Ultraviolet radiation and cutaneous malignant melanoma

Jhappan, Chamelli; Noonan, Frances P.; Merlino, Glenn

doi:10.1038/sj.onc.1206450

Cited by 242 publications

(210 citation statements)

References 174 publications

(153 reference statements)

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“…Ultraviolet (UV) radiation induces basal and squamous cell carcinoma and cutaneous malignant melanoma in humans [1][2][3] and is therefore a major environmental concern. UV radiations exert their toxic effects by causing DNA damage, which depends mainly on the wavelength.…”

Section: Introduction Introduction Introduction Introductionmentioning

confidence: 99%

“…In addition, to determine the relative toxicity of each wavelength tested, we quantified the viabilities of cells irradiated with the 4 different wavelengths at 100 mJ/cm 2 For determining the LD50 of the 4 tested wavelengths, we exposed PC12 cells to 25-800 mJ/cm 2 of 250-, 270-, and 290-nm radiations and to 125-8000 mJ/cm 2 of the 310-nm radiation.…”

Section: Introduction Introduction Introduction Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

Masuma

Kashima

Kurasaki

et al. 2013

Journal of Photochemistry and Photobiology B: Biology

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Ultraviolet (UV) radiations present in sunlight are a major etiologic factor for many skin diseases and induce DNA damage through formation of cyclobutane pyrimidine dimer (CPD). This study was conducted to determine the toxicological effects of different wavelengths (250, 270, 290, and 310 nm) and doses of UV radiation on cell viability, DNA structure, and DNA damage repair mechanisms in a PC12 cell system. For this, we evaluated cell viability and CPD formation. Cell survival rate was markedly decreased 24 h after UV irradiation in a dose-dependent manner at all wavelengths (except at 310 nm). Cell viability increased with increasing wavelength in the following order: 250 < 270 < 290 < 310 nm. UV radiation at 250 nm showed the highest cell killing ability, with a median lethal dose (LD50) of 120 mJ/cm2. The LD50 gradually increased with increase in wavelength. Among the 4 wavelengths tested, the highest LD50 (6000 mJ/cm2) was obtained for 310 nm. CPD formation decreased substantially with increasing wavelength. Among the 4 wavelengths, the proportion of CPD formation was highest at 250 nm and lowest at 310 nm. On the basis of LD50 values for each wavelength, PC12 cells irradiated with UV radiation of 290 nm showed maximum DNA repair ability, whereas those irradiated with the 310-nm radiation did not show any repair ability. Toxicity of UV radiation varied with wavelengths and exposure doses

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Section: Introduction Introduction Introduction Introductionmentioning

confidence: 99%

Section: Introduction Introduction Introduction Introductionmentioning

confidence: 99%

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

Masuma

Kashima

Kurasaki

et al. 2013

Journal of Photochemistry and Photobiology B: Biology

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“…One new animal model reinforces epidemiological findings that childhood sunburn is a significant risk factor for developing melanoma. Noonan and colleagues found that a single high dose of UV radiation was sufficient to produce melanoma-like tumors in neonatal, but not adult, mice if the skin cells expressed a growth factor that stimulates melanocytes [19,20]. Chin and colleagues established a second elegant genetic model of murine melanoma in which the INK4a gene deletion cooperates with Ras overexpression [21].…”

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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“…These species are among the very few animals in which melanoma can be induced by UV alone. The Xiphophorus is also actively used as a genetic model organism for the study of neuroblastoma, retinoblastoma, and other malignancies; however, this system is ultimately limited by its evolutionary distance from mammals (62).…”

Section: Spalax P53 Favors Growth Arrest But Not Apoptotic Target Gementioning

confidence: 99%

Evolution of p53 in hypoxia-stressedSpalaxmimics human tumor mutation

Ashur‐Fabian

Avivi

Trakhtenbrot

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

108

134

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The tumor suppressor gene p53 controls cellular response to a variety of stress conditions, including DNA damage and hypoxia, leading to growth arrest and͞or apoptosis. Inactivation of p53, found in 40 -50% of human cancers, confers selective advantage under hypoxic microenvironment during tumor progression. The mole rat, Spalax, spends its entire life cycle underground at decidedly lower oxygen tensions than any other mammal studied. Because a wide range of respiratory adaptations to hypoxic stress evolved in Spalax, we speculated that it might also have developed hypoxia adaptation mechanisms analogous to the genetic͞epige-netic alterations acquired during tumor progression. Comparing Spalax with human and mouse p53 revealed an arginine (R) to lysine (K) substitution in Spalax (Arg-174 in human) in the DNAbinding domain, identical to known tumor associated mutations. Multiple p53 sequence alignments with 41 additional species confirmed that Arg-174 is highly conserved. Reporter assays uncovered that Spalax p53 protein is unable to induce apoptosisregulating target genes, resulting in no expression of apaf1 and partial expression of puma, pten, and noxa. However, cell cycle arrest and p53 stabilization͞homeostasis genes were overactivated by Spalax p53. Lys-174 was found critical for apaf1 expression inactivation. A DNA-free p53 structure model predicts that Arg-174 is important for dimerization, whereas Spalax Lys-174 prevents such interactions. Similar neighboring mutations found in human tumors favor growth arrest rather than apoptosis. We hypothesize that, in an analogy with human tumor progression, Spalax underwent remarkable adaptive p53 evolution during 40 million years of underground hypoxic life.

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Ultraviolet radiation and cutaneous malignant melanoma

Cited by 242 publications

References 174 publications

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

Recent Advances in Melanoma Biology

Evolution of p53 in hypoxia-stressedSpalaxmimics human tumor mutation

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