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

The effect of chronic applications of HN2 on acute responses of DNA synthesis to UVB radiation was studied in Uscd strain hairless mouse skin in vivo. 0.1 mg of HN2 in 95% ethyl alcohol and the diluent were applied weekly to the backs of the mice for 69 wk. The mice were then exposed to 1.98 X 10(2) J/m2 of UVB energy and were sacrified 4 hours and 48 h post-irradiation. The effects on DNA synthesis were evaluated using TdRH3 as the radioactive tracer. The results of the study revealed that the chronic HN2 applications increased the number of basal cells in the DNA synthesis phase of the mitotic cycle. This was associated with acanthosis and cellular hypertrophy. 4 h post-irradiation there was the expected depression in DNA synthesis in both the HN2- and diluent-treated mice. In addition, 48 h post-irradiation the number of basal cells synthesizing DNA was accelerated in both the HN2- and diluent-treated mice. However, it was much more noticeable in the HN2-treated animals. Whether this increased activity is related to the additive carcinogenesis generated between UVB and HN2 remains to be determined.
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PMID:A study of the effect of chronic applications of nitrogen mustard (HN2) on acute responses of mammalian skin to UVB irradiation in vivo. 653 1

The influence of mechlorethamine (HN2, nitrogen mustard) on UV-induced carcinogenesis was examined in the hairless mouse skin in vivo. Noncarcinogenic amounts of topically applied HN2 and carcinogenic levels of UVB energy were used in the study. The HN2 applications significantly accelerated the appearance and growth of cutaneous tumors in this study. Thus HN2 acted as either a promoter or cocarcinogen for UV-induced cancer formation. Although the mechanism of this effect was not established, combinations of UVB radiation and HN2 topical therapy pointed to an increased incidence of cutaneous tumors in human skin.
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PMID:Effects of mechlorethamine (HN2, nitrogen mustard) on UV-induced carcinogenesis in hairless mouse skin. 658 24

Ornithine decarboxylase activity and polyamine concentrations were determined in the lungs of mice from 0 to 20 h after treatment with 12-O-tetradecanoylphorbol-13-acetate (17.7 nmol in 0.2 ml acetone/mouse). In CFLP mice, which responded to carcinogen with development of lung-adenomas, a single topical application of TPA to hairless mouse skin increased ornithine decarboxylase activity in the lung. In contrast, in C3H/He-mg mouse strain, which were resistant to lung-adenoma production, TPA application did not increase ODC activity of the lungs.
Carcinogenesis 1983 Oct
PMID:Effect of 12-O-tetradecanoylphorbol-13-acetate on polyamine metabolism in mice sensitive and resistant to lung-adenoma. 661 64

The effects of dietary lipid level, degree of saturation, and antioxidant supplements on ultraviolet-light (UV) carcinogenesis were studied in female albino hairless mice. Twelve groups of 42 animals each received a restricted, semipurified, isocaloric diet containing 4%, 12%, or 12% (60% hydrogenated) corn oil with or without antioxidants (2%, w/w). A regimen of escalating UV irradiation was employed until a cumulative dose of 142 J/cm2 had been delivered. Tumor development time in 50% of the population (TDT50) was derived from a cumulative distribution of time to tumor formation, which was estimated for all groups. Although there were no significant differences in TDT50s between animals receiving low and high unsaturated lipid dietary regimens, animals receiving hydrogenated corn oil demonstrated a significantly (p less than 0.01) greater TDT50 and fewer tumors per animal than those receiving either level of unsaturated corn oil. Antioxidants had no effect on TDT50s within any of the dietary groups. However, greater tumor multiplicity was observed in groups receiving unsaturated lipid and antioxidants. These data demonstrate that the degree of dietary lipid saturation modifies the carcinogenic response to UV and suggest that dietary lipid may modify the previously reported inhibitory effect of antioxidants on UV carcinogenesis. It may be concluded that adherence to dietary standards is as important as other experimental parameters when comparisons of UV effects are involved.
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PMID:Influence of dietary lipid upon ultraviolet-light carcinogenesis. 664 39

Nine groups of 32 hairless mice (16 males and 16 females in each) were painted on the back skin with approximately 200 microliters solution of urethan twice a week for up to 58 weeks. The following treatments were given: acetone alone, propylene glycol alone, 10% urethan in acetone, 15% urethan in propylene glycol, 20% urethan in acetone, 30% urethan in propylene glycol, 40% urethan in acetone, 75% urethan in propylene glycol, and approximately 100% melted urethan. Histological examinations revealed no development of general epidermal hyperplasia or inflammatory reactions. Tumors developed in skin, liver and lymph nodes, and one mouse also developed leukemic infiltrations in kidneys and lungs. The rate and yield of skin tumors were registered and statistically analyzed. The number of other tumors occurring was also recorded. The results confirm that urethan is a tumorigen for the lung and several other organs, and that it is also a complete carcinogen for hairless mouse skin, even in a dose as low as 10% urethan in acetone. There is also a significant dose-response relationship.
Carcinogenesis 1984 Jul
PMID:Urethan (ethyl carbamate) alone is carcinogenic for mouse skin. 673 52

