Notch1在腺样囊性癌组织中的表达及其对预后的影响

目的： 探讨腺样囊性癌 (adenoid cystic carcinoma,ACC)组织中Notch1的表达,分析其表达与临床病理资料间的关系及其对预后的影响。方法：运用免疫组化方法检测38例ACC患者及对照组正常口腔小涎腺中Notch1的表达,并对ACC病例进行随访,分析Notch1的表达与临床病理资料间的关系及其对预后的影响。结果：ACC病例组中Notch1总阳性率为81.6% (31/38),而正常口腔小涎腺阳性率为30% (9/30),Notch1在ACC及正常口腔小涎腺中的表达差异具有统计学意义 (P<0.05)。Notch1的表达与病理分型、T分期及侵犯相邻组织呈正相关 (r =0.550,P=0.002;r =0.741,P=0.001;r =0.523,P=0.005)。单因素分析显示：病理分型、淋巴结转移、Notch1的表达、T分期、侵犯相邻组织对患者的预后有影响 (P<0.05),且Notch1的表达和肿瘤分期是影响患者预后的独立危险因素。结论：ACC生长缓慢,但易复发且伴远处转移,Notch1在ACC的发生和发展中起重要作用,在评估其预后方面起一定作用。     

UHRF1在膀胱癌中的表达及临床意义

[目的]研究UHRF1在膀胱癌中的表达及临床意义.[方法]采用实时荧光定量逆转录聚合酶链反应(RT-PCR)和免疫组化法分别检测58例膀胱癌组织和20例相应正常组织中UHRF1的表达,并分析表达的差异与临床病理特征的关系.[结果]UHRF1 mRNA在膀胱癌中的表达量(107.0±24.3)高于正常组织的表达量(1.9±0.4),差异有显著统计学意义(P＜0.001);免疫组化显示UHRF1蛋白在膀胱癌组织中的阳性表达率为53.4％,正常组织中未见表达,两种组织的表达有明显差异(P＜0.001).UHRF1蛋白的表达与肿瘤分级(P=0.026)和分期(P=0.017)有关,与性别、年龄、肿瘤大小、数目无明显相关性(P＞0.05).[结论]UHRF1的表达在肿瘤组织中明显高于正常组织,且与病理分级、临床分期有关,UHRF1的过表达可能促进膀胱癌的进展.     

Keap1在乳腺癌组织中的表达及临床意义

[目的]探讨Keap1在乳腺癌组织中的表达.[方法]选取2013年1月至2015年12月在武汉市武昌医院肿瘤科收治的原发乳腺肿瘤患者,其中病理诊断为乳腺癌80例(乳腺癌组)和乳腺良性肿瘤300例(乳腺良性肿瘤组),两组都进行Keap1的免疫组化分析与临床资料的调查分析.[结果]乳腺癌组的Keap1阳性表达率为70.0％,乳腺良性肿瘤组为7.8％,乳腺癌组的Keap1阳性表达率明显高于乳腺良性肿瘤组(P＜0.05).在80例乳腺癌患者中,Keap1的阳性表达与患者的病理类型、临床分期、淋巴结转移情况等有相关性(P＜0.05).多元回归Logistic分析结果显示,临床分期、淋巴结转移与病理类型是影响乳腺癌患者Keap1阳性表达的主要独立危险因素(P＜0.05).[结论] Keap1在乳腺癌组织中呈现高表达,且与患者的临床分期、淋巴结转移与病理类型明显相关,参与乳腺癌的发生与发展.     

Gli1在食管鳞状细胞癌中的表达及与预后的关系

目的:探讨Hh信号通路关键因子Gli1在食管鳞状细胞癌(ESCC)中的表达及临床意义,并分析其与预后的关系.方法:食管鳞状细胞癌组织及癌旁正常食管组织各88例,采用免疫组织化学法检测Gli1的表达,另用Western-blot方法检测其中30例ESCC的Gli1的表达,Pearson卡方检验分析Gli1表达与临床病理特征之间的关系.单因素Kaplan-Meier法分析Gli1表达与预后的关系.Cox比例风险回归评估Gli1表达与预后的关系.结果:食管鳞状细胞癌组织中Gli1的表达在蛋白水平明显高于食管正常鳞状上皮,Gli1在ESCC中免疫组化阳性表达率为71.59％ (63/88),Gli1在癌旁正常食管鳞状上皮中免疫组化阳性表达率为6.82％ (6/88),差异有统计学意义(P＜0.05).Western blot法证实Gli1蛋白在ESCC组织中表达上调,与癌旁正常食管组织中的表达比较,差异有统计学意义(P ＜0.001).Gli1高表达与肿瘤病理分期及淋巴结转移密切相关(P＜0.05).单因素分析Kaplan-Meier法提示Gli1阳性表达组与阴性表达组生存率之间的差别有统计学意义(Log-rank test,P=0.005).结论:食管鳞状细胞癌中Gli1的表达比较普遍,与ESCC的预后密切相关,可作为预测转移潜能和预后判断的有价值的指标.     

