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   基因启动子甲基化 的翻译结果: 查询用时:0.12秒
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肿瘤学
皮肤病与性病
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基因启动子甲基化
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  promoter methylation
     2 To analyze the relationship between p16INK4a promoter methylation and the expression level of p16INK4a mRNA in epidermis from patients with psoriasis.
     2、分析银屑病表皮p16~(INK4a)基因启动子甲基化与p16~(INK4a)mRNA表达量的关系
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     The study of INK4a/ARF gene promoter methylation in bronchial squamous cell carcinomas(SCC).
     肺鳞癌INK4a/ARF基因启动子甲基化研究
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     Result:In NSE, there was no promoter methylation of FHIT gene, while in LSCC the rate of it was 24.4%(10/41), and it was related to the tumor pathological grade and lymph node metastasis(P<0.01).
     结果:在NSE组中,无一例出现FHIT基因启动子甲基化,而在LSCC组中,有24.4%(10/41)出现甲基化,且甲基化状态与病理分级及淋巴结转移有关(P<0.01);
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     Relationship between Expression and Promoter Methylation of p16~(INK4a) Gene in Ameloblastoma
     成釉细胞瘤中p16~(INK4a)基因启动子甲基化与表达相关性的研究
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     Analysis of promoter methylation of DBCCR1 gene in bladder transitional cell carcinoma
     膀胱移行细胞癌DBCCR1基因启动子甲基化分析
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  “基因启动子甲基化”译为未确定词的双语例句
     Analysis of methylation status of the promoter of mdr1 gene in K562 and K562/DNR cells
     K562和K562/DNR细胞中mdr1基因启动子甲基化状态的分析
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     Polymerase chain reaction (PCR) was used to amplify microsatellite loci BAT25、BAT26、BAT40、D2S123 and D5S346.MSI was analyzed by polyacrylamide gel electrophoresis.
     采用PCR扩增-聚丙烯酰胺凝胶电泳-硝酸银染法检测BAT25、BAT26、BAT40、D2S123、D5S346五个位点的MSI,甲基化特异性-PCR检测hMLH1基因启动子甲基化异常情况。
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     The frequence of the promoter hypermethylation of RASSF1A in breast cancer(65%) was significantly higher than in normal breast tissue(20%)and benign carcinoma (17%).
     乳腺癌组织的RASSF1A基因启动子甲基化频率(65%)明显高于正常乳腺组织(20%)和乳腺良性肿瘤(17%)(P<0.05)。
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     BACKGROUND&AIM: To study the aberrant methylation of the hMSH2gene promoter and its mRNA expression in the nickel sulfide(NiS)and anti_7,8,_dihydrodiol_9,10_epoxide benzo[a] pyrene(anti_BPDE)transformed16HBE cells and to explore the possible epigenetic mechanism for NiS and anti_BPDE carcinogenesis.
     背景与目的:对结晶型硫化镍(Nickelsulfide,NiS)及反式二氢二醇环氧苯并芘(anti_7,8,_dihydrodiol_9,10_epoxidebenzo[a]pyrene,BPDE)恶性转化及成瘤的人支气管上皮细胞(Humanbronchialepithelial,16HBE)hMSH2基因启动子甲基化状况及其mRNA表达进行研究,探讨镍及反式_BPDE的表遗传致癌机制。
短句来源
     There was significant correlation between methylation of FHIT gene promoter and expression of its protein(P<0.01).
     FHIT基因启动子甲基化与蛋白阳性表达有明显的相关性(P<0.01)。
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  相似匹配句对
     Methylation of gene promoter and chemorisistance
     基因启动子甲基化和化疗耐药
短句来源
     Promoter Methylation of Tumor Related Genes in Human Gastric Carcinoma
     胃癌相关基因启动子甲基化状态的研究
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     ③ CpG methylation around the promoter region was considered a possible mechanism of E-cadherin gene inactivation in human cancers;
     3)E-Cad基因启动子CpG岛甲基化
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     Analysis of the hypermethylation of p16 gene promotor in pituitary adenomas
     垂体腺瘤p16基因启动子甲基化分析
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     The complex methylation patterns of BRCA1 promoter
     BRCA1基因启动子复杂甲基化模式
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  promoter methylation
Numerous attempts to find mutations in exons of silenced genes failed, and at least half of the new candidate genes (RASSFIA, CACNA2D2, BLU, HYAL1, SEMA3B, RAR-β) proved to be inactivated by promoter methylation.
      
