P63和TTF-1在肺癌组织中的表达及意义

目的研究P63和TTF-1在肺癌各种类型组织中的表达及其意义。方法随机收集原发性肺癌组织标本53例（其中鳞癌16例,腺癌16例,小细胞癌14例,大细胞癌7例,均为中低分化程度癌组织）,采用免疫组织化学S-P法分别检测P63蛋白和TTF-1蛋白在各种类型肺癌组织中的表达并结合二者表达的结果进行分析。结果二者的表达在肺癌细胞中定位于细胞核,呈棕黄色。在肺鳞癌、肺腺癌、肺小细胞癌和肺大细胞癌中,P63的阳性表达率分别为93.8%（15/16）、37.5%（6/16）、21.4%（3/14）、28.6%（2/7）;TTF-1的阳性表达率分别为18.8%（3/16）、75%（12/16）、78.6%（11/14）、0%（0/7）。结论①P63在肺鳞癌中的表达水平较高,可以作为鉴别低分化鳞癌与低分化腺癌,小细胞癌的指标;②TTF-1在低分化腺癌和小细胞癌中的表达水平较高,对于肺癌组织类型和非癌组织的鉴别具有一定意义;③根据P63和TTF-1在肺癌组织的特异性表达,将二者联合起来有助于对低分化鳞癌和低分化腺癌以及低分化鳞癌和小细胞癌的鉴别诊断。     

ILK在肺鳞状细胞癌和肺腺癌的表达及其与临床病理特征和预后的关系

目的 探讨ILK在肺鳞状细胞癌和肺腺癌组织中的表达情况,及其与病理分型、肿瘤分化、分期、淋巴结转移及预后的关系。方法采用S-P免疫组织化学方法和Western Blot法,检测肺鳞状细胞癌和肺腺癌组织及相应癌旁肺组织中整合连接激酶（integrin-linkedkinase,ILK）的表达情况,并结合临床和病理资料进行分析。结果免疫组化结果显示：ILK在53／76（70％）的肺癌组织中阳性表达。其中鳞状细胞癌阳性率75％（33／44）,腺癌阳性率62．5％（20／32）,其表达与肺鳞状细胞癌的分化呈负相关（P〈0．01）,与临床分期（P〈0．01）、淋巴结转移（P〈0．01）呈正相关;与肺腺癌的临床分期（P〈0．01）和淋巴结转移（P〈0．01）正相关,与分化程度无相关性（P〉0．05）。同时,其表达与患者的生存时间呈负相关（P〈0．01）,与年龄、性别、肿瘤大小和组织类型等因素无关。Western Blot法进一步证实ILK在肺癌组织中的表达显著高于癌旁正常肺组织（P〈0．01）,其表达与肺癌的分化（P〈0．01）显著负相关。结论肺鳞状细胞癌和肺腺癌中,ILK与肺癌的侵袭和转移有关。ILK可作为判断肺鳞状细胞癌和肺腺癌预后的参考指标。     

钠／碘同向转运体在人不同组织学分型胃癌中的表达

目的研究钠／碘同向转运体（sodium-iodide symporter,NIS）在人不同组织学分型胃癌组织中的表达,分析NIS表达与胃癌组织学分型的关系。方法选取于中国医科大学附属第一医院肿瘤外科行手术治疗的180例患者的胃癌组织为研究对象。依据胃癌的组织学分型分为6组,其中乳头状腺癌30例,管状腺癌30例,低分化腺癌30例,黏液腺癌30例,印戒细胞癌30例,未分化癌30例。选取上述180例患者的癌旁组织及30例慢性胃炎患者的胃组织作为对照。采取免疫组织化学SP法对上述组织的石蜡切片进行染色。结果在人胃癌组织、人胃癌旁组织及人慢性胃炎组织中,NIS阳性细胞率分别为10．6％（19／180）、28．3％（51／180）和90％（27／30）。人胃癌组织与人胃癌旁组织相比（P〈0．01）、人胃癌组织与人慢性胃炎组织相比（P〈0．01）、人胃癌旁组织与人慢性胃炎组织相比（P〈0．01）,NIS阳性细胞率均具有显著统计学差异。在人乳头状腺癌、管状腺癌、低分化腺癌、黏液腺癌、印戒细胞癌及未分化癌中,NIS阳性细胞率分别为30％（9／30）、10％（3／30）、13．3％（4／30）、6．7％（2／30）、3．3％（1／30）和0（0／30）。人乳头状腺癌与人黏液腺癌相比（P〈0．05）、人乳头状腺癌与人印戒细胞癌相比（PGO．01）以及人乳头状腺癌与人未分化癌相比（P〈0．01）,NIS阳性细胞率均具有统计学差异。在人慢性胃炎组织及人胃癌旁组织中,NIS仅表达于胃黏膜细胞的细胞膜上,而在人胃癌组织中,NIS在癌细胞膜有表达,在细胞质也有较明显的表达。结论在人胃癌组织、癌旁组织、慢性胃炎组织中,NIS阳性细胞率依次增高。在本研究人各种组织学分型的胃癌中,随着胃癌恶性程度的增高,NIS表达呈现出减少的趋势。人胃癌组织NIS在癌细胞的细胞膜和细胞质均有表达,而?     