脑源性神经营养因子在涎腺腺样囊性癌中的表达及意义

[目的]探讨脑源性神经营养因子（BDNF）与涎腺腺样囊性癌（SACC）的关系。[方法]采用免疫组织化学方法检测45例SACC切片中BDNF的表达,并统计分析BDNF与SACC组织学分型、临床分期、神经侵犯和远处转移之间的关系。[结果]BDNF在SACC中的阳性表达率为84.4%（38/45）,BDNF表达强度与SACC的组织学分型和神经侵犯无明显关系（P〉0.05）,而与临床分期、远处转移关系密切（P〈0.05）。[结论]SACC中存在BDNF异常表达,而且BDNF可能促进了SACC的发生发展。     

涎腺腺样囊性癌中丝裂原激活蛋白激酶p38的表达及意义

目的 探讨丝裂原激活蛋白激酶p38(p38MAPK)在涎腺腺样囊性癌(SACC)中的表达及临床意义.方法 采用组织微阵列平台,运用免疫组化和原位杂交技术,检测52例SACC和11例正常涎腺组织中p38MAPK蛋白和mRNA的表达,并分析其与SACC 临床病理特征的关系.结果 正常涎腺组织和SACC组织中,p38MAPK蛋白的阳性表达率分别为36.4%和96.2%,差异有统计学意义(P＜0.01).p38MAPK蛋白表达与SACC的淋巴结转移、神经侵犯有关(均P＜0.05).正常涎腺组织和SACC组织中,p38MAPK mRNA的阳性表达率分别为45.5%和94.2%,差异有统计学意义(P＜0.01).p38MAPK mRNA表达与SACC的淋巴结转移、神经侵犯有关(均P＜0.05).SACC组织中,p38MAPK蛋白与mRNA的表达呈正相关(r=0.409,P＜0.01).结论 在SACC组织中,p38MAPK表达上调,p38MAPK通路可能与SACC的发生、侵袭和转移有关.

Abstract：

Objective To investigate the expression of p38 mitogen-activated protein kinase (p38MAPK) in salivary adenoid cystic carcinoma (SACC) tissues and their clinicopathologic significance.Methods The protein and mRNA expressions of p38MAPK were examined by immunohistochemistry and in situ hybridization, respectively, in 52 cases of SACC and in 11 normal salivary gland tissues adjacent to the tumors on a tissue microarray platform.Results The positive rate of p38MAPK protein expression in the paracancerous normal salivary gland tissues and that in SACC were 36.4% and 96.2%, respectively,showing a significant statistical difference (P ＜ 0.01 ).The protein expression of p38MAPK was positively correlated with the lymph node metastasis and nerve involvement (P ＜ 0.05 ).The positive rates of p38MAPK mRNA in the paracancerous tissues and in the SACC tissues were 45.5% and 94.2%,respectively, with a significant statistical difference (P ＜0.01 ).The mRNA expression of p38MAPK was positively correlated with the lymph node metastasis and nerve involvement (P ＜ 0.05 ).In the SACC, there was a notable positive correlation between the p38MAPK protein and mRNA expressions (r = 0.409, P ＜0.01).Conclusions The expression of p38MAPK is up-regulated in salivary adenoid cystic carcinoma.p38MARK may be involved in the tumorigenesis, development and metastasis of this cancer.     

泛素连接酶Hrd1在胃癌组织中的表达及意义

[目的]研究泛素连接酶Hrd1在胃癌组织中的表达及其与胃癌患者临床病理特征及预后的关系.[方法]收集60例胃癌患者手术切除组织,采用免疫组化SP法检测Hrd1在胃癌组织和癌旁组织中的表达情况.[结果]60例胃癌患者的组织中有38例Hrd1阳性表达,阳性率为63.3％,在癌旁正常组织中23例Hrd1阳性表达,阳性率为38.3％,在胃癌组织中明显高于癌旁组织(P＜0.05).Hrd1在胃癌组织中的表达与肿瘤的大小、TNM分期有关(P＜0.05);而与患者性别、年龄、分化程度及淋巴结转移、肿瘤发生部位等指标无明显相关性(P＞.05).Hrd1在胃癌组织中的表达与胃癌预后相关(P＜0.05).[结论] Hrd1表达与胃癌发生、发展有关,其在胃癌中的表达情况可以作为判断胃癌预后的参考指标.     

