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癌症的发展是一个复杂和多步骤的过程,在这个过程中一系列进行性改变导致体细胞的失控性增殖。癌细胞的特征是能够无约束地生长,能够侵袭到周围正常的组织,并能够转移到远处的器官。大多数肿瘤,包括神经系统的肿瘤,都是原发的。改变后细胞的遗传学破坏可能是由于遗传中的倾向性,细胞周期中DNA重排,病毒感染和整合;也可能是暴露在突变因子情况下,诸如离子辐射一类,这些因素可以使癌细胞的生长优于它的正常部分。通常广谱的肿瘤遗传学改变包括两类基因的改变:第一,癌基因的优势,它的出现导致细胞的改变;第二,隐性抗癌基因的缺乏,它的缺乏引起细胞的改变。后者通常又称为肿瘤抑制基因,生长抑制基因或隐性抗癌基因。可以相信正常细胞的增殖是在这些促进生长的原癌基因和抑制生长的抗癌基因的内在控制下进行的突变、重排、缺失或扩增而潜在地激活原癌基因导致肿瘤的形成。同样的事件可以发生在抗癌基因和抑癌基因的失活,干扰它们在细胞中作为细胞增殖的负性调控作用。本文主要介绍在GenBank中登录的与人脑肿瘤相关的抑癌基因的情况。
The development of cancer is a complex and multi-step process in which a series of progressive changes lead to the uncontrolled proliferation of somatic cells. Cancer cells are characterized by the ability to grow unconstrained, be able to invade the surrounding normal tissue, and be able to metastasize to distant organs. Most tumors, including those of the nervous system, are primary. Changes in the genetic damage of cells may be due to genetic predisposition, DNA rearrangement in the cell cycle, viral infection and integration; may also be exposed to the mutation factor, such as ionizing radiation, these factors can make cancer cells Grow better than its normal part. Often broad-spectrum oncological changes include two types of genetic changes: first, the advantages of oncogenes, which lead to cell changes; second, the lack of a recessive anti-cancer gene, and its lack of cellular changes. The latter is often referred to as a tumor suppressor gene, a growth inhibitory gene or a recessive anti-cancer gene. It is believed that the proliferation of normal cells is the result of the potential activation of protooncogenes resulting in tumor formation by mutations, rearrangements, deletions or amplifications under the intrinsic control of these growth-promoting proto-oncogenes and growth-inhibiting anti-oncogenes. The same events can occur in the inactivation of anti-oncogenes and tumor suppressor genes, interfering with their negative regulatory role in cell proliferation as cells. This article describes the case of human tumor-associated tumor suppressor genes registered in GenBank.