Two of these Hallmarks, Apoptosis Evasion and Tissue invasion & Metastasis will be outlined in further detail later in this review. .
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Cancer Cells.
How do they start?.
The initiation of cancer (carcinogenesis), is caused by a series of mutations. A mutation being a change to the structure of a gene via alteration to the DNA bases. DNA bases can be substituted, inserted, or deleted (Berg et al. 2002). 'The human genome is exposed to mutations during the life cycle because of many types of changes in the DNA' explains (Sohrabi et al. 2014). Mutations may be caused by carcinogenic agents, viruses or errors in the DNA replication or mitotic processes. However, some cells functions remain unaffected after a mutation has occurred. Carcinogenesis, as described by (King 1996), is a 'multistep mechanism resulting from the accumulation of errors in vital regulatory pathways.' In other words, cancer is the result of cumulative mutations that alter specific locations in a cell's DNA and thus change the particular proteins encoded by cancer-related genes at those locations (Gibbs 2004) .
An example of a carcinogenic agent that causes mutations is Ultraviolet light. UV light is described by (Berg et al. 2002) as a 'ubiquitous DNA-damaging agent'. Research by (Berg et.al 2002) shows that UV light covalently links adjacent pyrimidine residues (see fig. 1.3). These Pyrimidine dimers caused by UV light can't fit into a double helix, and so replication and gene expression are blocked until the abnormality is removed or repaired.
All cells, however, do have mechanisms in place to repair damaged DNA sequences. These mechanisms come in the form of DNA repair enzymes. Research from (Berg et al. 2002) describes 3 different pathways used in DNA repair. These pathways include direct repair, base-excision repair, and nucleotide-excision repair. 'In base-excision repair, the damaged base is removed and replaced.