山大学附属江门医院从2018年1月～2021年1月收治的100例NSCLC患者纳入研究组,另选取同期我院收治的肺部良性病变患者50例作为对照组。检测并比较两组CTC计数及血清CEA、NSE、Cyfra21-1、pro-GRP水平,分析NSCLC患者外周血CTC与临床病理特征和血清CEA、NSE、Cyfra21-1、pro-GRP水平的关系。此外,通过受试者工作特征（ROC）曲线分析外周血CTC和血清CEA、NSE、Cyfra21-1、pro-GRP诊断NSCLC的效能。结果：研究组外周血CTC计数及血清CEA、NSE、Cyfra21-1、pro-GRP水平均高于对照组,差异有统计学意义（P＜0.05）。Pearson相关性分析结果显示：NSCLC患者外周血CTC计数和血清CEA、NSE、Cyfra21-1、pro-GRP水平均呈正相关（P＜0.05）。TNM分期为Ⅲ～Ⅳ期、有吸烟史的NSCLC患者CTC阳性比例明显高于TNM分期为Ⅰ～Ⅱ期、无吸烟史的NSCLC患者（P＜0.05）。ROC曲线分析结果显示：CTC计数及血清CEA、NSE、Cyfra21-1、pro-GRP水平联合检测诊断NSCLC的曲线下面积最大。结论：NSCLC患者外周血CTC计数升高,与血清CEA、NSE、Cyfra21-1、pro-GRP水平均存在相关性,且CTC阳性与NSCLC恶性进展和患者吸烟史有关,联合检测上述指标诊断NSCLC可获得较为理想的效能。     

Brain metastasis in lung cancer: Building a molecular and systems-level understanding to improve outcomes

Lung cancer is a clinically difficult disease with rising disease burden around the world. Unfortunately, most lung cancers present at a clinically advanced stage. Of these cancers, many also present with brain metastasis which complicates the clinical picture. This review summarizes current knowledge on the molecular basis of lung cancer brain metastases. We start from the clinical perspective, aiming to provide a clinical context for a significant problem that requires much deeper scientific investigation. We review new research governing the metastatic process, including tumor cell signaling, establishment of a receptive tumor niches in the brain and evaluate potential new therapeutic options that take advantage of these new scientific advances.Lung cancer remains the largest single cause of cancer mortality in the United States (Siegel et al., 2015). This continues to be the clinical picture despite significant advances in therapy, including the advent of targeted molecular therapies and newly adopted immunotherapies for certain subtypes of lung cancer. In the vast majority of cases, lung cancer presents as advanced disease; in many instances, this advanced disease state is intimately associated with micro and macrometastatic disease (Goldberg et al., 2015). For both non-small cell lung cancer and small cell lung cancer patients, the predominant metastatic site is the brain, with up to 68% of patients with mediastinal lymph node metastasis eventually demonstrating brain metastasis (Wang et al., 2009).The frequency (incidence) of brain metastasis is highest in lung cancers, relative to other common epithelial malignancies (Schouten et al., 2002). Other studies have attempted to predict the risk of brain metastasis in the setting of previously non-metastatic disease. One of the largest studies to do this, analyzing historical data from 1973 to 2011 using the SEER database revealed a 9% risk of patients with previously non-metastatic NSCLC developing brain metastasis over the course of their disease, while 18% of small cell lung cancer patients without previous metastasis went on to develop brain metastasis as their disease progressed (Goncalves et al., 2016).The reasons underlying this predilection for the central nervous system, as well as the recent increase in the frequency of brain metastasis identified in patients remain important questions for both clinicians and basic scientists. More than ever, the question of how brain metastasis develop and how they can be treated and managed requires the involvement of interdisciplinary teams—and more importantly—scientists who are capable of thinking like clinicians and clinicians who are capable of thinking like scientists. This review aims to present a translational perspective on brain metastasis. We will investigate the scope of the problem of brain metastasis and the current management of the metastatic disease process in lung cancer. From this clinical starting point, we will investigate the literature surrounding the molecular underpinnings of lung tumor metastasis and seek to understand the process from a biological perspective to generate new hypotheses.     

