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1.
抑癌基因Rb与P53的研究进展   总被引:1,自引:0,他引:1  
Rb和453均为抑癌基因,Rb全长大约200kb,定位于人13号染色体的13p14.1,它所编码的104kD磷酸蛋白参与细胞周期的调控,调控细胞增值。而P53窒长16-20kb,定位于人17号染色体的17p13.1,它所编码的53kD磷酸蛋白可通过调控CIPI基因表达而调控细胞生长。在很多肿瘤中已发现Rb和P53基因的突变与缺失,揭示了这两种基因与肿瘤发生有密切关系。  相似文献   

2.
以30例胃癌组织和正常组织为研究对象,通过STR-PCR技术,对6号染色体6q24内的ZAC基因两侧的4个STR基因座进行杂合性缺失分析,统计这4个STR基因座在30例标本中的LOH频率,绘制它们的缺失图谱,得到了第4号和25号这两个样本中发生了包含ZAC基因在内的4285651bp的缺失,为进一步分析ZAC基因发生缺失的断裂点和查找ZAC基因表达下调的原因打下基础.  相似文献   

3.
浅谈肿瘤与抑癌基因   总被引:1,自引:0,他引:1  
癌基因激活和抑癌基因失活是各种肿瘤发生、发展的基础。而到目前为止 ,已发现了多种癌基因和抑癌基因。本文就与肿瘤有密切关系的主要几种抑癌基因的情况进行阐述 ,目的是为了使大家能对肿瘤与抑癌基因有更深刻地了解 ,并且对抑癌基因的深入研究和广泛应用将为中医的诊断、治疗、预后判断及预防提供更为有效的方法和手段  相似文献   

4.
射向肿瘤的“魔弹”──P ̄(16)张磊现代医学研究表明,肿瘤发生发展的根本原因是,参与细胞生长增殖调控的基因和参与细胞分化成熟调控的基因,这一矛盾统一体的失调或性质上的变异。癌基因或抑癌基因是这一矛盾统一体中两类基因的典型代表。前者是肿瘤生长的决定或...  相似文献   

5.
DNA甲基化是真核生物DNA的正常内源性修饰方式 ,它由DNA甲基化转移酶催化发生。但DNA甲基化异常在肿瘤发生中却起着极为重要的作用 ,它主要表现为抑癌基因高甲基化所致的基因失活和原癌基因低甲基化所致的基因激活 ,引起与细胞增殖、分化相关基因表达异常 ,造成细胞恶变形成肿瘤。文章总结了DNA甲基化异常对肿瘤相关基因表达的影响 ,在肿瘤发生中的可能机制及针对高甲基化的治疗方案  相似文献   

6.
随着科学技术的飞速发展,对肿瘤生物学行为的研究日渐深入,目前,人们已逐渐认识到肿瘤的本质是细胞基因组本身的改变,特别是癌基因的激活、抑癌基因失活及其相互关系的改变,因此人们认为癌症是一种基因疾病。本文,对近年来人胃癌组织中癌基因和抑癌基因表达的研究现状作一简单综述。 1 癌基因的研究 1981年weinberg等首先报道人癌基因分离成功,肿瘤研究开始进入了癌基因时代。癌基因(oncogenes)又称致癌基因,它是能将正常细胞转化为癌细胞的DNA片断,  相似文献   

7.
有关抑癌基因的名称很多,如隐性基因、抑癌基因、抗癌基因、癌抑制基因等它是一种抑制细胞生长和肿瘤形成的基因,在生物体内与癌基因的功能相互拮抗,共同保持生物体内正负信号相互作用的相对稳定。它在细胞中如果发生丢失、突变或失活,将促进细胞癌变。对抑癌基因的研究已成为当今细胞癌基因研究的热点,取得了一定的进展。  相似文献   

8.
基因活动异常是细胞癌变的根本原因。在人类的染色体上 ,与癌变有关的基因有 2类 :一类称癌基因(oncogene) ,其表达可导致癌症的发生 ;另一类称抑癌基因 (antioncogene) ,其表达可抑制癌症的发生和发展。本文从基因、基因产物及其作用 3个环节介绍癌基因和抑癌基因对细胞癌变过程的调控作用。1 癌基因、癌基因产物及其作用目前 ,世界上已发现癌基因 1 0 0多个 ,其中一些存在于病毒中 ,称病毒癌基因 (virusoncogene) ;另一些则存在于细胞中 ,称细胞癌基因 (cellularoncogene)。人体细胞内…  相似文献   

