《中国肺癌杂志》(2005年)第8卷文题索引

[按栏目顺序排列]第十一届世界肺癌大会专题肺癌基础研究和临床治疗的分子时代———第十一届世界肺癌大会评述(周清华)5∶361非小细胞肺癌围术期综合治疗的新概念(吴一龙)5∶367肺癌分子靶向治疗:更多的希望、更多的选择(韩宝惠)5∶370晚期非小细胞肺癌治疗新进展(张力)5∶375基因组学在肺癌研究中从基础向临床应用的转化(王艳萍、周清华)5∶378肺癌病因学和遗传易感性研究进展(朱文、周清华)5∶385肺癌筛查与早诊的新进展(车国卫、周清华等)5∶390肺癌流行病学研究进展(王瑾、许峰、周清华)5∶395非小细胞肺癌放射治疗进展(许峰、王瑾、周…     

日本肺癌学会总会第21届年会概况

日本肺癌学会总会第21届年会于1980年11月4日至5日在东京召开。主要学术活动内容为,1.邀请讲演:(1)外科在多学科处理肺癌中的积极作用(上海胸科医院吴善芳);(2)美国梅育中心发现早期肺癌的现状(美国梅育中心Robert S Fonta-na);(3)外科治疗肺癌的适应症(美国斯隆-凯特琳纪念中心Nael Martini)。2.特别报告:(1)高危险人群普查对肺癌早期发现的意义(成毛韶夫);(2)肺癌多学科治疗研究班(服部正次);(3)肿瘤补体免疫学研究和肺癌预后判断(河村一太)。3.肺癌展望:(1)肺癌细胞学诊断客观分析法的展望(高桥正宣);(2)肺癌的生物化学研究(牧田章);(3)粒子线     

联合化疗治疗肺癌合并上腔静脉综合征临床疗效分析

目的探讨联合化疗治疗肺癌合并上腔静脉综合征的疗效.方法分析2000年～2003年期间我科收治的32例肺癌合并上腔静脉综合征化疗病例.其中小细胞肺癌14例,非小细胞肺癌18例.小细胞肺癌采用EP方案(足叶乙甙,顺铂)或TP方案(拓普替康,顺铂)化疗,化疗开始先用氮芥(HN2)静脉冲击一次.非小细胞肺癌采用CAP方案(环磷酰胺,阿霉素,顺铂),LAP方案(异环磷酰胺,阿霉素,顺铂)或NP方案(盖诺,顺铂)化疗.同时配合脱水、利尿及激素治疗.结果小细胞肺癌CR4例,PR8例,有效率(CR+PR)85.7%.非小细胞肺癌有效率CR 1例,PR 12例,有效率(CR+PR)72.2%.结论联合化疗治疗肺癌合并上腔静脉综合征疗效显著确切,是临床上首选的治疗方法.     

肺癌微创治疗进展

正胸腔镜设备和相关外科技术经过近20年的发展和完善,胸腔镜肺癌肺叶切除术(VATS-lobec-tomy)外科治疗早期肺癌的近期和远期临床效果已无争议,而2006年颁布的美国国家综合癌症网络(NCCN)非小细胞肺癌治疗指引和2007年发表的美国胸部医师协会(ACCP)肺癌治疗指引把胸腔     

《中国肺癌杂志》(2006年)第9卷文题索引

[按栏目顺序排列]述评加强我国肺癌外科气道重建研究(周清华)1∶1肺癌气道重建隆凸合并心脏大血管切除重建术治疗局部晚期中心型支气管肺癌(周清华、刘斌、杨俊杰等)1∶2隆凸成形术治疗中心型肺癌41例(许林、俞明锋、袁方良等)1∶9气管隆凸切除与重建术在肺癌治疗中的应用(陈晓峰、张鹏、姜格宁等)1∶14肺癌袖状切除术与全肺切除术疗效比较分析(王长利、张真发、宫立群等)1∶18支气管肺动脉同时成形在中心型肺癌手术中的应用(王春利、张双平、马炎炎等)1∶22支气管肺动脉成形术治疗中心型支气管肺癌(张鹏、陈钢、刘毅梅等)1∶25隆凸切除重建…     

表皮生长因子在肺癌治疗中的应用

表皮生长因子(EGF)及受体信号通路在非小细胞肺癌(NSCLC)的发生和发展中起重要作用.本文综述肺癌EGF及其受体(EGFR)的一般特性、作用机制、生物学功能、酪氨酸激酶拮抗剂(TKI)在肺癌靶向治疗中的作用以及EGF肿瘤疫苗治疗NSCLC的价值.     