In experimental studies of u.v.-skin-carcinogenesis u.v.-radiation is usually given in discrete amounts over a protracted period of time. Epidermal polyamine profiles were investigated in hairless mice after single and multiple exposures to ultraviolet-B (u.v.B). Hairless mice were irradiated with u.v.B from FS40 sunlamps and sacrificed after 1, 5, 10 or 20 days of daily irradiation with 0.9 kJ/sq m u.v.B at 6, 24 or 48 h after the final irradiation. Epidermis was analyzed for ornithine decarboxylase (ODC) activity, and for its putrescine, spermidine and spermine content. Skin biopsies were examined for histological changes. As previously reported epidermal ODC activity was induced 6 h after one irradiation with u.v.B and reached a maximum activity at approximately 24 h. In contrast after 5, 10 or 20 daily irradiations with u.v.B the epidermal ODC activity was maximal at approximately 6 h after the final irradiation and by 24 h had returned towards control levels. The magnitude of the ODC activity measured 6 h after irradiation increased with the number of irradiations. A similar pattern was seen with epidermal putrescine levels where a marked shift from a peak at approximately 24 h after one irradiation with u.v.B to a peak at approximately 6 h after 20 days of irradiation with u.v.B occurred. Spermidine levels increased as the number of u.v.B exposures was increased and spermine levels tended to decrease. The spermidine/spermine ratio increased most rapidly during the first 5 exposures, and remained elevated through to 20 days of daily irradiation. Chronic irradiation with u.v.B results in rapid induction of ODC activity and putrescine accumulation in the epidermis, events also elevated by chemical or viral transformation.
Carcinogenesis 1983
PMID:Epidermal polyamine profiles after multiple exposures to ultraviolet radiation. 686 Dec 73

Four new dominant autosomal mutations influencing the development of skin and hair in the mouse were tested for allelism with each other and with hairless, hr. Three of the mutations probably constitute an allelic series and have been given the symbols Frl1, Frlb, and Frlc. The Frl series shows no evidence of linkage with hr. The fourth mutation, Hrn, is a dominant and homozygous viable allele at the hr locus. With the possible exception or Frlb, all mutants were of spontaneous origin. Because of their unique characteristics, these new mutants are of potential value as mouse model systems in studies of skin carcinogenesis and related areas of research.
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PMID:Four dominant autosomal mutations affecting skin and hair development in the mouse. 686 94

Sunscreens of low or high sun protection factors (SPF*) were tested for their ability to inhibit ultraviolet (UV) carcinogenesis in two varieties of hairless mice. Low protection (SPF = 2) reduced by 50% the number of albino animals developing tumors. High protection (SPF =15) prevented tumor formation. Tumorigenesis was totally prevented in the lightly pigmented variety with either sunscreen, demonstrating the added protection of melanin. In mice and man, UV-induced cancer is a cumulative process. Reducing the amount of UV light reaching the basal layer will retard that process.
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PMID:Sunscreens prevent ultraviolet photocarcinogenesis. 696 95

Irradiation of skin with ultraviolet light of sunburn range (UVB) leads to a large and rapid induction of the polyamine biosynthetic enzyme ornithine decarboxylase in the epidermis. Induction of epidermal ornithine decarboxylase also occurs following application of the tumor promoting agent 12-0-tetradecanoylphorbol-13 acetate and topical retinoic acid is able to block both this ornithine decarboxylase induction and skin tumor promotion. In the studies described below, topical application of retinoic acid to hairless mouse skin leads to a significant inhibition of UVB-induced epidermal ornithine decarboxylase activity. The degree of this inhibition was dependent on the dose, timing, and frequency of the application of retinoic acid. To show significant inhibition of UVB-induced ornithine decarboxylase the retinoic acid had to be applied within 5 hr of UVB irradiation. If retinoic acid treatment was delayed beyond 7 hr following UVB, then no inhibition of UVB-induced ornithine decarboxylase was observed. The quantities of retinoic acid used (1.7 nmol and 3.4 nmol) have been shown effective at inhibiting 12-0-tetradecanoyl phorbol-13 acetate induced ornithine decarboxylase. The results show that these concentrations of topical retinoic acid applied either before or immediately following UVB irradiation reduces the UVB induction of epidermal ornithine decarboxylase. The effect of retinoic acid in these regimens on UVB-induced skin carcinogenesis is currently under study.
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PMID:Retinoic acid modulation of ultraviolet light-induced epidermal ornithine decarboxylase activity. 705 47

Solar ultraviolet radiation at the surface of the earth is a recognized cause of skin cancer. Postulated anthropogenic reductions in the thickness of the ozone layer would lead to an increased amount of ultraviolet radiation and hence would be expected to increase the risk of skin carcinogenesis. This study uses hairless (Skh:HR) mice as an animal model to study this increased risk. The mice were exposed 5 days/week to graded doses of ultraviolet radiation from a xenon arc lamp attenuated by five different thicknesses of Schott glass filters (WG320) to simulate various ozone layer thicknesses. A Robertson-Berger sunburning ultraviolet meter was used as one of the forms of dosimetry. The results of the various exposure treatments are expressed as the percentage of animal with tumors (incidence) versus time after commencing irradiation and as cumulative tumor yield (average number of tumors per survivor) versus time. With any given filter, the time to 50% incidence is inversely related to daily dose in Robertson-Berger meter units. The time to 50% incidence for comparable Robertson-Berger meter doses through different filter thicknesses increases with increasing thickness. These results indicate that the effective dose for skin cancer induction may be estimated from the Robertson-Berger meter dose but that the Robertson-Berger meter response spectrum underestimates the photocarcinogenic effectiveness of the shorter wavelengths. The cumulative tumor yield data are also consistent with these conclusions. Alternate weighting of the source spectra with the acute-response action spectrum for mouse skin edema gave a better correlation between unit dose and time to a tumor response, independent of the source spectral distribution. This suggests that the mouse skin edema action spectrum, indistinguishable from a human skin erythema action spectrum for lambda greater than 295 nm, is similar in shape to the mouse skin photocarcinogenesis action spectrum for lambda greater than 295 nm.
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PMID:Simulated stratospheric ozone depletion and increased ultraviolet radiation: effects on photocarcinogenesis in hairless mice. 708 69


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