9.
细胞间隙连接通讯(GJIC)与肿瘤发生密切相关,大多肿瘤细胞的GJIC功能微弱或缺失。细胞发生转化后其GJIC功能降低或抑制。综述了GJIC的结构、功能,肿瘤中GJIC的变化,GJIC的抑瘤作用。  相似文献   

10.
肿瘤是一种基因疾病,其发病机制包括单核苷酸突变、拷贝数变异、插入/缺失等。人类对肿瘤经过数十年的研究,未获得突破性进展。肿瘤研究的关键是理解基因的改变在肿瘤发生、发展过程中发挥的作用。近些年单细胞测序技术的发展为探寻肿瘤发生中基因的改变提供了有力的工具。现通过肿瘤标志运用流式细胞术分选单个肿瘤细胞,并通过细胞测序获得大量信息,为肿瘤的治疗提出一个新方法—个体化治疗。  相似文献   

11.
本文概述了聚合酶链反应技术在癌基因、抑癌基因、端粒酶的活性、肿瘤病毒、肿瘤免疫的研究及常见肿瘤的检测及预后等方面的应用。  相似文献   

12.
目前,人们研究肿瘤的热点已经从癌基因转到抑癌基因,在已发现的数个抑癌基因中,p53、Fas、p16、Fhit、nm23、BLCAP与宫颈癌的关系密切,也是宫颈癌研究的热点.p53和p16基因通过调控细胞周期来抑制细胞增殖;Fas通过与其配体FasL或其单克隆抗体结合后,诱导Fas所在细胞凋亡;Fhit通过诱导细胞凋亡、细胞周期阻滞发挥着抑制肿瘤细胞增殖的作用;nm23则是通过改变nm23基因的编码产物二磷酸核苷酸激酶(NDPK)从而引起NTP产生不足,参与浸润、转移过程;BLCAP是一个新近发现的宫颈癌相关抑癌基因,其功能及性质尚不大清楚.  相似文献   

13.
p73 基因与p53 抑癌基因的比较   总被引:1,自引:0,他引:1       下载免费PDF全文
p53 是一种肿瘤抑制基因,它的突变与50 %的人类肿瘤发生有关。p73 基因编码的蛋白质,无论在结构上,还是在功能及调节上均与p53 蛋白相似,且与肿瘤的发生密切相关,本文对此方面的研究结果进行了比较,并对p73 能否作为候选抑癌基因进行了讨论.  相似文献   

14.
siRNA抗肝癌国内研究进展   总被引:1,自引:0,他引:1  
综述了国内siRNA在肝癌治疗中的研究现状.在肝癌治疗中,运用siRNA技术构建相应的siRNA载体,分别作用于与肝癌发生相关的癌基因、抑癌基因及其他相关因子等,可在一定程度上抑制癌基因表达、抑癌基因突变、细胞周期素的过度表达、过度表达的生长因子和受体以及肝癌细胞的侵袭转移能力.这些方面的研究均取得了可喜的成果,部分研究已从体外试验过渡到体内试验,为肝癌的临床治疗奠定了基础.siRNA技术为肝癌以及其他肿瘤的治疗开辟了一条新途径.但siRNA技术作为一项即将应用于临床的新技术仍存在许多问题,因此,作为临床治疗目前条件尚不成熟,仍需进一步研究.  相似文献   

15.
Postherpetic neuralgia (PHN) is a severe sequela of herpes zoster (HZ). Until now, only age and pain severity were considered predisposing factors for the development of PHN. We evaluated 49 patients with acute phase HZ, 10 of whom developed PHN (Group A) and 39 of whom did not develop PHN (Group B). Twenty-five healthy volunteers similar in age and gender distribution to the study group were recruited as controls (Group C). Numbers of serum CD3+ (pan-T lymphocytes), CD4+ (helper/inducer), and CD8+ (suppressor/cytotoxic) lymphocytes were decreased significantly in Groups A and B relative to the control group, but there were no statistical differences between Groups A and B. Interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, IL-8, and IL-10 were significantly elevated in Groups A and B relative to Group C. IL-6 was significantly higher in Group A than in Group B, and was significantly positively correlated with pain severity scored on a visual analog scale. Therefore, we suggest that the inflammatory response, especially that of IL-6, in the acute phase of HZ may be associated with hyperalgesia and the development of PHN. Project (No. 2008ZYC07) supported by the Zhejiang Medical Bureau of China  相似文献   

