Topic
Skin Carcinoma
About: Skin Carcinoma is a research topic. Over the lifetime, 297 publications have been published within this topic receiving 7460 citations.
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TL;DR: There was a disproportionate increase in basal cell carcinoma in young women and men residing in Olmsted County, Minnesota, which may lead to an exponential increase in the overall occurrence of nonmelanoma skin cancers over time as this population ages.
Abstract: ContextThe incidence of nonmelanoma skin cancer is increasing rapidly among
elderly persons, but little is known about its incidence in the population
younger than 40 years.ObjectivesTo estimate the sex- and age-specific incidences of basal cell carcinoma
and squamous cell carcinoma in persons younger than 40 years in Olmsted County,
Minnesota, and to evaluate change in incidence over time; to describe the
clinical presentation, rate of recurrence and metastasis, and histologic characteristics
of these tumors in this population-based sample.DesignPopulation-based retrospective incidence case review.SettingResidents of Olmsted County, Minnesota, a population with comprehensive
medical records captured through the Rochester Epidemiology Project.ParticipantsPatients younger than 40 years with basal cell carcinoma or squamous
cell carcinoma diagnosed between 1976 and 2003.Main Outcome MeasuresIncident basal cell carcinomas and squamous cell carcinomas and change
in incidence of these tumors over time.ResultsDuring the study period, 451 incident basal cell carcinomas were diagnosed
in 417 patients and 70 incident squamous cell carcinomas were diagnosed in
68 patients. Of these tumors, 328 were histologically confirmed basal cell
carcinomas and 51 were histologically confirmed squamous cell carcinomas.
Overall, the age-adjusted incidence of basal cell carcinoma per 100 000
persons was 25.9 (95% confidence interval [CI], 22.6-29.2) for women and 20.9
(95% CI, 17.8-23.9) for men. The incidence of basal cell carcinoma increased
significantly during the study period among women (P<.001)
but not men (P = .19). Nodular basal cell
carcinoma was the most common histologic subtype; 43.0% of tumors were solely
nodular basal cell carcinoma and 11.0% had a mixed composition, including
the nodular subtype. The incidence of squamous cell carcinoma was similar
in men and women, with an average age- and sex-adjusted incidence per 100 000
persons of 3.9 (95% CI, 3.0-4.8); the incidence of squamous cell carcinoma
increased significantly over the study period among both women (P = .01) and men (P = .04).ConclusionsThis population-based study demonstrated an increase in the incidence
of nonmelanoma skin cancer among young women and men residing in Olmsted County,
Minnesota. There was a disproportionate increase in basal cell carcinoma in
young women. This increase may lead to an exponential increase in the overall
occurrence of nonmelanoma skin cancers over time as this population ages,
which emphasizes the need to focus on skin cancer prevention in young adults.
524 citations
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TL;DR: It is reported here that UV irradiation impairs TGF-beta/Smad pathway in human skin by down-regulation of TbetaRII, with attendant reduction of type I procollagen production, a critical molecular mechanism in the pathophysiology of photoaging.
Abstract: Ultraviolet (UV) irradiation from the sun reduces production of type I procollagen (COLI), the major structural protein in human skin. This reduction is a key feature of the pathophysiology of premature skin aging (photoaging). Photoaging is the most common form of skin damage and is associated with skin carcinoma. TGF-β/Smad pathway is the major regulator of type I procollagen synthesis in human skin. We have previously reported that UV irradiation impairs transforming growth factor-β (TGF-β)/Smad signaling in mink lung epithelial cells. We have investigated the mechanism of UV irradiation impairment of the TGF-β/Smad pathway and the impact of this impairment on type I procollagen production in human skin fibroblasts, the major collagen-producing cells in skin. We report here that UV irradiation impairs TGF-β/Smad pathway in human skin by down-regulation of TGF-β type II receptor (TβRII). This loss of TβRII occurs within 8 hours after UV irradiation and precedes down-regulation of type I procollagen expression in human skin in vivo. In human skin fibroblasts, UV-induced TβRII down-regulation is mediated by transcriptional repression and results in 90% reduction of specific, cell-surface binding of TGF-β. This loss of TβRII prevents downstream activation of Smad2/3 by TGF-β, thereby reducing expression of type I procollagen. Preventing loss of TβRII by overexpression protects against UV inhibition of type I procollagen gene expression in human skin fibroblasts. UV-induced down-regulation of TβRII, with attendant reduction of type I procollagen production, is a critical molecular mechanism in the pathophysiology of photoaging.
