卵巢上皮性癌中 Notch -1和 Jagged -1的表达及临床意义

目的:检测Notch-1和Jagged-1基因蛋白在卵巢上皮性肿瘤中的表达,探讨二者在卵巢上皮性癌发生、发展、浸润、转移中的作用。方法:应用免疫组织化学(immunohistochemistry,IHC)方法检测75例卵巢上皮性癌和54例良性上皮性肿瘤中Notch-1和Jagged-1基因的蛋白表达情况,并分析其与临床病理特征之间的关系。结果:Notch-1和Jagged-1在卵巢上皮性癌组织中的表达明显高于良性上皮性肿瘤组织(P<0.01)。Notch-1和Jagged-1在卵巢上皮性癌中表达与组织分化程度有关,中低分化组的表达明显高于高分化组(P<0.05)。临床分期及有无淋巴结转移组中,二者的蛋白表达无明显差异(P>0.05)。在卵巢上皮性癌中两种蛋白表达呈明显正相关(r=0.295,P<0.05)。结论:Notch-1和Jagged-1可能与卵巢上皮性癌的发生及癌细胞的分化有关,且二者在其发生、发展过程中可能起协同作用。     

赫赛汀对乳腺癌SK-BR3细胞Notch-1信号通路的影响及意义

探讨赫赛汀对乳腺癌SK-BR3细胞Notch-1蛋白的影响及其作用机制,认识Notch-1信号通路在乳腺癌细胞形成赫赛汀耐药中的意义。方法:选用HER-2过表达乳腺癌SK-BR3细胞及HER-2非过表达乳腺癌MDA-MB-231细胞,免疫细胞化学法和Western blot法检测两细胞株中Notch-1蛋白的表达;应用赫赛汀处理SK-BR3细胞,Western blot法检测HER-2、Notch-1通路活性分子Notch-1IC的蛋白表达;RT-PCR法检测Notch-1靶基因HES-1 mRNA的表达;免疫共沉淀法检测SK-BR3细胞中Notch-1与HER-2是否存在相互作用。结果:Notch-1IC核定位水平及Notch-1IC蛋白表达水平在HER-2过表达乳腺癌细胞（9.37±0.64）中明显低于HER-2非过表达乳腺癌细胞（21.665±1.11）,P<0.01;赫赛汀处理SK-BR3细胞后,与未处理组比较,细胞内Notch-1IC蛋白及HES-1 mRNA水平均明显增高（P<0.01,P<0.01）,HER-2蛋白表达水平在处理前后未发生明显变化（F=0.973,P>0.05）;免疫共沉淀结果显示Notch-1与HER-2蛋白之间存在共沉淀。结论:Notch-1蛋白在HER-2过表达乳腺癌细胞中活性下降;HER-2与Notch-1结合,可能负性调控Notch-1;赫赛汀活化的Notch-1信号通路,可能与细胞耐药发生有关。      

甲状腺癌组织EG-1和VEGF-C及p53表达及临床意义的探讨

目的:研究EG-1、VEGF-C和p53在甲状腺癌组织中的表达及其临意义.方法:用RT-PCR方法检测80例甲状腺癌和33例良性甲状腺疾病组织中EG-1基因表达情况,应用免疫组化技术检测VEGF-C和p53的表达.结果:61.50%(49/80)患者的甲状腺癌标本中EG-1 mRNA阳性,而良性甲状腺结节中阳性表达率为21.21%(7/33).EG-1表达组和未表达组总生存曲线分析存在差异(P<0.01),同时EG-1 mRNA在甲状腺癌组织中的表达与年龄、淋巴结转移、肿瘤分期和病理类型等因素有关(P<0.05),与VEGF-C蛋白显著相关(P<0.001),与p53蛋白无相关性.多因素Cox回归分析显示,EG-1表达是预测甲状腺癌生存率的独立预后因素,其中 EG-1表达组死亡风险与EG-1未表达组相比明显增高(RR=4.010,P=0.013),甲状腺癌EG-1基因表达组和未表达组生存率差异有统计学意义,P<0.01.EG-1基因表达组预后差,EG-1基因表达组与未表达组死亡风险危险度比值为4.010,P<0.05.结论:EG-1 mRNA在甲状腺癌组织中的表达与VEGF-C蛋白显著相关,与p53蛋白无相关性.EG-1可能成为评价甲状腺癌预后的重要分子生物学标记.     