Adult lung stem cells and their contribution to lung tumourigenesis

The isolation and characterization of lung stem and progenitor cells represent an important step towards the understanding of lung repair after injury, lung disease pathogenesis and the identification of the target cells of transformation in lung carcinogenesis. Different approaches using prospective isolation of progenitor cells by flow cytometry or lineage-tracing experiments in mouse models of lung injury have led to the identification of distinct progenitor subpopulations in different morphological regions of the adult lung. Genetically defined mouse models of lung cancer are offering new perspectives on the cells of origin of different subtypes of lung cancer. These mouse models pave the way to further investigate human lung progenitor cells at the origin of lung cancers, as well as to define the nature of the lung cancer stem cells. It will be critical to establish the link between oncogenic driver mutations recently discovered in lung cancers, target cells of transformation and subtypes of lung cancers to enable better stratification of patients for improved therapeutic strategies.     

Differences between TNM classification and 2-[18F]FDG PET parameters of primary tumor in NSCLC patients

BackgroundThe aim of the study was to compare the TNM classification with 2-[¹⁸F]FDG PE T biological parameters of primary tumor in patients with NSCLC.Materials and methodsRetrospective analysis was performed on a group of 79 newly diagnosed NSCLC patients. PET scans were acquired on Gemini TF PET/CT scanner 60–70 min after injection of 2-[¹⁸F]FDG with the mean activity of 364 ± 75 MBq, with the area being examined from the vertex to mid-thigh. The reconstructed PET images were evaluated using MIM 7.0 Software for SUV_max, MTV and TLG values.ResultsThe analysis of the cancer stage according to TNM 8^th edition showed stage IA2 in 8 patients, stage IA3 — 6 patients, stage IB — 4 patients, IIA — 3 patients, 15 patients with stage IIB, stage IIIA — 17 patients, IIIB — 5, IIIC — 5, IVA in 7 patients and stage IVB in 9 patients. The lowest TLG values of primary tumor were observed in stage IA2 (11.31 ± 15.27) and the highest in stage IIIC (1003.20 ± 953.59). The lowest value of primary tumor in SUV_max and MTV were found in stage IA2 (6.8 ± 3.8 and 1.37 ± 0.42, respectively), while the highest SUV_max of primary tumor was found in stage IIA (13.4 ± 11.4) and MTV in stage IIIC (108.15 ± 127.24).ConclusionTNM stages are characterized by different primary tumor 2-[¹⁸F]FDG PET parameters, which might complement patient outcome.     

血管内皮生长因子与肺癌治疗

肺癌是世界上主要癌症杀手之一,大部分肺癌病人都死于肿瘤转移所引起的并发症.由于现在大部分的肺癌病人预后不佳,因此寻找新方法、新途径治疗尤为重要.抗血管生成是目前的肿瘤治疗研究热点之一.对目前以抗血管内皮生成因子为手段的肺癌治疗方面的研究作一综述.     

外泌体源性miRNAs在肺癌发生发展中的作用

外泌体(exosomes)是细胞分泌的纳米级细胞外囊泡.外泌体通过释放其内的生物活性大分子,比如微小RNA(microRNA,miRNA)到受体细胞,从而介导细胞间交流通讯. MiRNAs作为一类主要在转录后水平负向调控靶mRNAs的非编码RNAs,其在外泌体中含量最为丰富.在肺癌中,miRNAs经肿瘤细胞分泌的外泌体转运释放而发挥重要的作用.本文主要讨论了外泌体源性miRNAs在肺癌发生发展的各个阶段,包括血管生成、细胞增殖、侵袭转移、免疫逃逸、耐药等方面的作用,以及其在作为新型肺癌诊断和预后标志物方面的临床价值.     