21世纪肺癌外科的挑战与机遇

自 1933年Ｇｒａｈａｍ施行全肺切除术治疗肺癌 ,开创肺癌外科治疗里程碑以来 ,肺癌外科治疗已取得了长足的进步。回顾近 70年来 ,人类肺癌外科治疗的历史大体上可以分为以下几个阶段 :(1) 4 0和 5 0年代肺癌外科治疗以全肺切除术为经典术式 ;(2 ) 6 0年代开始认识到全肺切除术并不是理想的肺癌外科治疗术式 ,并逐渐认识到肺叶切除术较之全肺切除术的优越性 ;(3) 70年代以最大限度地切除肺癌和最大限度地保留肺功能为肺癌外科治疗的主要指导思想 ,并创立了各种支气管、隆凸切除成形术式 ;(4 ) 80年代认识到区域淋巴结清扫在肺癌外科手术中的…     

(2001年)第4卷文题索引[按栏目顺序排列]

述评　在新世纪肺癌会不会“低头”(孙燕 ) 1∶4　为 2 1世纪我国肺癌分子生物学的发展和腾飞而奋斗 (周清华等 ) 1∶8　肺癌侵袭转移研究在新世纪面临的挑战 (陆应麟等 ) 2∶81　非小细胞肺癌治疗现状及进展 (廖美琳等 ) 3∶1 6 1　肺癌多学科综合治疗的现状和展望 (吴一龙 ) 4∶2 4 1　 2 1世纪肺癌外科的挑战与机遇 (周清华等 ) 6∶40 1专题笔谈　学习《1 999年ＷＨＯ/ＩＡＳＬＣ肺和胸膜肿瘤组织学分类》的体会 (谢作煊 ) 4∶2 75肺癌循证医学研究　肺癌患者端粒酶表达的ｍｅｔａ分析 (刘瑾等 ) 4∶2 99肺癌分子生物学　人非小细胞肺癌…     

《中国肺癌杂志》（2004年）第7卷文题索引

[按栏目顺序排列 ]述评　 晚期非小细胞肺癌化疗周期的新争议 (韩宝惠 ) 1∶1　加强我国肺癌分子靶向治疗基础和临床研究 (周清华、孙燕 )4∶2 67肺癌分子靶向治疗　 非小细胞肺癌生物靶点治疗的动向 (廖美琳 ) 4∶2 70　Anewhorizonoftargetedtherapyinmanagementoflungcancer(TonyMok) 4∶2 76　Targetedtherapyinnon smallcelllungcancer(Shou ChingTang) 4∶2 84　肺腺癌组织特异性自杀基因治疗实验研究 (赵立军、李强、白冲等 ) 4∶2 90　转染nm2 3 H1基因靶向阻断人大细胞肺癌细胞株L9981Wnt信号传导通路 (付军科、周清华、朱文…     

中医药治疗肺癌对患者血清CA-125的影响

背景与目的:CA-125已经是公认的卵巢癌标志物,在长期的临床观察中发现血清CA-125在肺癌诊治中具有一定的诊断及判定预后的价值.本研究探讨中医药治疗术后与不能切除肿瘤的肺癌患者时对血清CA-125的影响;同时探讨血清CA-125与肺癌临床分期及病理学类型相关性.方法:用微粒学酶免分析法检测30例健康人及60例肺癌患者中医综合治疗方案治疗前后血清CA-125水平,并作对比分析.结果:血清CA-125在肺癌患者的值(91±45)与健康人(18±5)相比,差异有非常显著性,(P＜0.001),血清CA-125在ⅢA/ⅢB及Ⅳ期肺癌患者中值分别为85±21及142±25,与Ⅰ/Ⅱ期患者的35±11相比,差异有非常显著性(P＜0.001)肺腺癌患者CA-125水平(127±31)与鳞癌(58±27)及小细胞癌(56±26)相比,差异有非常显著性(P＜0.001).ⅢA/ⅢB及Ⅳ期肺癌患者中医药综合治疗方案治疗后CA-125值分别为(36±11;87±15)于治疗前(85±21;142±25)相比,差异有非常显著性.(P＜0.001).但对于Ⅰ/Ⅱ期患者治疗后(33±10)与治疗前(35±11)相比,差异无显著性(P＞0.05).结论:中医药治疗肺癌,在Ⅲ/Ⅳ期的肺癌患者可显著的降低血清CA-125水平,在Ⅰ/Ⅱ期的肺癌患者也有明显的降低血清CA-125水平的趋势.血清CA-125水平与肺癌患者临床分期、病理类型有关.     