非小细胞肺癌中HMGA2的表达与细胞增殖的关系

目的探讨High mobility group A2 protein（HMGA2）的表达对非小细胞肺癌生长、转移的影响,与临床病理参数和细胞增殖的关系。方法应用免疫组化法检测38例非小细胞肺癌组织（23例鳞癌,15例腺癌）及癌旁的正常肺组织标本中HMGA2和Ki-67的表达。结果HMGA2和Ki-67在癌旁的正常肺组织中均不表达,而在肺癌组织中的表达阳性率分别为39．47％、44．74％,二者在肺癌组和癌旁的正常肺组织组之间差异有显著性（P〈0．05）。HMGA2的表达在伴淋巴结转移的肺癌组织明显高于不伴有淋巴结转移的肺癌组织（P〈0．05）,而与其他临床病理参数包括肿瘤的分化程度、肿瘤大小和TNM分期以及细胞增殖指标Ki-67之间没有相关性。结论本研究显示HMGA2在非小细胞肺癌组织中异常表达,可能与肺癌的发生和进展有关。     

Survivin在肺鳞癌、腺癌中的表达及其与Ki67和p53表达的关系

目的探讨survivin在肺鳞癌、腺癌中的表达和意义及其与Ki67、p53表达的相关性。方法采用免疫组织化学SP法检测survivin、Ki67和p53在112例肺鳞癌、腺癌中的表达情况。结果Survivin、Ki67和p53的阳性率分别为59．8％（67／112）、46．4％（52／112）和51．8％（58／112）,survivin的表达与肺癌的低分化（P=0．009）和淋巴结转移正相关（P=0．014）;Ki67和p53的表达分别与肺鳞癌、腺癌的低分化程度负相关（P〈0．05）。Survivin与Ki67和p53在肺鳞癌、腺癌中的表达分别正相关（P〈0．01）。结论Survivin的表达与肺鳞癌、腺癌的低分化和淋巴结转移正相关;Ki67和p53的表达分别与肺鳞癌和腺癌的低分化程度相关,survivin、Ki67和p53三者的协同表达可能是促进肺癌的恶性进展的重要因素。     

252例胸膜恶性肿瘤的临床病理分析

目的：探讨胸膜恶性肿瘤的病理类型、肿瘤所占比例、临床病理特征及鉴别诊断。方法：结合病理形态学及免疫组化方法对252例胸膜恶性肿瘤进行诊断及鉴别诊断。结果：252例胸膜恶性肿瘤包括胸膜穿刺活检120例,胸腔镜活检25例,伴有胸膜转移的恶性胸水107例;男性143例,女性109例,年龄19—87岁,平均年龄59．9岁。临床主要症状是胸闷、气短、咳嗽、胸痛等。CT表现为胸膜增厚、胸水（90％）、多发或单发胸膜结节和原发器官占位性病变。活检病例中,转移性癌86例（34．1％）,包括肺腺癌64例（25．4％）,小细胞癌11例（4．4％）,鳞癌11例（4．4％）,恶性间皮瘤47例（18．7％）,滑膜肉瘤9例（3．6％）,非霍奇金淋巴瘤3例（1．2％）;恶性胸水病例病例中转移性癌95例（37．7％）,包括肺腺癌85例（33．7％）,小细胞癌6例（2．4％）,鳞癌2例（0．8％）,乳腺腺癌2例（0．8％）,恶性间皮瘤8例（3．2％）,非霍奇金淋巴瘤4例（1．6％）。结论：胸膜恶性肿瘤中以转移性腺癌多见,其次为恶性间皮瘤,结合形态学及免疫组织化学检测不同标志物的表达有助于诊断胸膜恶性肿瘤的种类。     

