ULTRAVIOLET RADIATION ‐ INDUCED MALIGNANT MELANOMA IN Monodelphis domestica

Ley, Ronald D.; Applegate, Lee Ann; Padilla, R. Steven; Stuart, Thomas D.

doi:10.1111/j.1751-1097.1989.tb04123.x

Cited by 208 publications

(151 citation statements)

References 13 publications

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“…For example, 70 weeks of exposure to UV irradiation alone caused 5 of 13 Monodelphis domestica opossums to develop melanocytic tumors [16]. Administration of a topical carcinogen, 7,12-dimethylbenz(a)anthracene (DMBA), and UV irradiation induced melanomas in hairless and newborn mice [17].…”

Section: Uv Light and Melanomamentioning

confidence: 99%

Recent Advances in Melanoma Biology

Perlis

Herlyn

2004

The Oncologist

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The incidence and mortality rates of melanoma have increased at annual rates of 2%-3% for the last 30 years. Disseminated disease is largely refractory to cytotoxic chemotherapy and is almost universally fatal. Several recent advances in melanoma biology offer new strategies for potentially treating this aggressive malignancy. This review focuses on three significant advances involving tumor initiation, etiology, and progression. New experimental models reveal a direct role for UV-B light in initiating melanomas in human skin. Studies on E-and N-cadherin elucidate the importance of local homeostatic mechanisms in regulating tumor progression. Finally, several discoveries concerning apoptotic mechanisms in melanoma suggest strategies for future treatments.

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Section: Uv Light and Melanomamentioning

confidence: 99%

Recent Advances in Melanoma Biology

Perlis

Herlyn

2004

The Oncologist

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“…The South American opossum Monodelphis domestica, which lacks a DNA repair mechanism, develops melanomas at a high rate after approximately 1 year of UV treatment. 6 The administration of 7,12 -dimethylbenz[ a]anthracene ( DMBA ) followed by croton oil and UV leads to melanoma in mouse skin. 7 Administration of UVB to human skin in which bFGF is overexpressed leads to pigmented lesions with highgrade atypia resembling lentiginous forms of malignant melanoma.…”

mentioning

confidence: 99%

p53 alone or in combination with antisense cyclin D1 induces apoptosis and reduces tumor size in human melanoma

et al. 2002

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Melanoma incidence is growing at a faster rate than any other human malignancy. Wild -type ( wt ) p53 is important in both G 1 and G 2 cell cycle arrest, and cyclin D1 ( CD1 ) is necessary for G 1 !S progression in melanoma cells. We reported that an adenoviral vector containing wt p53 significantly reduced [ 3 H ]thymidine uptake in melanoma cells containing mutant but not wt p53. Subsequently we showed that CD1 decreased melanoma proliferation and increased apoptosis. We now extend these findings by evaluating the effect on preformed melanomas of ( 1 ) intratumoral therapy with wt p53 alone, ( 2 ) wt p53 in combination with antisense ( AS ) CD1, both short ( 14 days ) and longer term, and ( 3 ) doubling the dose or repeat doses of wt p53 or AS CD1. Two melanoma cells lines that metastasize in SCID mice ( 451 and 1205 ) were used, one containing a p53 mutation ( 451 ) and the other a normal p53 gene sequence ( 1205 ). Compared to injection with a control adenoviral vector containing -galactosidase ( LacZ ), intratumoral injection of wt p53 slowed the growth of tumors formed from 451 cells. Using 5Â10 8 plaque forming units as our standard intratumoral dose, neither doubling the dose of LacZ, p53 or AS CD1, nor repeat doses of the vectors, was as effective as combined therapy with wt p53 + AS CD1, which resulted in the shrinkage of all tumors treated and 4 / 7 ( 57% ) tumors vanished. No tumors treated with wt p53 or AS CD1 alone vanished. Wt p53 + AS CD1 treatment resulted in significantly more cells undergoing apoptosis compared to either therapy alone. In summary, combining the separately effective treatment vectors p53 and AS CD1 led to an enhanced growth -suppressive and apoptotic effect, supporting a role for combination gene therapy to treat human malignant melanoma.

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“…These studies have documented maximal carcinogenicity in the UVB region (21,22). Animal models have been proposed for melanoma; some action spectrum data have been derived from a fish model, which suggests substantial carcinogenic potential for UVA, but the relevance of these experiments to the disorder in human remains to be clarified (23)(24)(25)(26).…”

Section: The Linkmentioning

confidence: 99%

Overview of ultraviolet radiation and cancer: what is the link? How are we doing?

Weinstock

1995

Environ Health Perspect

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Sun exposure has now been established as the most important avoidable cause of nonmelanoma skin cancer (NMSC) and melanoma. With specific reference to melanoma, there are several key issues that remain to be resolved. These include definition of the action spectrum, the importance of systemic effects of sun exposure, whether a tan is protective, the risk of tanning booth exposures, and the efficacy of sunscreens. Also the role, if any, of sun exposure in noncutaneous malignancies remains to be established. Melanoma incidence and mortality have increased dramatically over the past several decades, but these increases have now slowed, and for mortality among those 15 to 45 years of age, decreasing rates are now observed. Improving the coverage of the Surveillance, Epidemiology, and End Results (SEER) registries by requiring pathology laboratories in non-SEER areas to report cancers among SEER area residents will allow correct interpretation of these trends in the future at minimal cost. The available data on trends in NMSC incidence and mortality are suboptimal but suggest a pattern of declining mortality despite increasing incidence. Trends in NMSC morbidity have not been defined. Establishing NMSC registries in a few diverse sentinel areas would allow more reliable inference and monitoring. Techniques are being developed for reducing sun exposures and increasing early detection of skin cancers in the general population, but improved monitoring of incidence, mortality, and morbidity is required to monitor the effects of current and future ozone depletion and to evaluate prevention and early detection measures. -Environ Health Perspect 103(Suppl 8): 251-254 (1995)

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ULTRAVIOLET RADIATION ‐ INDUCED MALIGNANT MELANOMA IN Monodelphis domestica

Cited by 208 publications

References 13 publications

Recent Advances in Melanoma Biology

Recent Advances in Melanoma Biology

p53 alone or in combination with antisense cyclin D1 induces apoptosis and reduces tumor size in human melanoma

Overview of ultraviolet radiation and cancer: what is the link? How are we doing?

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