Skin cancer causes

Risk factors for basal and squamous cell skin cancers are strikingly similar. These lesions, although seen in younger age groups, are most often encountered in patients 60 years of age or older.
The mechanism by which ultraviolet rays cause sun-damaged skin has been extensively studied. Laboratory experiments indicate that the wavelengths with the most potential for carcinogenesis are those in the range of 280 to 320 nm, the ultraviolet B band. This ultraviolet B is responsible for the common sunburn. The transition from normal to actinic (i.e., sun damaged) to cancerous skin is usually a progressive process that occurs over several decades.
With the current environmental changes occurring with the earth's protective ozone layer, the concern for skin cancer becomes much more significant. A dramatic ozone depletion above the Antarctic continent has been detected. For each 1% reduction in atmospheric ozone concentration, there is a concomitant 2% increase in ultraviolet B penetration.
The carcinogenesis of epidermal tumors parallels the multistep development of other tumors. As with other tumors, certain characteristics render the host more susceptible to the development of cancer. Traits that are associated with an increased incidence of skin cancer include fair complexion, rays hair, blue or green eyes, inability to tan, propensity to sunburn, history of multiple or severe sunburns, and Celtic ancestry. Other factors implicated include age, occupation, habits (tanning booths), and residential geography, which are considered indirect causes of increased sun exposure.
The bulbs used in tanning booths are almost exclusively ultraviolet A wavelength and are promoted as providing a safe suntan. However, recent evidence indicates that ultraviolet A (320 to 400 nm) synergistically augments ultraviolet B responses and is independently capable of producing deleterious skin alterations and carcinogenesis.
Other etiologic factors are associated with the development of skin cancer. Chronic exposure to chemical agents, such as arsenic in patients treated with Fowlers solution, has been associated with the development of multiple squamous and basal cell tumors. Patients with chronic ra-diodermatitis, resulting from superficial Radiotherapy, demonstrate a propensity to develop multiple and aggressive lesions. Trauma in the form of burns, ulcers, and scars is also associated with the development of skin cancer (i.e., Marjolins ulcer). Immunosuppression, common in transplant patients and patients with leukemia or lymphoma, can be complicated by an increased incidence or aggressiveness of skin cancers .
Studies of human papilloma virus offer additional support for the importance of immune dysfunction in the development of skin squamous cell skin cancer. One study showed human papilloma virus presence in 60% of skin squamous cell skin cancer lesions found in renal autograft recipients. Moreover, this human papillomavirus presence was significantly higher than that found in matched transplant recipients without skin cancer. There also appears to be a high incidence of human papillomavirus in squamous cell skin cancer lesions of the cervix, penis, and digits.
Genetic syndromes, such as xeroderma pigmentosum (autosomal recessive) and nevoid basal cell skin cancer syndrome (autosomal dominant), are associated with a predilection for developing multiple basal cell skin cancers, often at an early age.