survivin和caspase-3在非小细胞肺癌中的表达及相关性研究

目的：研究survivin和caspase-3蛋白在非小细胞肺癌中的表达情况,分析二者的作用机制及相关性。方法：采用免疫组化KIT染色法,检测survivin和caspase-3在60例NSCLC组织和20例正常肺组织中的表达情况。结果：肺癌组织中的survivin阳性表达率（61．67％）明显高于正常肺组织（5％）;Ⅲ期的survivin阳性表达率（76．92％）明显高于Ⅰ＋Ⅱ期（50％）;均有显著性差异（P〈0．05）;而与年龄,病理类型,组织分化程度,淋巴结转移情况无关。肺癌组织中caspase-3阳性表达率（43．33％）明显低于正常组织（85％）;高＋中分化组的caspase-3阳性表达率（58．06％）明显高于低分化的（27．59％）;鳞癌组织中的caspase-3阳性表达率（56．25％）高于腺癌组织（28．57％）;均有显著性差异（P〈0．05）;而与年龄,TNM分期,淋巴结转移情况无关。结论：survivin在非小细胞肺癌中表达上调,而caspase-3却下降,且二者的表达呈负相关,提示survivin可能参与肺癌的发生发展,且抑制caspase-3的激活而抑制凋亡;caspase-3的失活可能导致肿瘤细胞的增殖。     

非小细胞肺癌中肿瘤标志物CEA、SCC、NSE表达水平的临床分析

目的分析和探讨肿瘤标志物CEA、SCC、NSE在非小细胞肺癌临床预诊中的价值。方法对83例非小细胞肺癌患者和50例健康人进行肿瘤标志物CEA、SCC、NSE检测,从非小细胞肺癌不同分期、不同病理类型及综合阳性率等方面进行观察分析。结果非小细胞肺癌组CEA阳性率各期均在50%以上,NSE阳性率随肿瘤分期递增,平均为51.8%,二者的测定值Ⅲb、Ⅳ期均明显高于Ⅱ、Ⅲa期(P<0.01);SCC阳性率25%~33.3%,测定值各期差异不显著(P>0.05)。CEA以腺癌阳性率最高,测定值腺癌组明显高于其他组(P<0.01);SCC鳞癌组的阳性率和测定值均高于其他组(P<0.05);NSE鳞癌和大细胞未分化癌阳性率均在50%以上,测定值鳞癌、大细胞未分化癌和其他类型明显高于腺癌组(P<0.01)。不同病理类型综合阳性率的表达:有一项以上阳性者鳞癌为71.1%,腺癌为81.3%,大细胞未分化癌为80%,其他类型为100%。结论CEA、SCC、NSE三者联合检测综合阳性率明显提高。NSE敏感性高,特异性差,可作为肺癌早期诊断的辅助手段。     

MCM7与RACK1在肺癌中的表达及其临床意义

目的探讨MCM7与RACK1在各类型肺癌中的表达及其相关性。方法收集肺腺癌150例、鳞癌150例、大细胞癌20例和小细胞癌50例及其癌旁正常肺组织石蜡标本,采用免疫组织化学S-P法检测各类型肺癌组织和癌旁正常肺组织中MCM7与RACK1的表达,并分析二者与肺癌临床病理因素的关系。结果 MCM7与RACK1在癌组织中的表达明显高于癌旁正常肺组织;χ~2检验结果显示肺癌中MCM7与RACK1的表达均与肺癌的病理分级、淋巴结转移、组织学分类和临床TNM分期相关;Pearson相关性分析结果显示,肺癌中MCM7与RACK1的表达呈正相关;Kaplan-Meier法分析显示MCM7与RACK1高表达患者生存时间缩短。结论肺癌中MCM7与RACK1的表达呈正相关,二者表达在肺癌中起促进作用,可作为检测肺癌细胞的增殖状态、新的判断预后的重要因子,以其为靶向进行临床治疗的重要指标。     

老年宫颈癌50例临床及预后分析

目的：探讨老年宫颈癌的临床病理特征及预后影响因素。方法：对50例老年宫颈癌患者的临床特点及生存情况进行回顾性分析。结果：鳞状细胞癌45例（90．0％）,腺癌4例（8．0％）,透明细胞癌1例（2．0％）;≤Ⅱa期占16．0％,≥Ⅱb期占84．0％;主要临床症状为绝经后不规则阴道流血,全组1、3、5年生存率分别为82．0％,66．0％,54．0％。多因素分析结果显示病理类型、临床分期及淋巴结转移情况是老年宫颈癌患者预后的独立影响因素（均P〈0．05）。结论：KPS评分≥70分、鳞癌、临床分期为Ⅰ期、Ⅱ期,无淋巴结转移的患者预后较好,病理类型、临床分期及淋巴结转移情况是老年宫颈癌患者预后的独立影响因素。     

