As Berger et al state for prostate cancer:
We identified a median of 3,866 putative somatic base mutations (range: 3,192–5,865) per tumor; the estimated mean mutation frequency was 0.9 per megabase. This mutation rate is similar to that observed in acute myeloid leukemia and breast cancer but 7–15 fold lower than rates reported for small cell lung cancer and melanoma17–19. The mutation rate at CpG dinucleotides was more than 10-fold higher than at all other genomic positions. A median of 20 non-synonymous base mutations per sample were called within protein-coding genes. We also identified six high-confidence coding indels (4 deletions, 2 insertions) ranging from 1 to 9 base pairs (bp) in length, including a 2bp frameshift in the tumor suppressor gene, PTEN.
Similarly for melanoma the Nature discussion by Hayden states:
The team also confirmed some findings from earlier studies
including the effect that sun exposure can have on the mutation rate of
tumour DNA. Tumours from areas of the body that are not frequently
exposed to sunlight had around 3 to 14 mutations every million base
pairs, whereas one patient who was known to have had high levels of sun
exposure had 111 mutations every million base pairs.
The relationship between sun exposure and mutation rates
adds to the evidence for the role of sun exposure in melanoma
development, says Laura Brockway-Lunardi, director of scientific
programmes for the non-profit Melanoma Research Alliance in Washington
DC, which helped to fund the work.
We also note that these mutations may or may not be related in some sequence or pathway. We would also not that for the melanoma mutations the 3-14 for non sunlight exposed and the 111 for sunlight exposed is significant and causal. However we have also argued that such might also be the case for backscatter X ray scanning as now used by the US Government to an excessive degree.
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