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. 2010:4:176.
doi: 10.3332/ecancer.2010.176. Epub 2010 Sep 22.

The protective effect of amifostine on ultraviolet B-exposed xeroderma pigmentosum mice

Sl Henry  1 , D Christiansen, Fr Kazmier, Cl Besch-Williford, Mj Concannon
Affiliations

The protective effect of amifostine on ultraviolet B-exposed xeroderma pigmentosum mice

Sl Henry et al. Ecancermedicalscience. 2010.

Abstract

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/cm(2) 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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Figures

Figure 1:
Figure 1:
No tumours developed in non-exposed control mice (above, left) throughout the nine-month study period. Squamous cell carcinoma developed in all ultraviolet B-exposed mice, most commonly on the ears (above, right) and nose (below, left). All ultraviolet B-exposed mice developed ocular keratitis (below, left and right), with the exception of those receiving high-dose amifostine.
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References

    1. Kwa RE, Campana K, Moy RL. Biology of cutaneous squamous cell carcinoma. J Am Acad Dermatol. 1992;26:1–26. doi: 10.1016/0190-9622(92)70001-V. - DOI - PubMed
    1. Marks R. An overview of skin cancers: incidence and causation. Cancer. 1995;2(Suppl 75):607–12. doi: 10.1002/1097-0142(19950115)75:2+<607::AID-CNCR2820751402>3.0.CO;2-8. - DOI - PubMed
    1. Romerdahl CA, Kripke ML. Advances in the immunobiology of the skin: implications for cutaneous malignancies. Cancer Metastasis Rev. 1986;5:167–78. doi: 10.1007/BF00046429. - DOI - PubMed
    1. Copeland NE, Hanke CW, Michalak JA. The molecular basis of xeroderma pigmentosum. Dermatol Surg. 1997;23:447–55. doi: 10.1016/S1076-0512(97)00104-0. - DOI - PubMed
    1. Bruce AJ, Brodland DG. Overview of skin cancer detection and prevention for the primary care physician. Mayo Clin Proc. 2000;75:491–500. doi: 10.4065/75.5.491. - DOI - PubMed

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