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Biomedical subjects

J H Epstein

Publications and source records attributed to J H Epstein.

At least 19 recordsLinked to original sources
PubMed1992

3-Aminobenzamide can act as a cocarcinogen for ultraviolet light-induced carcinogenesis in mouse skin.

Chronic irradiation (three times a week) with ultraviolet B light of the skin of hairless mouse Uscd (Hr) strains resulted in the induction of skin tumors after 25 to 41 weeks. Topical applications of 3-aminobenzamide (3AB; 0.1 or 1 M) after each irradiation significantly shortened the earliest time of onset of tumors to 13 to 25 weeks and increased the number of animals that developed tumors over 41 weeks from 67% without 3AB to 73% and 81% with 0.1 and 1 M 3AB, respectively. 3-Aminobenzamide has previously been shown to inhibit radiation-induced transformation in vitro. In vivo, 3AB has the opposite effect, indicating the need for caution in extrapolating from in vitro systems to carcinogenesis in vivo.

Animals↗
PubMed1992

Experimental models for primary melanoma.

The nonmelanoma skin cancers squamous cell carcinomas (SCC) and basal cell carcinomas (BCC) are by far the most common malignancies that occur in the United States each year. The third most common skin cancer, malignant melanomas (MM), accounted for 3% of all reportable cancers in the United States in 1991. The incidence of and mortality due to MM have been increasing at an alarming rate over at least the past 4 decades. As a result of this epidemic, there have been intense efforts to develop appropriate experimental models to examine the etiology and biology of this cancer. Benign and malignant melanocytic tumors have been produced in dogs, mice, guinea pigs, hamsters and gerbils with chemical carcinogens such as 7,12 dimethyl(a)benzanthracene (DMBA) and chemical promoters. Perhaps the most extensive and thorough studies using these chemicals were accomplished in the Weiser-Maple guinea pig model, in which radial and vertical stage growth occurred similar to human MM growth patterns. However, such stimuli are unlikely to be related to the human experience. Many investigators have considered ultraviolet radiation (UVR) from the sun to be intimately involved with the melanoma epidemic. Thus, a number of models have been developed to examine this possible relationship. These have included irradiation of DMBA-induced benign melanocytic tumors in pigmented hairless mice, chemical promotion of UVR-induced tumors in haired mice and the induction of melanomas by UVR in the South American opossum. In addition, a melanocytic growth was produced with psoralens plus UVA in a haired mouse. All of these melanomas required chronic UVR exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Repair of pyrimidine(6-4)pyrimidone photoproducts in mouse skin.

The induction and repair of cyclobutane pyrimidine dimers and pyrimidine(6-4)pyrimidone photoproducts in the epidermal DNA of ultraviolet-irradiated hairless mice were determined by radioimmunoassay. Few cyclobutane dimers were excised by 48 h after ultraviolet (UV) irradiation, whereas 50% of the (6-4) photoproducts were removed by 6 h, correlating with previously determined rates of unscheduled DNA synthesis in mouse skin. After this initial rapid phase of (6-4) photoproduct excision, a slower phase was observed between 6 and 48 h. These repair kinetics contrast with those for fibroblast cell cultures derived from mouse tissues irradiated with UV light yielding similar levels of damage. Although the initial rate of (6-4) photoproduct repair in cultured fibroblasts and epidermal cells was similar, the extent of repair in cultured cells was significantly greater, with most of the damage removed by 24 h. The kinetics for (6-4) photoproduct repair in mouse epidermal cells suggest that a significant population, such as terminally differentiated keratinocytes, may have a reduced repair capacity and that the culture process may select for more rapidly proliferating, repair-proficient stem cells.

Animals↗
PubMed1979

Photoimmunology.

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Allergy and Immunology↗
PubMed1979

Stimulation of ultraviolet-induced carcinogenesis by 1,3-Bis(2-chloroethyl)-1-nitrosourea.

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.

Administration, Topical↗
PubMed1978

Dermatology.

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Animals↗
PubMed1978

Ultrastructural study of the nuclei in premitotic and repair DNA synthesis following UVB injury.

Ultrastructural changes in nuclei synthesizing DNA were studied by cytochemical technique. Guninea pigs ears were UVB irradiated and TdR-H3 was injected intradermally into the irradiated sites 1 hr before biopsy. Areas of the epidermis containing more than 80% of cells in DNA (repair or premitotic) synthesis identified by light microscopic autoradiography were selected and cut at 600 A. The glycolmethacrylate sections were stained with uranyl acetate and lead citrate, and consecutive sections were incubated with 0.01% pronase and 0.5% RNase before staining in order to observe DNA. In cells undergoing DNA repair, the zone of DNA became discontinuous and DNA was scattered throughout the entire karyoplasm as small aggregates and fine filaments. Nuclei in S-phase showed essentially the same change, but quantitatively the disappearance of DNA from the nuclear membrane and distribution in the karyoplasm became much greater. These changes were not seen in specimens treated without cytochemical technique.

Animals↗
PubMed1978

Photocarcinogenesis: a review.

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.

Animals↗
PubMed1978

Recommendations for future research on ultraviolet radiation carcinogenesis.

Recommendations for future research on photocarcinogenesis were developed during an international conference on UVR carcinogenesis. Areas covered in the recommendations include research at the molecular biology level, human (especially epidemiologic aspects), physical (including instrumentation), and biologic studies (stressing animal models). The recommendations also propose the establishment of central supply and service sources for photocarcinogenesis research as well as the establishment of interdiscipilinary training programs related to research in photocarcinogenesis.

Animals↗
PubMed1977

Immunofluorescent studies of epidermal protein during UV induced carcinogenesis.

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.

Animals↗
PubMed1977

Solar urticaria.

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Antibodies↗
PubMed1977

Photoallergy.

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Humans↗