Advances in the immunobiology of the skin. Implications for cutaneous malignancies

Romerdahl, Cynthia A.; Kripke, Margaret L.

doi:10.1007/bf00046429

Cited by 6 publications

(3 citation statements)

References 78 publications

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“…As is evident from Figures 2 and 3, the magnitude and the range of protection against lethal virus infection associated with S.C. injection of DHEA were considerably greater than when DHEA was fed in the diet. Recent reports show that the skin may have unique immune functions [Romerdahl, 1986;Streilein, 19831. Indeed the skin is known to contain a population of cutaneous immune cells, which includes the epidermal Langerhans cells and keratinocytes that produce an epidermal thymocyte-activating factor, similar to IL-1 [Sauder, 19841; in the murine system the Thy-lC dendritic epidermal cell.…”

Section: Discussionmentioning

confidence: 99%

Protection against acute lethal viral infections with the native steroid dehydroepiandrosterone (DHEA)

Loria

Inge

Cook

et al. 1988

Journal of Medical Virology

178

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A significant protective effect of a native adrenal steroid, dehydroepiandrosterone (DHEA), was demonstrated in studies of two lethal viral infection models in mice: systemic coxsackievirus B4 and herpes simplex type 2 encephalitis. The steroid was active either by long-term feeding or by a single subcutaneous injection. A closely related steroid, etiocholanolone, was not protective in these models. Histopathological analysis, leukocyte counts, and numbers of spleen antibody forming cells in the coxsackievirus B4 model suggests that DHEA functions by maintaining or potentiating the immune competence of mice otherwise depressed by viral infection. DHEA was not effective in genetically immunodeficient HRS/J hr/hr mice and did not demonstrate antiviral activity in vitro. While the molecular basis for DHEA's effect on the immune system is not known, studies by others suggest that it may counteract the stress related immunosuppressive effects of glucocorticoids stimulated by viral infection. Because DHEA is a native steroid that has been used clinically with minimal side effects, the utility of DHEA in the therapeutic modulation of acute and chronic viral infections including the acquired immune deficiency syndrome deserves intensive study.

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Section: Discussionmentioning

confidence: 99%

Protection against acute lethal viral infections with the native steroid dehydroepiandrosterone (DHEA)

Loria

Inge

Cook

et al. 1988

Journal of Medical Virology

178

View full text Add to dashboard Cite

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“…The incidence of chemically induced melanoma in mice can be enhanced by treatment with tumor-promoting agents such as croton oil. Studies dating back to 1963 have demonstrated that UV radiation could be used in combination with chemical treatment to induce melanoma in mice, but could not act as a complete carcinogen (Epstein et al, 1967;Romerdahl et al, 1989;Husain et al, 1991).…”

Section: Genetically Engineered Mouse Modelsmentioning

confidence: 99%

Ultraviolet radiation and cutaneous malignant melanoma

2003

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Recent years have seen a steady rise in the incidence of cutaneous malignant melanoma worldwide. Although it is now appreciated that the key to understanding the process by which melanocytes are transformed into malignant melanoma lies in the interplay between genetic factors and the ultraviolet (UV) spectrum of sunlight, the nature of this relation has remained obscure. Recently, prospects for elucidating the molecular mechanisms underlying such gene-environment interactions have brightened considerably through the development of UV-responsive experimental animal models of melanoma. Genetically engineered mice and human skin xenografts constitute novel platforms upon which to build studies designed to elucidate the pathogenesis of UV-induced melanomagenesis. The future refinement of these in vivo models should provide a wealth of information on the cellular and genetic targets of UV, the pathways responsible for the repair of UV-induced DNA damage, and the molecular interactions between melanocytes and other skin cells in response to UV. It is anticipated that exploitation of these model systems will contribute significantly toward the development of effective approaches to the prevention and treatment of melanoma.

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“…Exposure to solar ultraviolet radiation, particularly ultraviolet B (UVB), is the predominant cause of most skin cancers acting through mechanisms of DNA damage (either directly or via free-radical generation) and immune system inhibition [2, 3]. The development of skin cancer is also linked to several patient characteristics, including fair skin, light hair and eye colour, the tendency to burn rather than tan, and family history [2].…”

Section: Introductionmentioning

confidence: 99%

ecancermedicalscience

Henry

Christiansen

Kazmier

et al.

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Background:Amifostine is a pharmaceutical agent that is used clinically to counteract the side-effects of chemotherapy and radiotherapy. It acts as a free radical scavenger that protects against harmful DNA cross-linking. The purpose of this study was to determine the effect of amifostine on the development of skin cancer in xeroderma pigmentosum (XP) mice exposed to ultraviolet B radiation (UVB).Methods:Twenty-five XP mice were equally divided into five groups. Group 1 (control) received no amifostine and no UVB exposure. Group 2 also received no amifostine, but was exposed to UVB at a dose of 200 mJ/cm2 every other day. The remaining groups were subjected to the same irradiation, but were given amifostine at a dose of 50 mg/kg (group 3), 100 mg/kg (group 4), or 200 mg/kg (group 5) immediately prior to each exposure.Results:No tumours were seen in the control group. The animals in group 2 (no amifostine) developed squamous cell carcinoma (SCC) at 3.5–4.5 months (mean 3.9 months). Groups 3 and 4 (low- and medium-dose amifostine) developed SCC at 4.0–7.0 months (mean 5.3 months), representing a statistically significant delay in tumour presentation (p = 0.04). An even greater delay was seen in group 5 (high-dose amifostine), which developed SCC at 7.0–9.0 months (mean 8.5 months, p < 0.001 versus groups 3 and 4). Ocular keratitis developed in all animals except the unexposed controls and the high-dose treatment group.Conclusion:Treatment with amifostine significantly delays the onset of skin cancer and prevents ocular keratitis in UVB-exposed XP mice.

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Advances in the immunobiology of the skin. Implications for cutaneous malignancies

Cited by 6 publications

References 78 publications

Protection against acute lethal viral infections with the native steroid dehydroepiandrosterone (DHEA)

Protection against acute lethal viral infections with the native steroid dehydroepiandrosterone (DHEA)

Ultraviolet radiation and cutaneous malignant melanoma

ecancermedicalscience

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