Endothelial cells and angiogenesis intensity in lung cancer

We focused our studies on single endothelial cells (ECs) scattered in extracellular matrix in lung cancer tumors. Neovascularization was evaluated in 100 tumors obtained from patients operated for lung cancer, in relation to histological type, tumor differentiation and clinical stage of the disease. Angiogenic objects (single endothelial cells and microvessels) were identified by immunohistochemistry using monoclonal antibodies against von Willebrand factor. The count of angiogenic objects per 1 mm2 in each section was determined in a "hot spot" located at the margin of the tumor. We used an arbitrary scale of angiogenesis intensity: 1 - 0-200, 2 - 201-400, 3 - >400 angiogenic objects/mm2. A majority (57%) of the examined cases belonged to the group 2. The angiogenesis intensity measured by the single EC numbers/mm2 correlates with the histological type and the differentiation of the tumors. There was no such a correlation when the angiogenesis intensity was measured by counting total angiogenic objects (microvessels + EC) number/mm2. Single EC number/mm2 in different histological types of cancer were as follows: 162+/-121 in squamous cell (SqCC), 194+/-71 in adenocarcinoma (AdC), 225+/-145 in large cell (LCC), 264+/-52 in small cell (SCC), 279+/-173 in combined cancer. The differences between the EC counts in the different histological types of lung cancers were statistically significant in the following pairs: SqCC vs SCC (p=0.0233) and AdC vs SCC (p=0.0409).The correlation between EC count in the "hot spot" and the grade of tumor differentiation was statistically significant for G1 vs G4 (p=0.0007) and G1 vs G2 (p=0.0411). Our results suggest that higher numbers of EC/mm2 may confirm rapid development of angioneogenesis. These relations should be examined in larger series of cases.     

Circulating anti-p53 antibodies in lung cancer and relationship to histology and smoking

Anti-p53 antibodies were examined in the plasma of 112 lung cancer patients by ELISA in order to study the distributions in lung cancer patients and the determinants of these antibodies in relation to lung cancer. Twenty (17.9 %) lung cancer patients were found to have anti-p53 antibodies. The distribution of the antibodies by histological type was 7/48 (14.6 %) adenocarcinoma, 8/32 (25.0 %) squamous cell carcinoma, 3/7 (42.9 %) small cell lung cancer, 0/4 large cell carcinoma, 0/8 adenosquamous cell carcinoma and 2/13 (15.4 %) other types. By ethnicity, 8/44 (18.2 %) Caucasians, 4/20 (20.0 %) Hispanics and 8/48 (16.7 %) African-Americans were positive for anti-p53 antibodies, with no significant differences among the groups (p=0.5137). The antibody positivity rates were higher in lung cancer patients 55 years or older (21.2 %) than in the patients under 55 years (7.4 %). The positive rates of the antibodies were 14.3 % in non-smokers, 16.7 % in ex-smokers and 19.1 % in current smokers, with heavy smokers (41 pack-years) having the highest positive rate (28.6 %), but none of these differences were statistically significant (p > 0.05). Seven controls who had anti-p53 antibodies were all ex-smokers or current smokers and some had occupational exposures. No anti-p53 antibodies were found in 41 non-smoking controls. These results suggest that the development of anti-p53 antibodies in pulmonary carcinogenesis and its association with smoking and other carcinogenic exposures deserve further study.     

Histologic and cytologic patterns of lung cancer in 2,580 men and women over a 15-year period

This paper describes the relative frequencies and changes in the morphologic patterns of lung cancer, as documented in the histologic and cytologic specimens from 2,580 patients diagnosed and treated at Duke University Medical Center over a period of 15 consecutive years. During the first five years, the relative frequencies of the various types of lung cancers were, in descending order, squamous cell carcinoma (43.1%), large cell undifferentiated carcinoma (22.5%), adenocarcinoma of the acinar type (18.6%), small cell undifferentiated carcinoma (11.6%), bronchioloalveolar carcinoma (3.5%) and adenosquamous carcinoma (0.7%). During the second and third five-year periods, squamous cell carcinoma remained the most common neoplasm, but declined to 35.7%, while adenocarcinoma of the acinar type became the second most common lung cancer at 22.0%. The absolute and relative incidences of lung cancer in women showed a striking increase from 21.8% to 29.9%. During this same period, adenocarcinoma of the acinar type replaced squamous cell carcinoma as the most common primary lung cancer in women.     

