本文的主要内容是导致癌症的原因，首先，为了找到癌症的细胞基础，关键在于解决癌细胞与正常细胞的不同之处。这两者有几个不同的特征(Sedic et al.， 2016)。例如，正常细胞的形状是扁平的，而癌细胞的形状是圆形的。癌细胞膜的出现是不稳定的。不存在接触抑制。癌细胞没有静止。细胞周期约为14小时，正常细胞周期一般为22小时。癌细胞没有衰老。他们是无序的，显示更高的血管生成。癌细胞的生长是侵袭性的，细胞内有明显的转移。本篇英国市场营销论文代写文章由英国论文通AssignmentPass辅导网整理，供大家参考阅读。
First, in order to find the cellular base of cancer, the key lies in addressing the way in which cancer cells are different from normal cells. There are several characteristics on which these two differ (Sedic et al., 2016). The shape of a normal cell for example is flat while that of a cancer cell is rounded. Appearance of membrane in cancer cells is turbulent. Inhibition of contact is not present. There is no quiescence in cancer cells. The time for cell cycle is around 14 hours which generally in normal cells is 22 hours. The senescence of cancer cells is not present. They are disorganized and show higher angiogenesis. Growth of cancer cells is invasive with metastasis apparent in the cells.
Cells have various distinct processes for restricting the division of cells, repairing the damage of DNA and preventing the cancer development. Due to this, it is apparent that cancer develops in a multiple step procedure wherein several processes can fail prior to an essential mass reaches and cells start to be cancerous (Mendelsohn et al., 2014). Most cancers specifically come as cells start acquiring mutation series making them to divide in a fast manner escaping inner and external division controls and avoiding cell death programing. A hypothetical example can be provided here. A cell first starts losing out on its activity within the inhibitor of cell cycle. This is an event which makes the descendants of cells divide in a rapid manner. There is unlikeliness that these are cancerous but they might result in formation of a tumour of benign nature (Clevers, 2011). This is a cell mass dividing at a larger pace but there is no potential in this to consider invading other near tissues. With some time, mutations start taking place within individual descendant cells resulting to cause enhanced activity with regard to positive regulator in the cell cycle. Such a mutation might not result in causing cancer in itself but the cell offspring would divide in a fast pace resulting in creation of a large cell pool wherein third base of mutation might occur. One cell eventually might start gaining sufficient mutations for taking over the cancer cell features and this might give rise to a tumour of malignant nature. These are cells in groups dividing in an excessive manner with the ability of invading near-by tissues. With progress of tumour, the cells generally take up more mutations (Dancey et al., 2012). Cancers in the advanced stage have key genome based changes inclusive of mutations at larger scale such as entire chromosomes being duplicated or lost altogether. In certain situations, these changes come because of mutation inactivation within the genes keeping stability in genomes.
Such genes result in encoding proteins with the ability of sensing and repairing the damage of DNA, intercepting the chemicals that bind DNA, maintaining the caps of telomere over the chromosomes ends and other essential roles for maintenance are also played. Therefore, when cells have a stability factor with non-functional genome, the descendants might reach the mutations critical mass required for can in a faster manner than general cells.
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