Identification and analysis of DNA repair mechanisms that contribute Assignment

Identification and analysis of DNA repair mechanisms that contribute to resistance against nucleoside analogues - Assignment Example For instance of repair pathways are homologous recombination (HR), trans-lesion synthesis (TLS), non-homologous end joining (NHEJ), nucleotide excision repair (NER), base excision repair (BER) and mismatch repair (MMR) (Martin et al., 2010). When there are double-strand breaks in the DNA strands and the replication forks, HR and the NHEJ pathways are at work to repair it. In the case of modified or incorrect basis, which can happen in DNA synthesis, the BER path works to remove them. When there are chemically induced damages to DNA or UV damage, the NER pathway removes the damage. MMR is the pathway repairing deletion, mismatch or insertion mutations that happen in the DNA and TLS pathways makes the polymerases bypass modified bases which can disrupt the replication forks. In other cases, multiple protein pathways take part in maintaining the genetic wholeness in different cell cycles, stopping the aberrant or anomalous cells from dividing. Thus, the daughter cells inherit the correc t genomic information (Martin et al. 2010). There are various mutations are happened at the same time, the repair process misses some of mutations and become part of DNA (Loeb, Loeb 2000). Currently, there are 346 genes, which are associated with the development of cancer and this number keeps increasing. In some cases these genes are mutated only in cancer cells, not in the normal cells. In other cases genes may show increased levels of deregulated. In both cases, the result can be a significant decrease in the effectiveness of the genes, which may lead to change pathways both in the cancer cell and the body itself (Huang, Wallqvist & Covell 2006). This suggests that mutations are very essential part of cancer formation. It is observed that when human cancer is first detected, there are already thousands of different mutations. Also, information that cancer can be passed from one generation to the next, means that some of those mutations are inherited in the genes (Loeb, Loeb 2000) . Cancer is characterised by a high rate of somatic cells cloning themselves. These cells do not go by the normal growth regulation mechanisms acting in a cell. This is why these cells can multiply far more rapidly than a normal cell would. In a similar way, mechanisms controlling apoptosis are also not working normally, which means that the cancerous cell does not die when it should (Evan, Vousden 2001). Most tumours that develop in the human body are substantially heterogeneous. This suggests that many mutations occur in the cancer cells leading to the creation of tumours and to the change in function of normal cells compared to cancerous cells (Loeb Loeb & Anderson 2003. That is why cancer can be seen as a disease, or many diseases, which happen because of genetic abnormalities piling up in the cells (Huang, Wallqvist & Covell 2006). In each generation of cancer cells, significant mutation occurs within different cells, and those that develop mutations that facilitate cancer grow th 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 (Wang et al, 2002). One important factor in the treatment of cancer is that therapeutic killing cancer cells, which make the cancer go into remission, can also make it more resistant to treatment in a similar manner to how some microorganisms can become