The usefulness of a panel of immunostains in the diagnosis and differentiation of metastatic malignancies in pericardial effusions

Pericardial effusions are not uncommon in patients with an advanced malignancy Rarely malignancies may present initially with a pericardial effusion. Cytological examination of pericardial fluid may be valuable in differentiation of these cases. However, a metastatic tumour in serous effusion may not always show the functional differentiation of the primary tumour. In such a situation, although a wide range of special studies have been suggested for the diagnosis of malignancy we have found the use of a panel of a few common immunostains to be useful in confirming or suggesting the site of a primary tumour. The material for this study consisted of 76 pericardial fluids obtained between January 1991 and October 1998 from 46 males (mean age 59 years) and 30 females (mean age 52 years). Metastatic malignancy was diagnosed in 22 of the 76 patients and in 7/22 cases pericardial effusions were the initial presentation. The subsequent follow-up in the seven cases revealed adenocarcinoma of lung (n = 2), small cell anaplastic carcinoma of lung (n = 1), squamous cell carcinoma lung (n = 1), melanoma leg (n = 1), non-Hodgkin's lymphoma retroperitoneal lymph nodes (n = 1) and carcinoma of the breast (n = 1). Of the remaining 15 cases with a known history of malignancy, eight had cancers (three adeno; two small cell; one poorly differentiated, and two squamous cell types) of the lung; breast (n = 3); colon (n = 1); melanoma (n = 2) and non Hodgkin's lymphoma (n = 1). Immunostains which were useful in the diagnosis were EMA, CEA, cytokeratin, B72.3, HMB45, vimentin, S100, LCA, L26 and kappa and lambda light chains.     

Natural killer (NK)-resistant human lung cancer cells are lysed by recombinant interleukin-2-activated NK cells

Natural killer (NK) cells are active in host defence against tumors. In order to determine if NK cells have the capacity to lyse human lung cancer cells, we evaluated blood NK cell activity against human lung carcinoma lines representing each of the commonest histological types of lung cancer, NCI-H157 (large cell), LICM107 and NCI-H146 (small cell), NCI-H226 (squamous cell), and LICM26 (adeno), and compared the results to their activity against a standard NK-sensitive target, K562, using a 16-hr 51Cr-release assay. At effector to target (E:T) ratios up to 50:1, NK activity was very low against each of the lung cancer cell lines compared to the K562 cells (NCI-H157 10 +/- 2%, LICM107 12 +/- 2%, NCI-H146 14 +/- 5%, NCI-H226 8 +/- 5%, and LICM26 7 +/- 3%, compared to K562 60 +/- 3%, P less than 0.001, for each compared to K562 cells). Recombinant interleukin 2 (IL-2) produced a dose-dependent augmentation of NK activity against each of the lung cancer cell lines, with doses as low as 0.25 U/ml being effective. The highest level of boosting was seen against NCI-H157 cells where NK activity (E:T, 50:1, IL-2, 250 U/ml) increased from 9 +/- 2 to 56 +/- 7%, P less than 0.001). Only brief exposure to IL-2 was necessary for augmentation to occur, with as little as 5 min being required for activation, although increased exposure times produced increased levels of augmentation. NK cells appeared to be the IL-2-responsive lytic cell population in these experiments as Leu 11b-depleted lymphocytes expressed little IL-2-mediated augmentation of activity against these target cells, and most of this IL-2-mediated augmentation of activity was located in the large granular lymphocyte-enriched fraction of the lymphocyte population. We conclude that normal blood NK cell activity against human lung cancer cell lines is low but that this activity can be markedly augmented by brief exposure of NK cells to low doses of recombinant IL-2, suggesting a potential role for IL-2 in the immunotherapy of human lung cancer.     

Presence of human papillomavirus genome in human tumor cell lines and cultured cells.

