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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Topical application of retinoic acid (RA) solutions greatly enhanced the response of hairless mouse skin to a moderate dose of simulated sunlight. Tumors appeared much earlier, and in much greater numbers, in animals treated daily with 1 or 10 micrograms of RA in methanol immediately after 2 h exposure to a xenon arc filtered through 2 mm of Schott WG 320 glass (approximately equivalent in human erythema effectiveness to 5 min of mid-summer noon solar exposure in northern mid-latitudes), compared to mice treated with light and methanol only. The higher amount of RA, in combination with light, produced moderate epidermal hyperplasia and some scaling and transient erythema, but no gross ulceration or inflammation of skin. The lower amount of RA, though about equally effective in carcinogenesis, produced minimal epidermal hyperplasia compared to the ultraviolet radiation + methanol control.
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PMID:Enhancement of experimental photocarcinogenesis by topical retinoic acid. 47 13

Previous observations and experiments have shown that the potent carcinogenic wavelengths for skin cancer in man are found in the 290- to 320-nm range, although shorter and longer wavelengths can also have an effect. The short wavelength limit (290 nm) is determined by thesolar emission reaching the earth's surface, a parameter that varies greatly with season, time, and atmopheric conditions. The long wavelength limit (320 nm) was based on observations of the effect of window glass filtration and on comparison of the effect of mid and long UV radiation. It provide little information as to the efficacy of wavelengths in this range. We performed a series of experiments to provide more specific comparative data by testing the hypothesis that the action spectrum for carcinogenesis parallel that for erythema. Albino mice were exposed the emission of a diffraction grating monochromator (5 nm half power bandwidth) at 290, 300, 310, and 320 nm. Energy levels were proportional to valves for the erythema spectrum of untanned Caucasian human skin. Exposures were given thrice weekly until 50% of the mice had developed tumors. Squamous cell carcinomas developed at approximately the same rate and frequency when the UV exposure was proportional to that for erythema, which indicated a decreasing potency from 300 to 310 to 320 nm. No tumors occurred in mice exposed to 290 nm.
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PMID:Action spectrum for ultraviolet carcinogenesis. 75 77

When 300, 310, or 320 nm monochromatic UV energy was given to albino mice in amounts proportional to its erythemal effectiveness, skin tumors developed on the exposed ears of the mice at approximately the same time and the same rate in all three groups. Thus the long wavelength limit of the carcinogenesis action spectrum paralleled that of the erythema action spectrum. No tumors were found in mice exposed to a 290-nm UV wavelength nor in those exposed to low dosages at 310 nm. All tumors observed in the group exposed to 300 nm were squamous cell carcinomas; 3 sarcomas and 5 squamous cell carcinomas were seen with the more penetrating doses of a 310-nm UV wavelength.
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PMID:Data on the action spectrum for ultraviolet carcinogenesis. 120 37

Butylated hydroxytoluene (BHT) and certain carotenoid pigments have been found to inhibit photocarcinogenesis in animal models. In addition, BHT protects against UV-B-induced erythema and UV-B induction of ornithine decarboxylase. Studies on the photoprotective mechanism(s) of BHT suggested that changes in the physico-chemical properties of the keratin of the stratum corneum layer of skin occurred, leading to increases in UV absorption of that tissue. These changes might be exerted via the anti-radical action of BHT that retards oxidation and prevents cross-linking of the keratin chains, resulting in a diminution of UV-B radiation reaching potential target sites. The carotenoids beta-carotene, canthaxanthin and phytoene also inhibit UV-B carcinogenesis. beta-Carotene and canthaxanthin are excellent quenchers of singlet oxygen, and all three pigments can quench free radicals. beta-Carotene and canthaxanthin have been shown to quench singlet oxygen/free radical reactions in the skin of porphyric mice, and these two pigments as well as phytoene have been found to quench excited species formed on irradiation of mouse skin by UV-B.
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PMID:Protective role of butylated hydroxytoluene and certain carotenoids in photocarcinogenesis. 188 65

