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DNA Damage and Cancer
Last updated on 14 January 2009
DNA damage is very frequent and appears to be a fundamental problem for life. DNA damage is also the underlying cause of mutations leading to cancer.
In human cells, the estimated average number of DNA damages occurring per hour is about 800, and the number per day is about 19,200 (Vilenchik and Knudson, 2000). The incidence of DNA damage is likely higher than this in cells subject to unfavorable conditions such as inflammation or tobacco smoke exposue. Most DNA damages are removed by DNA repair enzymes (Bernstein et al., 2002), but these repair processes are not 100% efficient.
In dividing cells, DNA damages, if not repaired, cause errors during DNA synthesis leading to mutations that can give rise to cancer. Thus individuals with an inherited impairment in DNA repair capability are often at increased risk of cancer (Bernstein et al., 2002). Because human somatic cells are diploid, mutant genes are most often recessive when they arise in a somatic cell, and they usually do not initially express because of the presence of the wild-type copy of the homologous gene. However, recessive mutations can express when there is a loss of heterozygosity (LOH). This condition may arise in a number of ways including mutation in the homologous gene, occurrence of aneuploidy (loss of a chromosome) for the homologous chromosome, or by recombination with the homologous chromosome.
Although most mutations, upon expression, are likely to have a deleterious or neutral effect on the cells that harbor them, some will provide a growth advantage. The growth advantage may arise from an increased rate of cell division or a decreased rate of cell death. Such cells will tend to proliferate at the expense of neighboring cells to give rise to a field of mutant cells (Bernstein et al., 2008). Within such a field, further DNA damage may give rise to a cell with a second expressing mutation that provides a further proliferative advantage relative to surrounding cells. This new double mutant will expand, forming a secondary field within the first field. Repetition of this process, often over decades, may give rise to a pre-malignant field and ultimately to cancer.
http://en.wikipedia.org/wiki/Nonsense_mutations
Excerpt:
In genetics, a nonsense mutation is a point mutation in a sequence of DNA that results in a premature stop codon, or a nonsense codon in the transcribed mRNA, and in a truncated, incomplete, and usually nonfunctional protein product. It differs from a missense mutation, which is a point mutation where a single nucleotide is changed to cause substitution of a different amino acid. Some genetic disorders, such as thalassemia and DMD, result from nonsense mutations.
Stop codon
From Wikipedia, the free encyclopedia
In the genetic code, a stop codon (or termination codon) is a nucleotide triplet within messenger RNA that signals a termination of translation.[1] Proteins are based on polypeptides, which are unique sequences of amino acids. Most codons in messenger RNA correspond to the addition of an amino acid to a growing polypeptide chain, which may ultimately become a protein. Stop codons signal the termination of this process by binding release factors, which cause the ribosomal subunits to disassociate, releasing the amino acid chain.
In the standard genetic code, there are several stop codons:
In the standard genetic code, there are several stop codons:
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