Abstract
Animal studies as early as the 1920s suggested that vitamin A deficiency leads to squamous cell metaplasia in numerous epithelial tissues including the skin. However, humans usually die from vitamin A deficiency before cancers have time to develop. A recent long-term cohort study found that high dietary vitamin A reduced the risk of cutaneous squamous cell carcinoma (cSCC). cSCC is a form of nonmelanoma skin cancer that primarily occurs from excess exposure to ultraviolet light B (UVB). These cancers are expensive to treat and can lead to metastasis and death. Oral synthetic retinoids prevent the reoccurrence of cSCC, but side effects limit their use in chemoprevention. Several proteins involved in vitamin A metabolism and signaling are altered in cSCC, which may lead to retinoid resistance. The expression of vitamin A metabolism proteins may also have prognostic value. This article reviews what is known about natural and synthetic retinoids and their metabolism in cSCC.
Highlights
Cutaneous squamous cell carcinoma is a form of keratinocyte carcinoma, known as non-melanoma skin cancer
Topical retinoid acid (RA) accelerated [119], inhibited [120], or had no effect [121] on photocarcinogenesis. These differences could be due to timing or dose of RA. These variable effects of RA may be due to differences in the background strain of the hairless gene mutation, as different mouse strains have different susceptibility to Cutaneous squamous cell carcinoma (cSCC) and different levels of endogenous retinoids [122,123]
Oral retinol or the second-generation aromatic retinoid etretinate at two high doses did not alter photocarcinogenesis in hairless mice [124]. These studies suggest a complex relationship between ultraviolet light B (UVB), cSCC development, and RA signaling
Summary
Cutaneous squamous cell carcinoma (cSCC) is a form of keratinocyte carcinoma, known as non-melanoma skin cancer. Standard treatment of cSCC is surgical removal and/or radiation, which is effective in most patients. The “cure” is temporary: 91% of patients who have cSCCs surgically removed develop an additional tumor within 10 years, and high-risk patients have greater tumor recurrence [13]. In the southern half of the U.S, death from cSCC is similar to several other cancers and higher than melanoma, renal, and oropharyngeal carcinomas [15]. This high risk is due to the presence of an aggressive tumor, multiple tumors, or immunosuppressed patients [17]. Detection of high-risk aggressive tumors leads to better treatments
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