All tumor-promoting phorbol esters induce inflammation in mouse skin. The correlation between promoting and inflammatory activities is only partial, however, indicating that only some events in inflammation may be closely coupled to the process of tumor promotion. Resiniferatoxin (RTX), an extremely inflammatory phorbol-related diterpene, acts as an ultrapotent analog of capsaicin to stimulate and then to block the neurogenic inflammatory pathway. In CD-1 mice, we have used pretreatment with RTX to show that the erythema and edema responses to phorbol and 12-deoxyphorbol esters in significant part involve this neurogenic inflammatory pathway. We report here that mouse strains with differing sensitivities to phorbol-ester-induced promotion displayed marked differences in the effect of pretreating with RTX on the edema response following phorbol-12-myristate-13-acetate (PMA) application. In the highly promotion-sensitive SENCAR mouse, RTX pretreatment had little inhibitory effect; the edema response to PMA was similar with or without RTX pretreatment 6 h before PMA application. On the other hand, in C57BL/6J mice, which are resistant to promotion by phorbol esters under the usual protocols, the edema response to PMA was totally eliminated by RTX pretreatment during the first 8 h after PMA administration. DBA/2J mice, which are similar to CD-1 mice in their susceptibility to PMA promotion, responded similarly to CD-1: the edema response was blocked partially by RTX pretreatment during the early phase (up to 8 h) of inflammation. Our results suggest that the RTX-resistant component of PMA-induced edema may correlate better with the sensitivity to promoting action than does the overall inflammatory response.
Carcinogenesis 1990 Apr
PMID:Effect of resiniferatoxin pretreatment on the inflammatory response to phorbol-12-myristate-13-acetate in mouse strains with different susceptibilities to phorbol ester tumor promotion. 232 99

Exposure to sunlight can produce both acute and long-term effects. Acute changes include erythema, photosensitivity, and immunologic alterations. Long-term consequences include carcinogenesis and photoaging. All effects can be minimized by photoprotection. This article reviews the adverse effects of sun exposure and strategies to reduce photodamage.
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PMID:Photoaging/photodamage and photoprotection. 200 93

Psoralen photochemotherapy (PUVA) is widely used in the treatment of psoriasis. Some therapy regimen have been associated with increased risk of skin cancer. Free radical species are thought to play a role in psoralen phototoxicity and photocarcinogenesis. It has been reported that the antioxidant butylated hydroxytoluene (BHT) inhibits acute phototoxicity by PUVA but does not reduce therapeutic efficacy. It has also been shown that BHT inhibits UVB-induced erythema, tumorigenesis and induction of ornithine decarboxylase (ODC) activity--ODC activity is thought by some to be associated with tumor promotion. Therefore, we have investigated the effect of BHT on psoralen tumorigenesis and PUVA-induced epidermal ODC activity. SKH-Hr-1 hairless albino mice were treated with topically applied 8-MOP and exposed to UVA (3X weekly) for 31 weeks with and without BHT administered either in the diet or topically. Induction of ODC activity was determined in similar experimental groups 24 h after a single exposure to UVA. Neither route of BHT administration had any effect on 8-MOP phototumorigenesis. However, BHT when administered in the diet reduced induction of ODC activity by 40% (p less than 0.05). These data indicate different mechanisms for UVB- and PUVA-induced carcinogenesis and again bring into question the relationship between induction of ODC activity and photocarcinogenesis.
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PMID:Effects of butylated hydroxytoluene upon PUVA-tumorigenesis and induction of ornithine decarboxylase activity in the mouse. 249 83

