癌基因激活

肿瘤的发生是原癌基因激活、抑癌基因失活以及凋亡相关基因失调等诸多因素综合作用的结果。

The development of tumor results from complex action among multiple factors such as oncogene activation , anti-oncogene inactivation , disturbance of apoptosis related gene and so on .

蛋白激酶C在细胞生长、分化、肿瘤促进、癌基因激活及恶性化的细胞信号传导过程中发挥主要作用。

Protein kinase C ( PKC ) plays an important role in cell & signal transduction during cellular growth and differentiation as well as in tumor promotion , oncogene activation and carcinogenesis .

与MTHFR失活有关的广泛低甲基化引起染色体失稳和原癌基因激活促进了肿瘤的发展。

Global hypomethylation associated with MTHFR inactivation contributes to development of cancer by destabilizing the chromosome and activating oncogenes .

NB的发生与神经母细胞分化过程中多种癌基因激活、抑癌基因失活和基因表达改变有关。

Tumorigenesis of neuroblastoma involves multiple genetic changes such as the activation of proto-oncogenes , inactivation of tumor suppressor genes and alterations of gene expression during the process of neuroblast differentiation .

癌变是一个复杂的过程，是由癌基因激活，抑癌基因和细胞死亡机制失活相互作用而出现的。

Cancer is a complex process by the interaction of oncogenes activation and tumor suppressor gene and the mechanism of cell death inactivation .

胃癌的发生、发展与多种因素相关，其中原癌基因激活、抑癌基因失活及肿瘤转移抑制基因失活起着重要作用。

Development of gastric cancer related to many factors including activation of oncogene , inactivation of tumor suppressor genes and tumor metastasis suppressor gene .

基因组的不稳定导致的癌基因激活、抑癌基因丢失或失活是肿瘤发生的机制之一。

Activation of oncogene and loss of functions of tumor suppressor genes resulting from instability of human genome is one of the mechanisms in tumorigenesis .

研究表明，骨肉瘤的发生机制与原癌基因激活和抑癌基因失活等基因改变有密切关系。

According to the latest study , the pathogenesis of osteosarcoma is closely related to the activation of oncogenes and the inactivation of tumor suppressor genes .

细胞凋亡与肿瘤的发生密切相关，由于癌基因激活或抑癌基因失活导致的细胞周期失控，细胞凋亡不足，是许多肿瘤发生的重要机制。

Cell apoptosis was closely related to the generation of the rumour because of the oncogene activation or anti-oncogene inactivation which could lead the cell cycle out of control .

分子生物学研究表明，肺癌的发生是一个多因素共同参与、多阶段的复杂生物学过程，与癌基因激活、抑癌基因失活密切相关。

Molecular biology studies have shown that lung cancer is a complexity of multi-stage biological process with multi-factors being involved , including activation of oncogene and inactivation of tumor suppressor gene .

近年来有关膀胱肿瘤发病的分子机制一直是研究的热点，其中包括基因突变、原癌基因激活、抑癌基因失活及凋亡失衡等多种发病机制。

In recent years , molecule mechanisms about Bca is always the hot point , such as gene mutation , protooncogene activation , anti-oncogene inactivation , apoptosis disequilibrium and so on .

在癌症的发病机制的研究中，逐步而有序的基因改变引发的癌基因激活和肿瘤抑制基因的失活被认为是人类癌症发病重要的分子生物学机制。

In the pathogenesis of cancer research , and gradually and orderly genetic changes caused by oncogene activation and inactivation of tumor suppressor genes in human cancer is considered an important mechanism of the molecular biology .

背景和目的：研究表明，肿瘤是一类多基因疾病，是由于端粒酶激活、癌基因激活或抑癌基因失活等引发的多因素、多阶段及多基因变异的综合病变过程。

Background and Aim : Carcinoma is a type of multi-gene disease , and a complex process involved multi-factor , multi-stage and multi-gene mutation , which caused by activation of telomerase and cancer gene , devitalization of suppressor gene .

胃癌的发生是一个多阶段、多基因改变累积的过程，其中癌基因激活以及抑癌基因失活起着重要作用。

The generation and development of gastric cancer are more than a multi-gene and multi-stage changing process , in which the activation of cancer gene mutation and inactivation of tumor suppressor gene play an important role in the development of gastric cancer .

