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

To estimate the influence of topical treatment with DMBA and induced tumors on delayed hypersensitivity, the response of spleen lymphocytes to PHA in vitro and macrophage migration inhibition with PHA were studied in DMBA-treated hairless mice. DNA synthesis and blastic transformation of cultured lymphocytes decreased after 6-12 weeks of DMBA application. Lymphocyte response to PHA gradually diminished during the experiment, as compared with control animals. Since the malignant transformation of skin tumors was not observed before 16 weeks of DMBA carcinogenesis, it seems that derangements in cellular immunity preceded the malignant proliferation. The increase in spleen weight and the absence of PHA-induced inhibition of macrophage migration in hairless mice with malignant tumors may also be related to the influence of the tumor itself on the lymphatic system of experimental animals.
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PMID:Immunological phenomena in harmless mice during experimental carcinogenesis induced with long-term topical application of 7, 12-dimethylbenzanthracene (DMBA). 4 67

Clinical observations and epidemiologic studies indicate that the sun is the primary stimus for most human skin can formation. However, investigations directly confirming this association as well as defining the action spectra, time-dose relationships, energy level requirements, etc., have been confined to animal experimentation. Studies in which gross methods are used indicate that the experimental carcinogenic action spectrum falls primarily between 280 and 320 nm. Quantitative studies and tumor promotion investigations indicate that UV-induced cancer formation begins with the initial exposure. Heat, wind, and moisture stimulate UV carcinogenesis. Also, exogenous chemicals may influence carcinogenesis as photosensitizers such as 8-MOP, as additive carcinogens as noted with DMBA, or as promoters as described for Croton oil, retinoic acid, and BCNU. Qualitative studies indicate that progressive alterations occur in the epidermal-dermal basement membrane and dermal conncecive tissue and mucopolysaccharides associated with the progressive development of epidermal cancers. Malignant melanomas have also been induced experimentally in hairless mice with UV energy. Mechanistically, immunologic alterations and effects on DNA have received the most attention. Tumor-specific antigenicity as well as antigen deletion has been demonstrated. Immune suppression by antilymphocyte serum and certain chemicals has led to stimulation of tumor development. Perhaps the most exciting new information relates to the demonstration that chronically UV-irradiated mice have not rejected highly antigenic UV-induced cancers. This indicated that UV irradiation specifically altered the immunologic responses of the animals to these tumors. Within recent years, the influence of DNA injury and repair on cutaneous carcinogenesis has received a great deal of attention. This has been partly due to the demonstration of defective repair of UV-induced DNA damage in patients with XP. The primary photosensitive problem in these patients is an inordinate sensitivity to the carcinogenic effects of sunlight. However, correlation of DNA injury and repair directly with cancer formation has not been accomplished.
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PMID:Photocarcinogenesis: a review. 38 36

Previous studies with agar diffusion technique demonstrated that antibodies produced in rabbits by injection of urea extractable proteins of rat cornfied cells cross react with proteins extracted from normal epidermis of hairless mice using the same technique. In the present study we investigated by indirect immunofluorescence microscopy the immunoreactivity of epidermal proteins in normal and ultraviolet light (UVB) induced hyperplasia and malignant transformation. Reactivity to the antibody was seen over the entire epidermis of nontreated skin and hypertrophied epidermis which occurred at 6-8 weeks after initiation of UVB irradiation. However, the reactivity diminished when malignant changes took place in the epidermal cells. Almost complete disappearance of the immunoresponse was observed in squamous cell carcinoma produced by further UVB radiation. These results suggest that the reactivity of this urea extractable protein serves as an additional immunologic marker for normal epidermal cells. Alterations in the immunoreactivity parallels UVB induced carcinogenesis.
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PMID:Immunofluorescent studies of epidermal protein during UV induced carcinogenesis. 40 10

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

The effect of a dietary antioxidant mixture on 3-methylcholanthrene mediated carcinogenesis in hairless mice was investigated. The antioxidant mixture significantly reduced the frequency of premalignant lesions and their subsequent development into tumors. The similarities in response of chemical and UV light-carcinogenesis to these antioxidants suggest some congruity in the mechanisms of the carcinogenic process.
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PMID:The mitigating effect of dietary antioxidants on chemically-induced carcinogenesis. 62 Jul 19