乳腺癌组织Notch1和JAG1蛋白表达与分子分型相关性研究

目的 Notch信号通路在乳腺癌中存在异常表达,但在不同分子分型乳腺癌中的表达情况鲜见报道.本研究将探讨不同分子分型乳腺浸润性导管癌组织中Notch1和JAG1蛋白表达及其与临床病理特征之间的关系.方法 收集滨州医学院附属医院病理科2012-01-06-2014-12-30存档的乳腺浸润性导管癌病例240例,根据ER、PR、HER2、Ki-67免疫组化结果分为管腔A型、管腔B型、HER2过表达型及三阴性型4组,每组60例,采用免疫组化En-Vision法检测不同分子分型乳腺癌中Notch1、JAG1蛋白的表达情况,对各分型乳腺癌组织的阳性表达率进行统计学分析.结果 各分型乳腺癌组织中Notch1的阳性表达差异有统计学意义(P=0.010,P＜0.05),其中三阴性乳腺癌(86.67％)与管腔A型(56.67％)比较(P＜0.001),HER2过表达型(83.33％)与管腔A型(56.67％)比较,差异均有统计学意义,P＜0.001;Notch1的阳性表达与淋巴结转移相关(P=0.017,P＜0.05),与临床分期(P=0.005,P＜0.01)、组织学分级(P=0.009,P＜0.01)显著相关,与ER表达(rs=-0.206,P=0.001,P＜0.01)、PR表达(rs=-0.187,P=0.005,P＜0.01)显著负相关,而与患者年龄、肿块大小无关.各分型乳腺癌组织中JAG1的阳性表达差异有统计学意义(P=0.035,P＜0.05),以三阴性乳腺癌阳性表达率最高,但各组间两两比较差异无统计学意义;JAG1阳性表达与ER表达(rs=-0.142,P=0.015,P＜0.05)、PR表达(rs=-0.127,P=0.035,P＜0.05)呈负相关;Notch1和JAG1之间无明显相关性.结论 Notch1阳性表达与ER、PR表达显著负相关,与乳腺癌的组织学分级、淋巴结转移及临床分期密切相关,并在HER2过表达型,尤其是三阴性乳腺癌组织中存在高表达,有可能成为三阴性乳腺癌新的治疗靶点.     

NCAM在涎腺腺样囊性癌组织中的表达及其意义

[目的]探讨涎腺腺样囊性癌中NCAM表达及其意义。[方法]采用免疫组化SP法和原位杂交法对20例正常涎腺组织和46例涎腺腺样囊性癌（SACC）组织中NCAM蛋白和NCAM mRNA表达进行检测。[结果]SACC组织中NCAM蛋白表达较高，阳性率为73．91％，与正常组织之间具有显著性差异（P〈0．01）：SACC组织中NCAM mRNA表达较强，阳性率为71．74％，与正常组织之间具有显著性差异（P〈0．01）；在有复发和转移的SACC组织中，NCAM蛋白和NCAM mRNA表达阳性率均达90％。与无复发和转移的SACC组织中NCAM蛋白和NCAM mRNA表达阳性率相比，具有显著性差异（P〈0．05）。[结论]NCAM与SACC的发生发展具有一定的相关性，与SACC转移行为关系不大，但可能在SACC的神经浸润中起介导作用。     

p27在涎腺腺样囊性癌组织中的表达及其意义

目的 探讨涎腺腺样囊性癌(SACC)中p27的表达及其意义.方法 采用免疫组化Envision法和原位杂交法对20例正常涎腺组织和46例SACC组织中p27蛋白和p27 mRNA表达进行检测.结果 正常组织中p27蛋白表达阳性率为100.0%,SACC组织中p27蛋白表达阳性率为65.2%,两者之间表达差异具有显著统计学意义(P<0.01);正常组织中p27 mRNA表达阳性率为100.0%,SACC组织中p27 mRNA表达阳性率为87.0%,两者之间表达差异无统计学意义(P>0.05).结论 p27蛋白表达与腺样囊性癌组织的发生、发展密切相关;p27基因与肿瘤的关系则主要体现于p27蛋白水平而非基因水平的改变.     