For each gene, the rate of promoter methylation and changes in expression were estimated in tumor and morphologically intact paired specimens of breast tissue (N = 100).
      
BRAF mutations and hMLH1 promoter methylation appear to have negative predictive value for identifying individuals with HNPCC, but further studies are needed.
      
Inactivation of the p16 and p53 tumor suppressor genes through promoter methylation, gene mutation, or loss of heterozygosity appears to be important for carcinogenesis in Barrett's esophagus.
      
CHFR promoter methylation was detected in 39% of acute leukemia patients.
      
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Objective To elucidate the cause of abnormal Rb expression in esophageal cancer (EC). Methods Methylation of Rb gene promoter was examined with restriction endonuclease digestion and PCR amplification. Results Of the 30 specimens of EC, 10 (33.3%) had MspⅠ type hypermethylation of the Rb gene promoter while 12 (40.0%) had HpaⅡ type hypermethylation and one had both type of hypermethylation. In monkey fed with a single dose of NMBzA (30 mg/kg) on day 0, increasing hypermethylation of both types of the Rb gene...

Objective To elucidate the cause of abnormal Rb expression in esophageal cancer (EC). Methods Methylation of Rb gene promoter was examined with restriction endonuclease digestion and PCR amplification. Results Of the 30 specimens of EC, 10 (33.3%) had MspⅠ type hypermethylation of the Rb gene promoter while 12 (40.0%) had HpaⅡ type hypermethylation and one had both type of hypermethylation. In monkey fed with a single dose of NMBzA (30 mg/kg) on day 0, increasing hypermethylation of both types of the Rb gene promoter in esophageal epithelium was found on day 1,2 and 3 but reduced on day 5. Conclusion These data suggest that abnoromal expression of Rb gene may be related to hypermethylation of its promoter and carcinogen NMBzA can induce such hypermethylation in monkey esophageal epithelium.

目的分析Rb基因表达异常原因,研究Rb基因启动子甲基化状态和甲基苄基亚硝胺(NMBzA)对Rb基因启动子的影响。方法采用限制性核酸内切酶酶切和PCR扩增方法。结果33.3%的食管癌组织Rb基因启动子存在MspⅠ型高甲基化,40.0%的食管癌组织Rb基因启动子存在HpaⅡ型高甲基化。1例标本存在MspⅠ和HpaⅡ两种类型的高甲基化。恒河猴1次灌喂30mg/kgNMBzA后1,2,3天,其食管上皮Rb基因启动子HpaⅡ、MspⅠ类型甲基化逐渐增强;第5天其Rb基因启动子HpaⅡ、MspⅠ类型甲基化程度明显下降。结论食管癌组织中Rb基因表达异常可能与启动子高甲基化有关,NMBzA通过启动子甲基化对Rb基因调控产生影响。

Objective\ To investigate the inactivation of estrogen receptor (ER) in prostate cancer and its relation with methylation of gene promoter. Methods\ By using bisulfite genomic sequencing method, the methylation status of ER gene was studied in the prostate cancer cell line and microdissected prostate cancer samples. Results\ The ER gene promoter in prostate cancer cell line was methylated in 100%. ER mRNA was not expressed. Treatment of those cell lines with demethylating agent 5-aza-2-deoxycytidine restored...

