本文主要讲的是癌细胞分析，在癌症细胞中，p53通常不存在，它没有功能，比正常细胞活性更低(Sedic et al.， 2016)。这里可以引用一个例子，各种癌变的肿瘤由p53突变体组成，它们没有结合DNA的能力。由于p53是通过靶基因结合和转录激活来起作用的，突变蛋白的非结合性使其无法完成其任务。当p53存在缺陷时，DNA损伤的细胞可能从细胞分裂开始。本篇论文代写价格文章由澳洲论文通AssignmentPass辅导网整理，供大家参考阅读。
Within the cells of cancer, p53 often is not present, it is not functional and has less activity than in normal cells (Sedic et al., 2016). An example can be quoted here that various tumours which are cancerous consist of p 53 mutant forms which do not have the ability of binding the DNA. As p53 is responsible for acting through target genes binding and transcription activation, the mutant protein non-binding nature does not allow it to do its tasks. When there is defect in p 53, cells with DNA damage might start with division of cell.
Such divisions daughter cells have a likeliness of inheriting mutations because of mother cell unrepaired DNA (Mendelsohn et al., 2014). With time, cells consisting of p53 faults have a tendency of accumulating mutations and certain of them might cause the turn of proto-oncogenes into oncogenes and might also inactivate the suppressors of tumour. P53 is one gene which gets mutated most commonly within the cancers among humans and the cells of cancer without the mutation of p 53 have a likeliness of inactivating it by related procedures such as heightened protein activity causing recycling of p 53.
During the previous few years of research, it has become apparent that specific genes of tumour suppressor’s take the form of being inactivated not because of their structural modifications but as the genes get silenced through promoter sequences hypermethylation without DNA base sequence changes (Clevers, 2011). These changes occur as maintained in a stable manner by several cell division multiple rounds. In CpG, such methylation takes place within the DNA but it hardly happens within tissues of normal nature. Methylation, however, is detected within several human cancers tumour suppressor genes.