CYP1A1和GSTM1基因多态性与内蒙古人群肺癌易感性的关系

背景与目的 肺癌是严重危害人类健康的恶性肿瘤之一，其发病与肺癌人群中某些肺癌相关基因的遗传多态性有关。本研究旨在探讨细胞色素P4501A1（CYP1A1）基因多态性和谷胱甘肽硫转移酶M1（GSTM1）基因多态性与内蒙古人群肺癌易感性的关系。方法 用PCR-RFLP技术分析了原发性肺癌组和住院对照组（各163例）的CYP1A1、GSTM1基因的多态性、基因型分布频率和交互作用。结果 CYP1A1突变型和GSTM1基因缺陷型EGSTM1（-）]频率分布分别为36．8％、65．0％（病例组）和19．0％、48．9％（对照组），二者经χ^2检验差异有显著性（χ^2=12．82，P=0．000；χ^2=9．78，P=0．002）。CYP1A1突变型患肺癌的风险显著增加（OR=2．48，95％CI为1．51～4．08）。GSTM1（-）者患肺癌的风险也显著增加（OR=2．03，95％CI为1．30～3．17）。基因突变的协同分析发现CYP1A1突变型／GSTM1（-）在肺癌组和对照组中的分布频率分别为28．8％和8．0％，二者经χ^2检验有显著性差异（χ^2=23．883，P=0．000）。CYP1A1突变型／GSTM1（-）患肺癌的风险显著增加（OR=4．90，95％CI为2．50～9．83）。无论是在肺癌组还是在对照组，CYP1A1突变型／GSTM1（-）和CYP1A1非突变型／GSTM1（-）在性别间分布频率的差异均无显著性（肺癌组χ^2=0．797，P=0．372；对照组χ^2=0．670，P=0．761）。吸烟与肺癌易感性的统计学分析，结果显示吸烟与肺癌易感性有关（χ^2=14．197，P=0．000），吸烟者患肺癌的风险显著增加（OR=2．33，95％CI为1.50～3．62）。CYP1A1突变型与吸烟关系的协同分析发现，携带CYP1A1突变型基因的吸烟者较携带CYP1A1突变型基因不吸烟者易患肺癌（OR=4．44，95％CI为2．40～8．32，χ^2=23．843，P=0．000）。GSTM1（-）与吸烟关系的协同分析中也发现，携带GSTM1（-）的吸烟者患肺癌的风险显著增加（OR=7．32，95％CI为3．39～15．50，χ^2=36．708，P=0．000）。结论 CYP1A1突变型和GSTM1（-）是内蒙古地区肺癌的易患因素，二者对肺癌的发生有协同作用，吸烟与肺癌的易感性也有关，CYP1A1突变型、GSTM1（-）与吸烟在肺癌的发生上也有相互促进作用。     

CYP1A1 (Ile462Val), CYP1B1 (Ala119Ser and Val432Leu), GSTM1 (null), and GSTT1 (null) Polymorphisms and Bladder Cancer Risk in a Turkish Population

We aimed to investigate bladder cancer risk with reference to polymorphic variants of cytochrome p450 (CYP)1A1, CYP1B1, glutathione S-transferase (GST) M1, and GSTT1 genes in a case control study. Polymorphismswere examined in 114 bladder cancer patients and 114 age and sex-matched cancer-free subjects. Genotypes weredetermined using allele specific PCR for CYP1A1 and CYP1B1 genes, and by multiplex PCR and melting curveanalysis for GSTM1 and GSTT1 genes. Our results revealed a statistically significant increased bladder cancerrisk for GSTT1 null genotype carriers with an odds ratio of 3.06 (95% confidence interval=1.39-6.74, p=0.006).Differences of CYP1A1, CYP1B1 and GSTM1 genotype frequencies were not statistically significant betweenpatients and controls. However, the specific combination of GSTM1 null, GSTT1 null, and CYP1B1 codon 119risk allele carriers and specific combination of GSTM1 present, GSTT1 null, and CYP1B1 432 risk allele carriersexhibited increased cancer risk in the combined analysis. We did not observe any association between differentgenotype groups and prognostic tumor characteristics of bladder cancer. Our results indicate that inheritedabsence of GSTT1 gene may be associated with bladder cancer susceptibility, and specific combinations ofGSTM1, GSTT1 and CYP1B1 gene polymorphisms may modify bladder cancer risk in the Turkish population,without any association being observed for CYP1A1 gene polymorphism and bladder cancer risk.     