Objective\ To investigate the inactivation of estrogen receptor (ER) in prostate cancer and its relation with methylation of gene promoter. Methods\ By using bisulfite genomic sequencing method, the methylation status of ER gene was studied in the prostate cancer cell line and microdissected prostate cancer samples. Results\ The ER gene promoter in prostate cancer cell line was methylated in 100%. ER mRNA was not expressed. Treatment of those cell lines with demethylating agent 5-aza-2-deoxycytidine restored ER mRNA expression in all the ER-negative cell lines. Of the prostate cancer tissue samples analyzed, 80% (8/10) in the low-grade group (grade Ⅰ and Ⅱ) and 95% (20/21) in the high-grade group (grade Ⅲ~Ⅴ) exhibited promoter methylation of ER gene. Conclusions\ The abnormal methylation of ER gene promoter in prostate cancer could result in the inactivation of ER gene. In the high malignant cells, this phenomenon was more common.\;

目的 探讨前列腺癌雌激素受体 (ER)的失活与其基因启动子甲基化的关系。方法 采用亚硫酸氢盐基因组测序法研究前列腺癌细胞系和显微解剖的前列腺癌标本的ER基因的甲基化状态。结果 前列腺癌细胞系ER基因启动子的甲基化率为 6 /6 ,且ERmRNA均不表达。将这些细胞用去甲基剂 5 氮 2 脱氧胞苷处理可以恢复所有ER阴性细胞系的ERmRNA的表达。 80 % (8/10 )的低分级前列腺癌 (Ⅰ、Ⅱ级 )和 95 % (2 0 /2 1)的高分级前列腺癌 (Ⅲ~Ⅴ级 )表现出ER基因启动子甲基化。结论 前列腺癌细胞ER基因启动子的异常甲基化可以导致该基因失活。在恶性度高的细胞 ,这种现象更为普遍。

Objective:O6 methylguanine DNA methyl transferase (MGMT) removes the methyl group from DNA adduct O6 methylguanine then to repair the damage.The MGMT gene has been shown to be silenced by promoter methylation in many human tumors.This study was designed to examine the relationship between the promoter methylation of the MGMT gene and esophageal squamous cell carcinoma.Methods:The promoter methylation of the MGMT gene was detected by methylation specific PCR in esophageal carcinoma tissues,tissues adjacent...

Objective:O6 methylguanine DNA methyl transferase (MGMT) removes the methyl group from DNA adduct O6 methylguanine then to repair the damage.The MGMT gene has been shown to be silenced by promoter methylation in many human tumors.This study was designed to examine the relationship between the promoter methylation of the MGMT gene and esophageal squamous cell carcinoma.Methods:The promoter methylation of the MGMT gene was detected by methylation specific PCR in esophageal carcinoma tissues,tissues adjacent to the tumors, and normal esophageal mucosa. Results:Among the 119 esophageal carcinomas,MGMT hypermethylation was detected in 46 cases(38.7%). In the 22 tissues adjacent to the tumors,5 (22.7%) was found to have this epigenetic alteration. All the 21 normal tissues were shown to be unmethylated.Conclusion:Hypermethylation of the MGMT promoter is a frequent molecular event in esophageal cancer and may be involved in carcinogenesis at the early stage.

目的:O6-甲基鸟嘌呤DNA甲基转移酶(MGMT)可以转移DNA加合物O6-甲基鸟嘌呤中的甲基,从而修复DNA损伤,许多肿瘤中发现MGMT基因启动子过甲基化导致该基因失活,我们研究了MGMT基因启动子甲基化状态与食管癌的关系。方法:采用甲基化特异性聚合酶链反应及测序方法分析食管癌、癌旁组织和正常食管上皮中MGMT启动子甲基化状态。结果:在检测的119例食管癌组织中,46例(38.7%)有MGMT基因启动子过甲基化;相应癌旁组织22例中也有5例(22.7%)出现MGMT基因甲基化,而21例正常食管上皮均无此种改变。结论:MGMT基因启动子过甲基化是食管癌中常见的分子事件,可能发生在癌变过程的早期阶段。

 
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