Sib patients with xeroderma pigmentosum (XP), XP90TO (42 years old, male) and XP92TO (40 years old, female, were assigned to group F by the complementation analysis in hybridized heterodikaryons. The XP90TO and XP92TO fibroblasts exhibited the typical XPF characteristics of a threefold higher sensitivity to the lethal effect of 254 nm UV and a reduced level of 12% unscheduled DNA synthesis (UDS) compared with normal cells. Clinically, both patients manifested moderate to severe acute sun sensitivity by age 8, pigmented freckles by age 10 and skin malignancies at higher ages (6 basaliomas at 42 years in XP90TO; 1 basalioma at 41 years in XP92TO). Despite the still currently sun-sensitive state, the patients showed normal minimal erythema dose (MED) at monochromatic wavelengths of 290, 300 and 305 nm but abnormally delayed peaking of erythema reaction at 48 h after exposure. After irradiation with more than 3 MED, XP92TO showed a long persistence of induced erythema for at least 7 days. A review of the 16 reported XPF patients indicated mild skin manifestations, no neurological abnormalities, and more delayed skin carcinogenesis at a lower frequency than that in XPA patients. In addition, we have collected clinical information from Japanese XP patients in rare complementation groups D and E and reviewed their clinical and photobiological characteristics.
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PMID:Late onset of skin cancers in 2 xeroderma pigmentosum group F siblings and a review of 30 Japanese xeroderma pigmentosum patients in groups D, E and F. 266 29

DNA photoproducts in epidermal basal cells caused by in vivo exposure to various wavelengths of ultraviolet B (UVB) light were studied by immunohistochemical and microfluorometric methods. Hairless mice were irradiated with UVB doses ranging between 6.3 and 100 mJ/cm2 at 280, 290, 297, 302 and 313 nm. A dose of 25 mJ/cm2 at 297 nm corresponded to a minimal erythema dose in the Hr/Hr mice. Immediately after the exposure, frozen skin sections were stained in situ with affinity-purified antiserum having a major specificity against UV-induced (6-4) photoproducts. Microfluorometric measurements of nuclear immunofluorescence intensities were then performed to quantitate the DNA lesions in epidermal basal cell nuclei. All wavelengths except 313 nm produced DNA photoproducts, and the induction was both dose and wavelength dependent. The most effective wavelength was 290 nm, followed by 297, 280 and 302 nm. The quantitative determinations indicated variations in the DNA photoproduct content between nuclei exposed to the same dose and wavelength. This may be due to shielding by other nuclei or to differences in the sensitivity to UVB irradiation among basal cells, resulting in non-random distribution of DNA-damaged cells. Hence, measurable amounts of UVB-induced (6-4) photoproducts are produced in hairless mouse epidermis following in vivo exposure with biologically relevant doses of narrow-banded UVB light.
Carcinogenesis 1989 Sep
PMID:UVB-induced (6-4) photoproducts in hairless mouse epidermis studied by quantitative immunohistochemistry. 267 Mar 3

A slight reduction of the ozone level over the northern hemisphere in the period 1969-1986 has been reported [D. Lindley, Nature (Lond.), 323: 293, 1988]. Ozone measurements performed in Oslo are in agreement with this. However, the ozone level for 1987 and 1988 was above normal, and no negative or positive trend is apparent for the last 10 years. The consequences of an ozone reduction for the fluence rate of carcinogenically effective sunlight was evaluated on the basis of recent action spectra for mutagenesis in cells, carcinogenesis in mice, and erythema induction in humans. Depending on the choice of action spectrum we find amplification factors (defined as percentage increase in yearly fluence of carcinogenically efficient sunlight per percentage reduction of the ozone level) between 1.1 and 1.3 at latitudes between 0 and 20 degrees and between 0.9 and 1.1 for Northern Europe. These estimates are significantly lower than 2.0, which is the value found when the calculations are based on the DNA absorption spectrum (R. B. Setlow, Proc. Natl. Acad. Sci. USA, 71:3363-3366, 1974).
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PMID:Ozone depletion and its consequences for the fluence of carcinogenic sunlight. 274 11


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