CYP1A1、GSTM1基因多态性及其联合作用与食管癌的易感性

目的探讨CYP1A1、GSTM1基因多态性及其联合作用与新疆汉族人食管癌易感性的关系。方法采用聚合酶链式反应-连接酶检测反应分析方法检测107例食管癌患者和204例非食管癌患者的CYP1A1(rs1048943、rs4646421和rs4646903)和GSTM1(缺失型和rs2071487)的基因型。结果CYP1A1基因rs1048943位点的等位基因和基因型频率在病例组和对照组之间比较,总体分布差异有统计学意义(χ² =5.52,P=0.019)。与A/A基因型相比,GG+AG基因型可增加食管癌的发病风险(OR=1.79,OR95%CI:1.10~2.92);GSTM1基因缺失型和非缺失型在病例组和对照组中的分布频率分别为68.69%、31.31%和48.39%、51.61%,在两组间的分布差异有统计学意义(χ²=10.55,P=0.001;OR=2.34,OR95%CI:1.40~3.91)。结论CYP1A1基因rs1048943位点多态性和GSTM1基因缺失型与新疆地区汉族人食管癌易感性有相关性。     

VEGFR1和MDR1在胃癌中的表达及意义

目的:探讨VEGFR1和MDR1在胃癌中的表达及意义.方法:采用免疫组化SP法检测VEGFR1和MDR1在胃癌中的表达及与分化程度的关系;比较VEGFR1和MDR1在胃癌中的表达相关性.结果:VEGFR1在高、中、低度分化胃癌的表达率依次为15/53(28%)、19/43(44%)、37/54(68%); 在低分化胃癌组织中的表达明显高于高分化和中分化胃癌组织(P＜0.05).MDR1在高、中、低度分化胃癌的表达率依次为18/53(34%)、21/43(48%)、41/54(76%); 在低分化胃癌组织中的表达明显高于高分化和中分化胃癌组织 (P＜0.05).结论:VEGFR1和MDR1在胃癌中的表达具有一致性,可能在胃癌的多药耐药中扮演重要角色.     

CYP1A1, GSTM1, GSTT1 and TP53 Polymorphisms and Risk of Gallbladder Cancer in Bolivians

The Plurinational State of Bolivia (Bolivia) has a high incidence rate of gallbladder cancer (GBC). However, the genetic and environmental risk factors for GBC development are not well understood. We aimed to assess whether or not cytochrome P450 (CYP1A1), glutathione S-transferase mu 1 (GSTM1), theta 1 (GSTT1) and tumor suppressor protein p53 (TP53) genetic polymorphisms modulate GBC susceptibility in Bolivians. This case-control study covered 32 patients with GBC and 86 healthy subjects. GBC was diagnosed on the basis of histological analysis of tissues at the Instituto de Gastroenterologia Boliviano Japones (IGBJ); the healthy subjects were members of the staff at the IGBJ. Distributions of the CYP1A1 rs1048943 and TP53 rs1042522 polymorphisms were assayed using PCR-restriction fragment length polymorphism assay. GSTM1 and GSTT1 deletion polymorphisms were detected by a multiplex PCR assay. The frequency of the GSTM1 null genotype was significantly higher in GBC patients than in the healthy subjects (odds ratio [OR], 2.35; 95% confidence interval [CI], 1.03-5.37; age-adjusted OR, 3.53; 95% CI, 1.29-9.66; age- and sex-adjusted OR, 3.40; 95% CI, 1.24-9.34). No significant differences were observed in the frequencies of CYP1A1, GSTT1, or TP53 polymorphisms between the two groups. The GSTM1 null genotype was associated with increased GBC risk in Bolivians. Additional studies with larger control and case populations are warranted to confirm the association between the GSTM1 deletion polymorphism and GBC risk suggested in the present study.     