16.
A small proportion of many cancers are due to inherited mutations in genes, which result in a high risk to the individual of developing specific cancers. There are several classes of genes that may be involved: tumour suppressor genes, oncogenes, genes encoding proteins involved in DNA repair and cell cycle control, and genes involved in stimulating the angiogenic pathway. Alterations in susceptibility to cancer may also be due to variations in genes involved in carcinogen metabolism. This review discusses examples of some of these genes and the associated clinical conditions caused by the inheritance of mutations in such genes.  相似文献   

17.
Insulin-like growth factor binding-protein-7 (IGFBP7) was obtained from our previous colonic adenocarcinoma (CRC) and normal mucosa suppression subtraction hybridization (SSH) cDNA libraries. By RT-PCR and immunohistochemistry, we found that IGFBP7 was overexpressed in CRC tissue compared to normal tissue. However, our in vitro experiments performed in 10 CRC cell lines showed that IGFBP7 expressed only in SW480 and Caco2 cell lines, which implied an underlying reversible regulatory mechanism. Using methylation-specific PCR (MSP) and bisulfite sodium PCR (BSP), we found that its expression was associated with DNA hypomethylation of exonl. This was further supported by the in vitro study which showed restored IGFBP7 expression after demethylation agent 5-aza-2'-deoxycytidine treatment. Correlation analysis between IGFBP7 expression and prognosis indicated that overexpression of IGFBP7 in CRC tissue correlated with favourable survival. Investigation of the functional role of IGFBP7 through transfection studies showed that IGFBP7 protein could inhibit growth rate, decrease colony formation activity, and induce apoptosis in RKO and SW620 cells, suggesting it a potential tumor suppressor protein in colorectal carcinogenesis. In conclusion, our study clearly demonstrated that IGFBP7 plays a potential tumor suppressor role against colorectal carcinogenesis and its expression is associated with DNA hypomethylation of exon 1.  相似文献   

18.
19.
Objective: In the present study, we have examined the safety and efficacy of recombinant adenovirus encoding human p53 tumor suppressor gene (rAd-p53) injection in patients with advanced non-small-cell lung cancer (NSCLC) in the combination with the therapy of bronchial arterial infusion (BAI). Methods: A total of 58 patients with advanced NSCLC were enrolled in a non-randomized, two-armed clinical trial. Of which, 19 received a combination treatment of BAI and rAd-p53 (the combo group), while the remaining 39 were treated with only BAI (the control group). Patients were followed up for 12 months, with safety and local response evaluated by the National Cancer Institute's Common Toxicity Criteria and response evaluation criteria in solid tumor (RECIST), respectively. Time to progression (TTP) and survival rates were also analyzed by Kaplan-Meier method. Results: In the combo group,19 patients received a total of 49 injections of rAd-p53 and 46 times of BAI, respectively, while 39 patients in the control group received a total of 113 times of BAI. The combination treatment was found to have less adverse events such as anorexia, nausea and emesis, pain, and leucopenia (P<0.05) but more arthralgia. fever, influenza-like symptom, and myalgia (P<0.05), compared with the control group. The overall response rates (complete response (CR)+partial response (PR)) were 47.3% and 38.4% for the combo group and the control group, respectively (P>0.05). Patients in the combo group had a longer TTP than those in the control group (a median 7.75 vs 5.5 months, P=0.018). However, the combination treatment did not lead to better survival, with survival rates at 3, 6, and 12 months in the combo group being 94.74%, 89.47%, and 52.63%, respectively, com-pared with 92.31%, 69.23%, and 38.83% in the control group (P=0.224). Conclusion: Our results show that the combination of rAd-p53 and BAI was well tolerated in patients with NSCLC and may have improved the quality of life and delayed the disease progression. A further study to better determine the efficacy of this combination therapy is warranted.  相似文献   

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