膀胱癌中CHK1和RAD51的表达及临床意义

目的 探讨细胞周期检测点激酶1 (cell cycle checkpoint kinase 1,CHK1)及DNA双链断裂修复蛋白RAD51在膀胱癌中的表达及意义.方法 采用免疫组织化学法检测104例膀胱癌组织和40例癌旁正常膀胱黏膜组织中CHK1及RAD51蛋白表达,并分析其与膀胱癌临床病理特征的关系.结果 膀胱癌组织中CHK1及RAD51蛋白表达均高于癌旁正常膀胱黏膜组织(均P ＜0.05).CHK1蛋白表达在膀胱癌的病理组织学分级、病理分期方面差异均有统计学意义(均P＜0.05),而在性别、年龄、肿瘤直径、单发/多发以及初发/复发方面差异均无统计学意义(均P＞0.05).RAD51蛋白表达在膀胱癌的病理组织学分级方面差异有统计学意义(P＜0.05),在病理分期、性别、年龄、肿瘤直径、单发/多发以及初发/复发方面差异均无统计学意义(均P＞0.05).膀胱癌组织中CHK1和RAD51蛋白表达呈正相关(r=0.223,P＜0.05).CHK1蛋白阴性表达组预后好于阳性表达组(P＜0.05),而RAD51蛋白表达阴性组和阳性组预后比较差异无统计学意义(P＞0.05).结论 CHK1和RAD51蛋白在膀胱癌组织中呈高表达,二者在膀胱癌发生、发展中起重要作用,并与膀胱癌的病理组织学分级及预后密切相关.     

四跨膜蛋白CD151调节结直肠癌Notch相关信号通路的研究

摘 要：［目的］ 研究CD151在结直肠癌Notch信号通路中的调节作用。［方法］ 通过Log-rank (Mantel-Cox) 分析TCGA数据库中CD151与结直肠癌患者生存期的关系，应用Western blot和实时定量聚合酶链反应（qRT-PCR）检测40例结直肠癌及癌旁组织以及慢病毒低表达CD151的HT29细胞株中Notch-1、Hes-1和Jagged-1的蛋白和mRNA的表达。［结果］通过分析TCGA数据库的数据得出CD151高表达的结直肠癌患者的2000d之内生存期明显低于CD151低表达的患者。在结直肠癌患者组织中CD151、Notch-1、Hes-1和Jagged-1的蛋白和mRNA的表达均高于癌旁组织（P均<0.05）。在敲低CD151的HT29-CD151-KD人结肠癌细胞株中，Notch-1、Hes-1和Jagged-1的蛋白和mRNA的表达明显降低（P均<0.05）。［结论］ CD151表达情况影响结直肠癌患者的生存期，CD151可明显下调结直肠癌Notch相关信号通路。     

儿童喉乳头状瘤组织中Toll样受体4及激活蛋白-1表达及相关性研究

目的:研究儿童喉乳头状瘤（juvenile onset laryngeal papilloma,JLP）中Toll样受体4（Toll-like receptor 4,TLR4）、激活蛋白-1（activator protein-1,AP-1）（通常是c-Jun和c-Fos的异源二聚体）蛋白的表达及其相互关系。方法:应用免疫组化法及RT-PCR检测JLP组织中TLR4和AP-1（c-Jun、c-Fos）的表达情况,分析两者表达的相关性及与JLP复发的相关性。结果:儿童JLP组织中TLR4和 AP-1（c-Jun、c-Fos）蛋白和mRNA均为阳性表达,与无复发组比较,复发组有显著性增高(P<0.01),与正常对照组比较,JLP两组均有显著性增高(P<0.01)。其中TLR4蛋白复发组和无复发组阳性率分别为83.33%和58.33%,c-Jun、c-Fos蛋白复发组阳性率分别为86.67%和83.33%,无复发组阳性率均为66.67%。TLR4 和AP-1（c-Jun、c-Fos）蛋白表达均与JLP的复发有明显相关性（P<0.05或者P<0.01）;JLP组织中TLR4和AP-1（c-Jun、c-Fos）表达两者呈正相关（P<0.01）。结论:TLR4及AP-1的高表达可能在JLP的发生发展机制中起着重要作用。     

子宫内膜癌组织PTEN和c-erbB-2蛋白表达临床意义的探讨

-2的阳性表达率明显高于正常子宫内膜和子宫内膜不典型增生,P<0.05; c-erbB-2阳性表达与子宫内膜癌的病理分级、临床分期、肌层浸润深度和淋巴转移相关(P<0.05),但与不典型增生的程度无关(P>0.05).在子宫内膜癌组织中PTEN的表达缺失率与c-erbB-2的过度表达呈正相关.结论:PTEN蛋白的表达缺失与子宫内膜癌的发生有关;c-erbB-2蛋白的高表达提示预后不良;PTEN和c-erbB-2联合检测可作为筛选复发转移高危因素的标志.     