A series of 47 human carcinoma cell lines and their cultured cells were examined for human papillomavirus (HPV) genomes with the use of an HPV detection kit (DNA-RNA hybridization, mixed HPV DNA probe of types 6, 11, 16, 18, 31, 33 and 35). Four of 8 cases of mild dysplasia, 3 of 9 cases of severe dysplasia, 3 of 7 cases of carcinoma in situ, 3 of 15 cases of uterine carcinoma and 5 of 6 cases of condyloma acuminatum were shown to contain the HPV DNA genome in primary cultured cells, while HPV was not detected in the third-passage cells except for the three cases of large cell, nonkeratinizing squamous cell carcinoma. HPV was also not detected in such normal tissues as uterine cervical squamous epithelium, uterine cervical columnar epithelium and endometrium. The presence of HPV DNA genomes was detected consistently in the passages of three lines (SKG-II, HKMUS and HKTUS; large cell nonkeratinizing squamous cell carcinomas of the uterine cervix) with the use of the Southern Blot method (DNA-DNA hybridization, mixed HPV probe of types 6, 11, 16 and 18). HPV type 16 DNA was detected in HKTUS, and HPV type 18 DNA was found in SKG-II and HKMUS. The other 44 cell lines, including ovarian carcinoma, endometrial carcinoma, sarcoma, gastric cancer, pancreatic cancer and rectal cancer, were negative for the HPV-6, HPV-11, HPV-16, HPV-18, HPV-31, HPV-33 and HPV-35 genomes under stringent hybridization conditions.     

Immunohistochemical analysis of the ubiquitin-conjugating enzyme UbcH10 in lung cancer: a useful tool for diagnosis and therapy

The ubiquitin-conjugating enzyme (UbcH10) plays important roles in the regulation of cell cycle progression. Recently, UbcH10 expression has been demonstrated in several human and experimental tumors, and proteasome inhibitors have been tested in trials for pulmonary neoplasms; however, the underlying mechanisms as well as the clinicopathological relevance of UbcH10 in the genesis and progression of lung cancer remain largely unknown. Therefore, the authors evaluated the expression of UbcH10 in human lung cancer and evaluated its possible diagnostic and prognostic use. They found that most cases of lung adenocarcinoma, squamous cell carcinoma, and large cell and small cell carcinoma were positive for UbcH10. The expression levels of UbcH10 progressively increased with decreasing degree of tumor differentiation. There was a statistically significant difference of UbcH10 positivity between grade I/III of lung adenocarcinoma (p=0.013) and squamous cell carcinoma (p=0.002). No significant differences were found between histological types (p=0.072). In the case of cell blocks prepared from pleural effusions, inflammatory and reactive mesothelial elements did not show appreciable UbcH10 expression, whereas neoplastic cells exhibited clear UbcH10 positivity. The results suggest that UbcH10 might represent a new and promising diagnostic and prognostic marker in both histologic and cytologic specimens of lung cancer.     

Detection of human papillomavirus in non-small cell lung carcinoma by polymerase chain reaction

Human papillomavirus (HPV) infection is one of the risk factors contributing to the pathogenesis of lung cancer. The aim of the study was to determine the presence of HPV in non-small cell carcinomas of the lung. The study included 40 tumors: 22 squamous cell carcinomas, 13 adenocarcinomas and 5 large cell carcinomas. HPV was found in 4 cases (10%). High risk HPV was present in 3 tumors: in one squamous cell carcinoma, one large cell carcinoma and one adenocarcinoma, while low risk HPV was detected in one adenocarcinoma.     

非小细胞肺癌组织MMP-2、MMP-9的表达与组织学类型及临床分期的关系

目的:探究非小细胞肺癌组织基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-9(MMP-9)的表达及其与患者组织学类型及其临床分期的关系。方法:选取2014年1月至2017年1月于我院进行就诊并确诊为非小细胞肺癌的96例患者为实验组,另选取30例肺良性病变患者为对照组,使用免疫组织化学的方法检测患者肺癌组织或肺良性病变组织中MMP-2、MMP-9的表达,并分析MMP-2、MMP-9的表达与患者组织学类型及临床分期之间的关系。结果:非小细胞肺癌组织MMP-2及MMP-9表达水平显著高于肺良性病变组织(P0.05)。非小细胞肺癌鳞癌组织MMP-2、MMP-9表达明显高于腺癌和腺鳞癌(P0.05),而鳞癌与腺鳞癌组织MMP-2、MMP-9表达相比差异无统计学意义(P0.05)。随着非小细胞肺癌临床分期的增加,癌组织MMP-2及MMP-9表达逐渐上升,各分期比较差异均具有统计学意义(P0.05)。结论:MMP-2、MMP-9在非小细胞肺癌组织中的表达水平明显上调,以鳞癌最高,且与临床分期显著相关,提示其对组织学类型、临床分期、病情评估和预后判断均具有一定的参考意义。