雷公藤红素对非小细胞肺癌细胞株H1299增殖与凋亡的影响

目的：研究雷公藤红素对非小细胞肺癌细胞株H1299的杀伤作用及相关调控机制。方法：用细胞计数法测定不同浓度雷公藤红素对H1299细胞增殖的影响;用流式细胞仪检测H1299细胞的细胞周期;用Western blotting检测剪切的（cleaved）聚ADP核糖聚合酶（PARP）、cleaved caspase-3和低氧诱导因子-1（HIF-1）的表达水平;用DCF-DA染色和荧光显微镜检测细胞内的活性氧（ROS）水平;用萤光素酶活性测定法检测NFκB的活性。结果：雷公藤红素以时间和剂量依赖性的方式抑制H1299细胞的增殖,并使细胞阻滞在G2/M期。同时,雷公藤红素显著上调cleaved PARP和cleaved caspase-3的表达,提高细胞内的ROS水平,并且抑制NFκB的活性。结论：雷公藤红素以时间和剂量依赖性的方式抑制H1299细胞的增殖,并诱导caspase依赖性的细胞凋亡,具体机制与细胞内ROS的积累和NFκB的活性抑制有关。     

Characteristics and consequences of passive smoking

Summary The consequences of passive smoking are well documented regarding the risk of lung cancer, obstructive ventilatory trouble, ischemic cardiopathy, infant disease of the respiratory ducts and of foetus growth delay caused by smoking during pregnancy. If the potential risk is much lower than the risk induced by active smoking, very few people can avoid exposure to smoke because of the large amount of active smokers in the French population. Rather than the characteristics of the emitting source and the particularities of smoking (speed and inhalation), it is mostly the ventilation of rooms where non-smokers are exposed to the smoker's smoke that constitutes the significant point. The consequences of environmental smoking on health would justify to take statutory decisions protecting the rights of the smokers. This is in accordance with the resolution passed by the European Community's Council and the Secretaries of Health of the member countries. More precisely, non smoking rules in closed rooms open to the public should be enforced, particularly in schools, hospitals and finally at the workplace.     

New insights into small‐cell lung cancer development and therapy

Small‐cell lung cancer (SCLC) accounts for approximately 15% of lung cancer cases; however, it is characterized by easy relapse and low survival rate, leading to one of the most intractable diseases in clinical practice. Despite decades of basic and clinical research, little progress has been made in the management of SCLC. The current standard first‐line regimens of SCLC still remain to be cisplatin or carboplatin combined with etoposide, and the adverse events of chemotherapy are by no means negligible. Besides, the immunotherapy on SCLC is still in an early stage and novel studies are urgently needed. In this review, we describe SCLC development and current therapy, aiming at providing useful advices on basic research and clinical strategy.     

Evidence of Mucin Secretion in Human Lung Adenocarcinoma Cell Lines NCIH650 and NCIH2077 and Effect of Select Secretagogues on Mucin Secretion

Mucins comprise an important class of tumor-associated antigens. The objectives of the present study were (a) to establish an in vitro model system using human non-small cell lung adenocarcinoma cell lines NCIH650 and NCIH2077 (b) provide evidence that these cell lines secrete mucin in culture conditions and (c) investigate the effects of select secretagogues on mucin secretion. The cell lines were established in ACL-4 medium containing several growth factors and retinoic acid and 5% fetal calf serum. The high molecular weight glycoconjugates secreted in the culture medium were purified by ammonium sulfate precipitation and Superose 6 and Superose 12 FPLC chromatography. The purified high molecular weight glycoconjugate fraction and the carcinoma cells were shown to have mucin by dot blot, Western blot and immunohistochemical analysis, respectively, using specific antibodies to purified major mucin, HTM-1. Also, incorporation experiments with mucin precursor ³H-glucosamine demonstrated that the cells indeed synthesize high molecular weight mucins. The effects of secretagogues such as, 8-bromocyclic AMP, ionomycin, phorbol-12-myristate-13-acetate and neutrophil elastase on mucin secretion were also investigated. Only 8-bromocyclic AMP and neutrophil elastase influenced mucin secretion. These studies provided strong evidence that the lung adenocarcinoma cell lines secrete high molecular weight mucins in culture conditions and only two of the four tested secretagogues significantly increased mucin secretion. Thus, this in vitro model system may be useful in determining alterations in mucin structure, if any, in lung adenocarcinomas as well as in studying the regulation of mucin gene expression.