Basal cell carcinoma, squamous cell carcinoma and melanoma of the head and face.

L Feller,J Lemmer,R A G Khammissa,M Altini,B Kramer

doi:10.1186/s13005-016-0106-0

Abstract

Ultraviolet light (UV) is an important risk factor for cutaneous basal cell carcinoma, cutaneous squamous cell carcinoma and cutaneous melanoma of the skin. These cancers most commonly affect persons with fair skin and blue eyes who sunburn rather than suntan. However, each of these cancers appears to be associated with a different pattern of UV exposure and to be mediated by different intracellular molecular pathways.Some melanocortin 1 receptor (MC1R) gene variants play a direct role in the pathogenesis of cutaneous basal cell carcinoma, cutaneous squamous cell carcinoma and cutaneous melanoma apart from their role in determining a cancer-prone pigmentory phenotype (fair skin, red hair, blue eyes) through their interactions with other genes regulating immuno-inflammatory responses, DNA repair or apoptosis.In this short review we focus on the aetiological role of UV in cutaneous basal cell carcinoma, cutaneous squamous cell carcinoma and cutaneous melanoma of the skin, and on some associated biopathological events.

Highlights

The skin of the head and face is habitually exposed to sunlight and there may be ultraviolet (UV)-induced chronic damage such as solar elastosis, actinic keratosis and lentigo, with possible consequent development of cutaneous squamous cell carcinoma, cutaneous basal cell carcinoma and cutaneous melanoma [1]
T cell-mediated immune responses against tumour-specific antigens may directly cause lysis of tumour cells, and activated inflammatory cells may non- destroy tumour cells by producing and secreting active biological mediators [63]. Both in dark and in light skin, UV can cause local immune suppression by altering antigen presentation by Langerhans cells, and by increasing expression of immunosuppressive neuropeptides, melanocortins, cytokines and inflammatory mediators released into the microenvironment by keratinocytes, melanocytes, neurocytes and mast cells [29, 64, 65]. This may diminish the capacity of the immune system to detect and to eliminate immunogenic initially transformed keratinocytes and melanocytes, and so to promote the growth of cutaneous basal cell carcinoma, cutaneous squamous cell carcinoma and cutaneous melanoma [29]
The risk of non-syndromal cutaneous basal cell carcinoma, cutaneous squamous cell carcinoma and cutaneous melanoma is associated with UV exposure, but the complex multifactorial relationship between the patterns of exposure to UV and the pathogenesis of these skin cancers is yet to be explained

Summary

Background

The skin of the head and face is habitually exposed to sunlight and there may be ultraviolet (UV)-induced chronic damage such as solar elastosis, actinic keratosis and lentigo, with possible consequent development of cutaneous squamous cell carcinoma, cutaneous basal cell carcinoma and cutaneous melanoma [1]. Like cutaneous squamous cell carcinoma, lentigo maligna melanoma typically affects chronically UV-exposed skin of the head and face, but the risk of other subtypes of melanoma is more related to intermittent, intense UV exposures [51, 53, 54]. Both in dark and in light skin, UV can cause local immune suppression by altering antigen presentation by Langerhans cells, and by increasing expression of immunosuppressive neuropeptides, melanocortins, cytokines and inflammatory mediators released into the microenvironment by keratinocytes, melanocytes, neurocytes and mast cells [29, 64, 65] This may diminish the capacity of the immune system to detect and to eliminate immunogenic initially transformed keratinocytes and melanocytes, and so to promote the growth of cutaneous basal cell carcinoma, cutaneous squamous cell carcinoma and cutaneous melanoma [29]

Conclusion

Findings

Ethical approval Not required