We present data from experiments designed to investigate the role of DNA interstrand cross-links induced by exposure to 8-MOP plus UVR and skin carcinogenesis. 8-MOP was administered topically to two strains of hairless mice, SKH:hairless-1 and HRS/J/An1, which were then exposed to UV light sources with emission in the range of 1) 300-400, 2) 320-400, and 3) predominantly 365 nm. We found no strain dependency for DNA cross-link production, but a marked strain-dependent difference in tumor susceptibility was noted. Only a small strain-dependent difference occurred in tumor incidence when TPA was administered after exposure to 8-MOP and 320-400 nm. These results suggest that the events concerned with tumor promotion are dependent on strain. Because the most effective tumorigenic wavelength spectrum was 300-400 nm, we investigated the possibility of interaction between lesions induced by the 300- to 320-nm wavelengths and the psoralen photoadducts. In the course of this experiment, we found that the tumorigenic effect was also dependent on the time interval between exposures to 8-MOP plus 365-nm light.
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PMID:Photosensitized reactions and carcinogenesis. 75 79

The influence of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) on ultraviolet-induced carcinogenesis was examined in hairless mouse skin in vivo. Noncarcinogenic amounts of topically applied BCNU and carcinogenic levels of UVB energy were utilized in the study. The applications of BCNU significantly accelerated the appearance and growth of the cutaneous tumors in this study. Thus, the BCNU acted as either a promoting or a cocarcinogenic agent for ultraviolet-induced cancer formation. Although the mechanism of this effect has not been established, avoidance of extensive sun exposure would probably be prudent when topical BCNU is being utilized therapeutically.
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PMID:Stimulation of ultraviolet-induced carcinogenesis by 1,3-Bis(2-chloroethyl)-1-nitrosourea. 76 Dec 13

Comparisons were made of cholesterol-5alpha, 6alpha-epoxide (CAE) levels in skin of hairless mice maintained on a regular or antioxidant supplemented diet and receiving chronic ultraviolet light (UVL) radiation over an 18-week period. Cholesterol-5alpha, 6alpha-epoxide levels in skin of animals on antioxidant supplemented diet, while reaching a peak four weeks after that of animals on regular diet, thereafter were consistently higher. Dietary antioxidants nevertheless had an inhibitory effect on UVL-induced tumors. These data are inconsistent with the theory of CAE involvement as an ultimate carcinogen in UVL-mediated carcinogenesis.
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PMID:Etiologic related studies of ultraviolet light-mediated carcinogenesis. 101 46

The carcinogenic effect of ultraviolet radiation (UVR) on the skin of hairless (hr) mice was modified by two immunosuppressive agents, rabbit anti-mouse lymphocytic serum (ALS), and 6-mercaptopurine (6MP). Daily exposure of mice to UVR resulted in multiple tumor production. Carcinogenesis was measured in terms of affected mice (prevalence) and numbers of tumors produced. By both criteria, photocarcinogenesis was enhanced by ALS but inhibited by 6MP.
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PMID:Modification of photocarcinogenesis by two immunosuppressive agents. 101 50

Flavins are reported to protect cellular DNA against UV irradiation injury in vitro. The possible photoprotective effects of riboflavin in vivo on UV-induced carcinogenesis were studied in three groups of HR-hairless mice. Group I served as control. Group II was painted daily with a 15 mg per ml solution of riboflavin. In Group III, drinking water was replaced with a 15 mg per ml solution of riboflavin in water. All three groups were simultaneously irradiated in a light box with two Westinghouse FS20 sunlamps from a distance of 30 cm for 5 min daily 6 days a week throughout the experiment. By the 11th month all surviving mice developed several histologically proven squamous cell carcinomas. The total numbers and times of onset of tumors did not vary in the three groups. Thus, no protective effect of massive amounts of riboflavin on ultraviolet-induced carcinogenesis in the hairless mouse could be demonstrated when such high dose rates of UV were used.
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PMID:The inefficacy of riboflavin against ultraviolet-induced carcinogenesis. 119 19


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