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Identification and analysis of DNA repair mechanisms that contribute to resistance against nucleoside analogues - Literature review Example

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Identification and analysis of DNA repair mechanisms that contribute to resistance against nucleoside analogues Contents Contents 2 1.0 Carcinogenesis and Cancer Treatment Resistance 3 2.0 Mechanisms in Cancer Cells 6 3.0 Nucleoside Analogues 7 3.1 Purine nucleobases and purine nucleoside analogues 10 3.2 Deoxyadenosine derivatives 11 3.3 Deoxycytidine analogues 11 4.0 Topoisomerases 12 5.0 The MRN complex 13 6.0 References 14 1.0 Carcinogenesis and Cancer Treatment Resistance Cellular DNA was once considered to be an inert substance, however, current molecular knowledge and research has developed considerably…
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Identification and analysis of DNA repair mechanisms that contribute to resistance against nucleoside analogues
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"Identification and analysis of DNA repair mechanisms that contribute to resistance against nucleoside analogues"

Download file to see previous pages Consequently, DNA is damaged frequently, and is repaired through pathways of repair and proofreading functions by DNA polymerase. Multiple mechanisms of repair within the cell act to balance these levels of mutation. However, the large number of mutations that occur means that every so often, the repair process misses these mutations and they become part of the DNA. This process can be the first step in carcinogenesis . There are currently 346 different genes that have been associated with the development of cancer, although this number continues to grow. In some cases these genes are mutated in cancer cells and not in normal cells. In other cases, genes may show substantial levels of deregulation. Both of these processes have the potential to significantly decrease the effectiveness of certain genes, leading to altered pathways within the cancer cell and the body itself . This suggests that mutations are a crucial part of the formation of cancer. Indeed, human cancer appears to have thousands of different mutations by the time that it is first detected. Furthermore, information that cancer can be inherited from one generation to the next suggests that some of these mutations can be passed along in genes . Cancer is characterised by high levels of clonal expansion of somatic cells. These cells are not subject to the normal growth regulation components of the cell cycle. Thus, they are able to proliferate beyond the normal constraints of tissue. Likewise, the controls over apoptosis are also circumvented . Most tumours that develop in the human body are substantially heterogeneous. This suggests that multiple mutations occur within human cancers driving the creation of tumours and the change in function between normal cells and cancerous cells . Thus, cancer can be considered to be a disease, or collection of diseases, that occurs due to genetic abnormalities accumulating within cells . In each generation of cancer cells, significant mutation occurs within different cells, and those that develop mutations that facilitate cancer growth are selected for, resulting in an increase in the prevalence of these cells. Mutations may be subtle, such as changes in the sequence of nucleotides, or more substantial, involving changes in the chromosomes themselves . One significant factor in cancer treatment resistance is that therapeutic killing cancer cells, while causing cancer to go into remission, can also act to select for resistance to treatment. This can result in a progression of tumour growth, with cells that cannot be targeted by the same treatment . Another form of resistance that can occur is based on the cells location in the division cycle. Cancer therapy tends to be most effective on cells that are rapidly replicating. Furthermore, resistance to treatment can often be stronger in some stages of the cell cycle than others . Cancer cells contain a wide range of mutations, and these mutations may act to drive the formation and progression of tu ...Download file to see next pagesRead More
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