Atypical protein kinase C iota is an oncogene in human non-small cell lung cancer

Protein kinase C (PKC) isozymes have long been implicated in carcinogenesis. However, little is known about the functional significance of these enzymes in human cancer. We recently showed that the atypical PKC (aPKC) isozyme PKCiota is overexpressed in human non-small cell lung cancer (NSCLC) cells and that PKCiota plays a critical role in the transformed growth of the human lung adenocarcinoma A549 cell line in vitro and tumorigenicity in vivo. Here we provide compelling evidence that PKCiota is an oncogene in NSCLC based on the following criteria: (a) aPKCiota is overexpressed in the vast majority of primary NSCLC tumors; (b) tumor PKCiota expression levels predict poor survival in patients with NSCLC; (c) the PKCiota gene is frequently amplified in established NSCLC cell lines and primary NSCLC tumors; (d) gene amplification drives PKCiota expression in NSCLC cell lines and primary NSCLC tumors; and (e) disruption of PKCiota signaling with a dominant negative PKCiota allele blocks the transformed growth of human NSCLC cells harboring PKCiota gene amplification. Taken together, our data provide conclusive evidence that PKCiota is required for the transformed growth of NSCLC cells and that the PKCiota gene is a target for tumor-specific genetic alteration by amplification. Interestingly, PKCiota expression predicts poor survival in NSCLC patients independent of tumor stage. Therefore, PKCiota expression profiling may be useful in identifying early-stage NSCLC patients at elevated risk of relapse. Our functional data indicate that PKCiota is an attractive target for development of novel, mechanism-based therapeutics to treat NSCLC.     

早期非小细胞肺癌ALK阳性患者的临床研究进展

肺癌是我国癌症死亡最主要的原因.其中非小细胞肺癌(non-small cell lung cancer,NSCLC)占肺癌患者的85%,且大部分患者初诊时即为晚期.针对晚期NSCLC患者,分子靶向治疗成为人们关注的热点.棘皮动物微管相关蛋白-间变淋巴瘤激酶(echinoderm microtubule-associated protein-like 4 gene and the anaplastic lymphoma kinase gene,EML4-ALK)是NSCLC最常见的分子靶点之一,其特异性的小分子酪氨酸激酶抑制剂(tyrosine kinase inhibitors,TKIs)已被批准应用于ALK阳性晚期NSCLC患者的治疗.然而,ALK融合基因对早期NSCLC患者预后的影响,以及ALK阳性的早期NSCLC患者应用TKIs的必要性等问题尚不明确.本文主要围绕ALK阳性NSCLC患者的检测进展,早期ALK阳性NSCLC患者的临床病理特征、预后、ALK-TKIs应用必要性等情况做一简要综述.     

Smoking and smoking cessation in relation to the development of co‐existing non‐small cell lung cancer with chronic obstructive pulmonary disease

Previous studies have identified a mixed‐phenotype of non‐small cell lung cancer (NSCLC) with co‐existing chronic obstructive pulmonary disease (COPD). Although NSCLC and COPD share a common risk factor in smoking, whether and how smoking may contribute to the coexistence of NSCLC with COPD (NSCLC‐COPD) is unclear. Our study suggests that cigarette smoking is the major risk factor for the development of NSCLC‐COPD, especially in females and among patients with squamous cell carcinoma subtype.     

Ras homologue enriched in brain is a critical target of farnesyltransferase inhibitors in non-small cell lung cancer cells

The purpose of this work is to study mechanisms underlying anti-tumor effects of farnesyltransferase inhibitors (FTIs) in non-small cell lung cancer (NSCLC). We demonstrate that mRNA and protein levels of Ras homologue enriched in brain (Rheb) are highly expressed both in NSCLC tissues and in NSCLC cell lines. Rheb expression levels correlate with phosphorylation of its downstream target S6 and the sensitivity of NSCLC cells to FTIs (R115777 and SCH66336)-induced growth inhibition and apoptosis. FTIs effectively and preferentially inhibited Rheb downstream signaling in NSCLC cells. Moreover, inhibition of Rheb functions by FTIs or dominant-negative Rheb mutants enhance the effects of cisplatin on NSCLC cells. Rheb-CSVL, a FTIs-resistant mutant, reduces the effects of FTIs on NSCLC cells. Our results suggest that Rheb is a critical target for FTIs therapy in NSCLC.     

非小细胞肺癌中伴神经内分泌分化及c-erbB-2表达的意义

 目的　探讨非小细胞肺癌(NSCLC) 伴神经内分泌分化(NE) 与原癌基因c-erbB-2 表达的关系。方法　观察非小细胞肺癌32 例,用免疫组织化学S-P 法来判定神经内分泌分化及c-erbB-2 表达特点。结果　NSCLC 中24 例有NE 分化,c-erbB-2 在伴NE 分化和无NE 分化的表达阳性率比较,差异有显著性,NE 分化的阳性率和癌细胞分化程度有显著性差异。c-erbB-2 阳性在淋巴结转移组表达与无淋巴结转移组表达相比有显著性差异。结论　c-erbB-2 的过表达在非小细胞肺癌中与其侵袭性的生物学行为密切相关。c-erbB-2 过表达可用来判断NE 分化的非小细胞肺癌预后。     

Frizzled-7-targeting antibody (SHH002-hu1) potently suppresses non–small-cell lung cancer via Wnt/β-catenin signaling