325 citations
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TL;DR: Results from the Nutritional Prevention of Cancer Trial conducted among individuals at high risk of nonmelanoma skin cancer continue to demonstrate that selenium supplementation is ineffective at preventing basal cell carcinoma and that it increases the risk of squamous cell carcinomas and total nonmelanie skin cancer.
Abstract: The Nutritional Prevention of Cancer Trial was a double-blind, randomized, placebo-controlled clinical trial designed to test whether selenium as selenized yeast (200 microg daily) could prevent nonmelanoma skin cancer among 1312 patients from the Eastern United States who had previously had this disease. Results from September 15, 1983, through December 31, 1993, showed no association between treatment and the incidence of basal and squamous cell carcinomas of the skin. This report summarizes the entire blinded treatment period, which ended on January 31, 1996. The association between treatment and time to first nonmelanoma skin cancer diagnosis and between treatment and time to multiple skin tumors overall and within subgroups, defined by baseline characteristics, was evaluated. Although results through the entire blinded period continued to show that selenium supplementation was not statistically significantly associated with the risk of basal cell carcinoma (hazard ratio [HR] = 1.09, 95% confidence interval [CI] = 0.94 to 1.26), selenium supplementation was associated with statistically significantly elevated risk of squamous cell carcinoma (HR = 1.25, 95% CI = 1.03 to 1.51) and of total nonmelanoma skin cancer (HR = 1.17, 95% CI = 1.02 to 1.34). Results from the Nutritional Prevention of Cancer Trial conducted among individuals at high risk of nonmelanoma skin cancer continue to demonstrate that selenium supplementation is ineffective at preventing basal cell carcinoma and that it increases the risk of squamous cell carcinoma and total nonmelanoma skin cancer.
262 citations
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TL;DR: A function of p21 is revealed as a suppressor of malignant but not benign skin-tumor formation and a determinant of the growth/differentiation potential of keratinocyte subpopulations.
Abstract: p21WAF1/Cip1 is one of the best characterized downstream targets of p53, and the growth suppressing function of this cyclin-dependent kinase inhibitor is well established. However, whether p21 exerts a tumor-suppressing function of its own remains to be established. We report here that, similarly to loss of p53, disruption of the p21WAF1/Cip1 gene results in a markedly increased susceptibility to chemically induced skin carcinoma formation, whereas the number of papillomas is reduced. Previous evidence indicates that malignant versus benign keratinocyte tumor formation is likely to involve distinct target-cell populations with a different commitment to differentiation. In parallel with the increased susceptibility to carcinoma formation, loss of p21WAF1/Cip1 was found to promote keratinocyte subpopulations with increased growth/differentiation potential, including clonal growth capability, reversible commitment to differentiation, and capability to generate all types of terminally differentiated keratinocytes present in vivo, not only in the interfollicular epidermis but also in hair follicles. Thus, these findings have revealed a function of p21 as a suppressor of malignant but not benign skin-tumor formation and a determinant of the growth/differentiation potential of keratinocyte subpopulations.
211 citations
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Johns Hopkins University1, Northwestern University2, City of Hope National Medical Center3, University of Washington4, University of Michigan5, University of Utah6, Roswell Park Cancer Institute7, University of South Florida8, University of California, San Francisco9, University of Nebraska–Lincoln10, Memorial Sloan Kettering Cancer Center11, Washington University in St. Louis12, University of Texas MD Anderson Cancer Center13, Duke University14, Seattle Cancer Care Alliance15, Ohio State University16, Fox Chase Cancer Center17, University Of Tennessee System18, University of Alabama at Birmingham19, Brigham and Women's Hospital20, Vanderbilt University21
201 citations