肿瘤是机体细胞失去正常调控而发生的一种异常增殖现象，癌基因激活和抑癌基因失活引起的细胞周期调控失常是肿瘤发生发展的重要原因。

Tumor is the result of abnormal proliferation of somatic cells deficient of normal regulation . The deregulation of the cell cycle caused by activation of oncogenes and inactivation of tumor suppressor genes plays a crucial role in the carcinogenesis and development of tumor .

目前肝癌发生发展的机制尚不完全清楚，可能的分子机制包括原癌基因的激活、抑癌基因的失活、DNA分子的损伤及染色体的不稳定等。

The potential molecular mechanisms include proto-oncogenes activation , tumor-suppressor genes inactivation , DNA abnormality and chromosomal instability .

背景与目的：5-杂氮-2′-脱氧胞苷是DNA甲基转移酶抑制剂，能使因甲基化而失活的抑癌基因重新激活，进而抑制肿瘤的生长。

BACKGROUND & OBJECTIVE : 5-Aza-2 ′ - deoxycytidine ( 5-Aza-CdR ) is an inhibitor of DNA methyltransferase ; it may reactivate methylated antioncogene , therefore , inhibit the growth of cancer cells .

MGMT基因的失活常导致原癌基因的激活。

The inactivation of MGMT gene may urge the proto oncogene activation .

近来有研究表明VEGF的表达是生长因子的刺激和癌基因的激活通过PI3K／AKT信号传导途径作用于HIF-1α而实现的。

Recent research demonstrated that PI3K / AKT signaling is required for VEGF expression through HIF-1 in response to growth factor stimulation and oncogene activation .

c-fms癌基因异常激活机制及携带AFP增强子反义c-fms与肝癌的研究

The study of abnormal activating mechanism of c-fms oncogene and antisense c-fms bearing AFP enhancer with hepatocellular carcinoma

已有许多资料表明，Ha-ras癌基因的激活与膀胱癌的发生发展有关。

Many data have suggested that activated Ha-ras oncogene is relevant to the occurrence and progression of bladder cancer .

RNA干扰（RNAi）技术是最有效的在转录后水平抑制基因表达的手段，而大肠癌的发生亦是癌基因的激活和失活共同作用的结果。

RNA interference ( RNAi ) technology is the most effective mean of suppressing gene expression in the post-transcriptional level , while the incidence of colorectal cancer is due to the oncogene activation and inactivation .

肿瘤内HIF-1的活性取决于HIF-1α，缺氧及某些癌基因的激活、抑癌基因的失活可使HIF-1α表达增加。缺氧是实体性肿瘤的常见特征，与治疗效果差及肿瘤恶性进展相关。

HIF-1 activity in tumors depends on the availability of the HIF-1 alpha subunit , the levels of which increase under hypoxic conditions and through the activation of oncogenes and / or inactivation of tumor suppressor genes .

结论：[1]肝外、肝内胆管瘢痕组织中c-myc和c-fos癌基因受激活，可能参与了成纤维细胞的分化增殖、胶原合成与降解以及对细胞因子的调控，并导致瘢痕增生。

Conclusion ( 1 ) c-myc and c-fos oncogenes are activated on biliary scar tissues , which may contribute to proliferation and differentiation of fibroblasts 、 synthesis and degradation of collagen and regulation of cytokines and induce abnormal scarring .

根据现代分子生物学理论，肿瘤的发生是一系列遗传学和表观遗传学（epigenetics）改变积累的结果，特别是癌基因的激活与抑癌基因的失活。

According to modern molecular biological theory , a series of genetic or epigenetic alterations , especially the activation of oncogenes and the inhibition of tumor-suppressor genes have major contributions to the development of cancers .

基因扩增是原癌基因恶性激活的重要机制之一。

Gene amplification is one of the major mechanisms for activation of oncogenes .

其发生、发展在本质上是由于细胞原癌基因的激活和抑癌基因的失活所致。

Its occurrence and development are due to the oncogene activation and inactivation of tumor suppressor genes .

前言胃癌的发生发展涉及多种原癌基因的激活和抑癌基因的失活。

The activation of oncogenes and inactivation of tumor suppressor genes were involved in carcinogenesis and progression of gastric cancer .

如果若干癌基因被激活，细胞无力排除也就演变成了癌细胞。

If several oncogenes are driven into action , the cell , unable to turn them off , becomes cancerous .

在启动阶段发生了一些特定基因表达不可逆的改变，尤其是细胞内一些原癌基因的激活。

During initiation stage , some irreversible processes including the alteration of specific genes and in particular the activation of celluar proto-oncogenes occurs .