胃癌组织HIF-1α表达与多药耐药因子及体外化疗药敏性的关系

目的:探讨胃癌组织乏氧诱导因子-1α(hypoxia-inducible factor-1α,HIF-1α)表达与P-糖蛋白(P-gp)、p53和Survivin及体外化疗敏感性的关系.方法:对63例胃癌新鲜肿瘤组织进行体外细胞培养化疗药敏性实验, 标本行上述指标免疫组化染色.结果:1)胃癌组织HIF-1α、P-gp、p53和Survivin阳性表达率分别为33.3%、71.4%、50.8%和66.7%.2)肿瘤HIF-1α表达与p53表达呈正相关(r=0.407 2, P<0.01), 与P-gp、Survivin表达无明显相关性(r=0.178 6、r=0.082 9, 均P>0.05), 其余因子之间表达均无明显相关性 (r=0.163 4～0.205 4, 均P>0.05).3) 10种化疗药物对4种蛋白阴、阳性表达组的肿瘤细胞平均抑制率不同.胃癌HIF-1α阳性表达组中, VCR、OPT、eADM和MTX对肿瘤细胞平均抑制率明显低于HIF-1α阴性表达组 (t=2.287～3.494, 均P<0.05).VCR、PTX、eADM、CDDP和MTX对胃癌细胞抑制率降低均与2种以上蛋白的过表达有关, 仅OPT、OXA的抑制率降低与一种因子阳性表达有关.结论: HIF-1α在胃癌组织中表达与部分化疗药物的耐药性有关, HIF-1α参与了肿瘤的化疗多药耐药性.     

c-Met及Notch-1对非小细胞肺癌患者预后的影响

目的:通过检测c-Met及Notch-1在非小细胞肺癌（non-small cell lung cancer,NSCLC）手术切除患者中的表达,探究其对患者预后的影响。方法:应用免疫组化方法检测收集到的106例NSCLC石蜡标本中c-Met和Notch-1的表达情况,分析c-Met和Notch-1表达与患者预后之间的关系。结果:c-Met表达与N分期、pTNM分期相关,Notch-1表达与N分期相关。c-Met和Notch-1阳性表达的患者均较阴性表达患者预后差（P<0.001）。相关分析显示,c-Met与Notch-1正相关（P<0.001）。c-Met与Notch-1联合分析发现,双阳性组患者预后最差,单阳性组其次,双阴性组最佳（P<0.001）。COX单因素分析发现,c-Met、Notch-1、T分期、N分期、pTNM分期是预后的风险因素。进一步COX多因素分析,结果显示c-Met表达为预后的独立风险因素（P<0.001）,而Notch-1表达与预后无关（P=0.732）。结论:c-Met及Notch-1联合检测可更精确的预测NSCLC患者预后风险。     

Cyclin D1和p27kip1在胃黏膜癌变过程中的表达

目的:探讨Cyclin D1和p27kip1蛋白在胃黏膜癌变过程中的表达及相互关系。方法:采用免疫组化SP法分别检测慢性浅表性胃炎(chron-ic superficial gastritis,CSG)、慢性萎缩性胃炎(chronic atrophic gastritis,CAG)、肠化生(intesti-nalm etaplasia,IM)、不典型增生(dysplasia,DYS)和胃癌(gastric carcinoma,GCA)组织中Cyclin D1和p27kip1的表达变化。结果:Cyclin D1的过表达随病变发展表达率逐渐增高,CAG组与CSG组比较,差异无统计学意义,P>0.05;IM、DYS、GCA组与CSG组比较,差异均有统计学意义,P均<0.05。p27kip1在上述黏膜中的表达呈递减趋势,CSG中最高,GCA组最低,CAG组和CSG组比较,差异无统计学意义,P>0.05;IM、DYS、GCA组与CSG组比较,差异均有统计学意义,P<0.05。Cyclin D1和p27kip1的表达呈负相关,γ=-0.53,P=0.000。结论:胃黏膜癌变过程中的Cyclin D1阳性表达呈递增趋势,p27kip1表达呈递减趋势;Cyclin D1和p27kip1表达变化发生在胃黏膜癌变早期,两者在胃癌黏膜癌变过程中的表达呈负相关提示两者可能存在相互抑制机制。     

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