UV RADIATION AND CUTANEOUS MALIGNANT MELANOMA
Chapter from book: Sunlight, Vitamin D and Skin Cancer, Second Edition, edited by Jörg Reichrath
Johan Emilian Moan,*1,2 Zivile Baturaite,1 Arne Dahlback2 and Alina Carmen Porojnicu1
lDepartment of Radiation Biology, Institute for Cáncer Research, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway; 2Institute of Physics, University of Oslo, Oslo, Norway. *Corresponding Author: Johan EmilianMoan—Email: j.e.moan@fys.uio.no
Abstract:
Essential features of the epidemiology and photobiology of cutaneous malignant melanoma (CMM) in Norway were studied in comparison with data from countries at lower latitudes. Arguments for and against a relationship between UV radiation (UV) from sun and artificial light and CMM are discussed. Our data indícate that UV is a carcinogen for CMM and that intermittent exposures are notably melanomagenic. This hypothesis was supported both by latitude gradients, by time trends and by changing patterns of tumor density on different body localizations. However, even though UV radiation generates CMM, it may also have a protective action and/or an action that improves prognosis.
There appears to be no, or even an inverse latitude gradient for CMM arising on non-UV exposed body localizations (uveal melanoma, CMMs arising in the vulva, perianal/anorectal regions, etc.). Furthermore, CMM prognosis was gradually improved over all years of increasing incidence (up to 1990), but during the past 20 y, incidence rates stabilized and prognosis was not improved significantly.
Comparisons of skin cancer data from Norway, Australia and New Zealand indicate that squamous cell carcinoma and basal cell carcinoma are mainly related to annual solar UVB fluences, while UVA fluences play a larger role of CMM.
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Arguments against a Relationship between UV and CMM
- 1. CMM is more frequent among people with occupations giving low accumulated UV exposures, so called white-collar workers, than among people with large accumulated UV exposures (farmers, fishermen, etc).15-17
- 2. The localization pattern of CMM on the body is different from that of SCC, which is clearly UV related.1
- 3. CMM appears to be uncommon among albino Africans; opposite to what is found for BCC and SCC.22
- 4. The incidence rate of CMM in sunny Australia (15-35° South) is only two times higher than in the high-latitude country Norway (> 59° North), while the incidence rates of BCC and SCC are 20 to 40 times higher in Australia.23 In some US populations there are a large north-south gradients of BCC and SCC, but no gradient of CMM.24
- 5. In Europe, which is populated mainly by Caucasians, CMM is more frequent in the north than in the south.23,25
- 6. Sun and artificial sources of UVB are efficient generators of vitamin D which seems to reduce carcinogenesis and tumor progression. It has been demonstrated that higher 25-hydroxyvitamin D3 levels, at CMM diagnosis, were associated with both thinner tumors and better survival from melanoma, independent of Breslow thickness.26-29
- 7. CMM may be a disease related to affluence, since the incidence rates appear to increase with increasing gross domestic product (GDP).10
- 8. A number of chemicals seem to be causing CMM. There is a possible relationship between polycyclic aromatic hydrocarbons (PAH), benzene, and/ or polychlorinated biphenyls (PCB) exposure of workers in the petroleum and automobile industry and an increased risk for CMM.30
- 9. UVA induces CMM neither inMonodelphis domestica nor in transgenic mice.31,32
- 10. Recently, the original Xiphophorus experiments of Setlow et al. were attempted to reproduce, but no CMM generating effect of UVA was found.33,34
Arguments for a Relationship between UV and CMM
- 1. In populations with similar skin type there is a clear latitudinal gradient, which is larger for BCC and SCC than for CMM. The UVB gradient is also larger than the UVA gradient. The incidence rate of CMM in sunny Australia is only two times higher than in the high-latitude country Norway, while the incidence rates of BCC and SCC are 20 to 40 times higher.25
- 2. CMM risk decreases with increasing pigmentation.35
- 3. Albino Africans lacking melanin have very high rates of BCC and SCC but low rates of CMM. This seems to suggest that melanin, which absorbs UVA, is a chromophore for CMM.22
- 4. Migration to more sunny countries increases the CMM risk.36,37
- 5. CMMs often arise in the borders of pigmented nevi.38,39
- 6. Sunburn episodes are risk factors for CMM and CMMs used to occur mainly on sun exposed skin.10,37,39-41
- 7. CMM patients often have low DNA repair capacity and low minimum erythema doses (MEDs).11,42-45
- 8. Lentigo maligna melanoma is clearly related to UV exposure.46
- 9. Patients with Xeroderma Pigmentosum (abnormal DNA repair) have at least 1000 times increased CMM risks.11,44,47
- 10. Some CMMs contain mutations pointing toward UV damage.9,12,48-50
- 11. CMM-resembling tumors can be induced in some animals by UV (examples: Angora goats, Sinclair swine, Monodelphis domestica (an opossum), white horses and Xiphophorus (a small swordfish).32
- 12. Patients with CMM have increased risk of BCC and SCC.51
- 13. Some reports indicate increased CMM risk for persons frequently using sunbeds. Most sunbeds emit relatively more UVA than the sun does.52-57
- 14. There seems to be little CMM protective effect of only UVB absorbing sunscreens. However, a broad-spectrum (UVB-UVA) sunscreen reduces risk of CMM.58-61
- 15. Around CMM lesions solar elastosis is found. Solar elastosis is related to accumulated UV exposure.26,62,63
- 16. Per unit skin area CMMs occurred more frequently on heavily exposed (face, scalp) than on rarely exposed (female breast) skin regions, although this is not always true for younger generations.8 The topless fashion was introduced in the early 1970-ies,64 and, before that time, very few cases of CMM on the breasts of women were registered.
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