Non–small-cell lung cancer (NSCLC) is one of the deadliest cancers worldwide, and metastasis is considered one of the leading causes of treatment failure in NSCLC. Wnt/β-catenin signaling is crucially involved in epithelial–mesenchymal transition (EMT), a crucial factor in promoting metastasis, and also contributes to resistance developed by NSCLC to targeted agents. Frizzled-7 (Fzd7), a critical receptor of Wnt/β-catenin signaling, is aberrantly expressed in NSCLC and has been confirmed to be positively correlated with poor clinical outcomes. SHH002-hu1, a humanized antibody targeting Fzd7, was previously successfully generated by our group. Here, we studied the anti-tumor effects of SHH002-hu1 against NSCLC and revealed the underlying mechanism. First, immunofluorescence (IF) and near-infrared (NIR) imaging assays showed that SHH002-hu1 specifically binds Fzd7⁺ NSCLC cells and targets NSCLC tissues. Wound healing and transwell invasion assays indicated that SHH002-hu1 significantly inhibits the migration and invasion of NSCLC cells. Subsequently, TOP-FLASH/FOP-FLASH luciferase reporter, IF, and western blot assays validated that SHH002-hu1 effectively suppresses the activation of Wnt/β-catenin signaling, and further attenuates the EMT of NSCLC cells. Finally, the subcutaneous xenotransplanted tumor model of A549/H1975, as well as the popliteal lymph node (LN) metastasis model, was established, and SHH002-hu1 was demonstrated to inhibit the growth of NSCLC xenografts and suppress LN metastasis of NSCLC. Above all, SHH002-hu1 with selectivity toward Fzd7⁺ NSCLC and the potential of inhibiting invasion and metastasis of NSCLC via disrupting Wnt/β-catenin signaling, is indicated as a good candidate for the targeted therapy of NSCLC.     

Ca/calmodulin-dependent protein kinase IIγ, a critical mediator of the NF-κB network,is a novel therapeutic target in non-small cell lung cancer

The molecular mechanism that triggers constitutive activation of nuclear factor-kappa B (NF-κB) in non-small cell lung cancer (NSCLC) remains elusive. In this present study, we demonstrated that Ca²⁺/calmodulin-dependent protein kinase IIγ (CaMKIIγ) is a critical molecular switch of continuous activation of NF-κB in NSCLC. We found that CaMKIIγ was aberrantly expressed in human NSCLC tissues and correlated well with the degree of malignancy. Functionally, CaMKIIγ promoted the growth and survival of NSCLC cells via direct activation of NF-κB and multiple oncogenic signaling pathways in NSCLC. Taken together, our findings described a previously uncharacterized role of CaMKIIγ in NSCLC, and suggest a novel potential therapeutic target for NSCLC treatment.     

Dickkopf家族蛋白在非小细胞肺癌中的作用机制和治疗应用的研究进展

非小细胞肺癌(Non-small cell lung cancer,NSCLC)占所有肺癌的80%~85%,是全世界发病率和致死率极高的恶性肿瘤。最初NSCLC对现有治疗的反应良好,但最终还是产生了耐药性。因此,有必要探索有效且新颖的治疗方法。随着对NSCLC研究的深入,发现Dickkopf家族蛋白(DKKs)的信号传导在NSCLC发展中扮演重要角色,DKKs是Wnt/β-catenin信号通路的重要调节因子,并与NSCLC细胞增殖、转移和侵袭密切相关。本文主要介绍了DKKs家族成员在NSCLC中的作用机制,讨论了DKKs在NSCLC治疗中的潜力,为进一步防治NSCLC提供了新思路。     

非小细胞肺癌MAGE-3基因产物的表达

目的　检测MAGE 3基因编码的抗原在非小细胞肺癌表达的情况 ,探讨MAGE 3抗原的表达与患者临床表现的关系 ,以及利用MAGE 3基因产物对非小细胞肺癌患者进行特异性免疫治疗的可能性。方法　用免疫组化LSAB的方法对石蜡包埋的组织切片进行MAGE 3抗原的检测。结果　 10 4例非小细胞肺癌原发灶肿瘤组织切片中 ,MAGE 3抗原阳性者 31例 ,阳性率 2 9.8%。MAGE 3抗原阳性患者肿瘤转移率 (30 .0 % )明显低于阴性患者的转移率 (5 6 .1% ,P <0 .0 5 ) ,MAGE 3抗原阳性患者 18个月的生存率 (88.2 % )明显高于阴性患者生存率 (5 2 .9% ,P <0 .0 1)。结论　非小细胞肺癌有较高比例的MAGE 3抗原表达 ,并与患者的预后相关。对MAGE 3抗原阳性NSCLC患者 ,可以利用MAGE 3抗原作为靶分子进行免疫治疗。