RB1CC1 activates the promoter and expression of RB1 in human cancer

RB1‐inducible coiled‐coil 1 (RB1CC1, also known as FIP200) is a tumor suppressor implicated in the regulation of RB1 (retinoblastoma 1) expression. However, the molecular mechanism of RB1 regulation by RB1CC1 has not been elucidated. Here, we demonstrate that nuclear RB1CC1 binds to the RB1 promoter using chromatin immunoprecipitation assays with anti‐RB1CC1 antibody. Luciferase assays with RB1 promoter reporter plasmids revealed that RB1CC1 activated the RB1 promoter through the 201 bp upstream GC‐rich region (from the initiation ATG). Electrophoretic mobility shift assay and Western blot analysis supported RB1CC1 binding to the GC‐rich region of the RB1 promoter. In addition, the C‐terminus of RB1CC1 was required for nuclear localization and subsequent RB1 promoter activation. Furthermore, the expression levels of RB1CC1 and RB1 significantly correlated with in vivo breast cancer tissues as determined by immunohistochemical analysis. These data indicate that nuclear RB1CC1 directly activates the RB1 promoter to enhance RB1 expression in cancer cells. Evaluation of RB1CC1 in various types of human cancer tissues is expected to provide useful information for clinical practice and future therapeutic strategies. © 2009 UICC     

Genetic Polymorphism of GSTP1, GSTM1 and GSTT1 Genes and Susceptibility to Chronic Myeloid Leukaemia

Background: The development of cancer results from an imbalance between exposure to carcinogens and the capacity of various enzyme systems engaged in activation or in the detoxification of xenobiotics. The aim of the present study is to investigate the association of GSTP1, GSTM1 and GSTT1 gene polymorphisms in susceptibility to Chronic Myeloid Leukaemia (CML). Methods: A total of 200 CML patients and 100 controls were enrolled in a case-control study with GSTM1 and GSTT1 analysis with PCR and GSTP1 analysis with PCR-RFLP. Results: The GSTT1 null genotype was significantly higher among CML patients suggesting that this genotype is associated with an increased risk of CML. It was found in 42% of cases as compared with 21% of the controls, (OR =2.78, 95% CI: 1.59 - 4.85; p-value =0.000). The presence of the GSTT1 genotype may thus be considered a protective factor for CML. The frequency of individuals carrying GSTM1 null genotype was slightly higher in the control group but this difference was not statistically significant. The GSTM1 null genotype was present in 35% of control cases and 34% of the CML patients, (OR=0.975, 95%CI: 0.58-1.58;p-value=0.863). Individuals with a combined GSTM1 null/GSTT1null genotype had an estimated 2.85-fold increased risk of CML, but no associated risk between GSTP1 Ile 105 Val polymorphism and CML was found (OR=1.99, 95% CI: 0.40 - 9.32; p-value = 0.417). Conclusions: No association between GSTP1 and GSTM1 with susceptibility to CML was found. GSTT1 genotype may be a protective factor for CML, while the null genotype shows association with developing CML.     

葡萄糖转运蛋白1和磷脂结合蛋白-1在子宫内膜癌中的表达及意义

背景与目的:探讨葡萄糖转运蛋白1(GLUT1)和磷脂结合蛋白.1(Annexin-1)在子宫内膜癌组织中的表达情况及其与临床病理参数之间的关系.材料与方法:采用免疫组化S-P法检测65例子宫内膜癌、27例非典型增生和21例增生期子宫内膜组织中GLUT1和Annexin-1的表达.结果:在增生期子宫内膜、非典型增生、子宫内膜癌的GLUT1阳性表达率分别为28.6%、59.3%、81.5%,呈递增趋势,组间两两比较,差异均具有统计学意义(P<0.05);Annexin-1阳性表达率分别为85.7%、55.6%、49.2%,呈下降趋势,其中子宫内膜癌与增生期子宫内膜比较差异有统计学意义(P<0.05).GLUT1高表达与子宫内膜癌的组织分级、肌层浸润深度有关(P<0.05),与病理分期、淋巴结是否转移、组织学类型无关(P>0.05);Annexin-1低表达与上述的临床病理参数皆无关(P>0.05).子官内膜癌中GLUT1与Annexin-1呈负性相关(r=-0.540,P=0.000).结论:Annexin-1低表达和GLUT1高表达可能对子宫内膜癌的发牛和发展具有促进作用,二者对子宫内膜癌早期诊断和预后预测有一定意义.     

DNA切除修复交叉互补基因1、乳腺癌易感基因、核苷酸还原酶1与非小细胞肺癌

 阐述了近年来非小细胞肺癌（NSCLC）化疗敏感性与DNA 切除修复交叉互补基因1 （ERCC1）、乳腺癌易感基因（BRCA1）、核苷酸还原酶1（RRM1）基因表达关系的研究进展，分析3个基因对NSCLC个体化化疗潜在的指导意义