Abstract
Ultraviolet radiation (UVR) is a known carcinogen participated for the development of skin cancers. Solar UVR exposure, particularly ultraviolet B (UVB), is the mostly significant environmental risk factor for the occurrence and progress of basal cell carcinoma(BCC). Both cumulative and intermittent high-grade UVR exposure could promote the uncontrolled replication of skin cells. There are also exsiting other contributing environmental factors that combine with the UVR exposure to promote the development of BCC. DNA damage in formation of skin cancers is considered to be a result of UVR toxicity. It is UVR that could activate a series of oncogenes simultaneously inactivating tumor suppressor genes and aberrant proliferation and survival of keratinocytes that repair these damages. Furthermore, mounting evidence demonstrates that inflammatory responses of immune cells in the tumor microenvironment plays crucial role in the skin tumorigenesis as well. In this chapter, we will follow the function of UVR in the onset and development of BCC. We describe the factors that influence BCC induced by UVR, and also review the recent advances of pathogenesis of BCC induced by UVR from the genetic and inflammatory aspects.
Highlights
Cutaneous cancer is the most common cancer type worldwide, and basal cell carcinoma (BCC) generally accounts for 75–80% of cases arising from the basal layer of the epidermis and its appendages [1,2,3]
We describe the factors that influence BCC induced by Ultraviolet radiation (UVR) and review recent advances in BCC pathogenesis induced by UVR from genetic and inflammatory aspects
Previous studies have demonstrated that the BCC incidence rate among patients with psoriasis receiving a large number (>100–200) of Psoralen and ultraviolet A (PUVA) treatments is significantly higher than expected, and this risk persists for some time after the discontinuation of PUVA therapy [38, 39]
Summary
Cutaneous cancer is the most common cancer type worldwide, and basal cell carcinoma (BCC) generally accounts for 75–80% of cases arising from the basal layer of the epidermis and its appendages [1,2,3]. Solar UVR exposure, in particular ultraviolet B (UVB), is the most significant environmental risk factor for the occurrence and progress of BCC. Both cumulative and intermittent high-grade UVR exposures could promote the uncontrolled replication of skin cells. Other risk factors for skin carcinogenesis exist, UVR exposure has still been attributed to the development of nearly 90% of NMSCs, such as squamous cell carcinoma (SCC) and BCC [13, 14]. As a primary risk factor, UVR could be combined with or influenced by other factors, such as general characteristics, UVR sources (such as sun exposure, tanning beds, and ultraviolet phototherapy), and other environmental factors (such as alcohol consumption, long-term chemical exposure, and photosensitive agents) to induce the onset of BCC
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