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Biomedical subjects

G Shklar

Publications and source records attributed to G Shklar.

At least 91 records · Page 5Linked to original sources
PubMed1982

Vitamin E inhibition of hamster buccal pouch carcinogenesis. A gross, histologic, and ultrastructural study.

Sixty-four young adult male and female golden hamsters (Mesocricetus auratus) were divided into four equal experimental groups of sixteen animals. In Group 1 animals the left buccal pouch was painted three times weekly with a 0.25 percent solution of 7, 12-dimethylbenz(a)anthracene (DMBA) in heavy mineral oil. In Group 2 animals the left buccal pouch was similarly painted with DMBA, but the animals also received 7 I.U. of vitamin E (alpha tocopherol) twice weekly on days alternate to the DMBA painting. The vitamin E was administered orally via a fine pipette. Group 3 animals were similarly painted with DMBA and received vitamin E vehicle by pipette. Group 4 animals served as untreated controls. Four animals in each group (two male, two female) were killed at 8, 10, 12, and 14 weeks. Buccal pouches were photographed and excised. Tumors were noted and measured in the left buccal pouches. The buccal pouches as well as major organs were fixed in formalin, sectioned in paraffin, and stained with hematoxylin and eosin. In the Group 2 animals receiving vitamin E, there was a significant delay in tumor formation so that by 12 to 14 weeks there were fewer tumors and their average size was smaller than those in the Group 1 and Group 3 animals painted with DMBA but receiving no vitamin E supplement. Microscopic examination revealed that there was less invasion of underlying tissues and less surface necrosis. The tumors in both control and vitamin E groups were well-differentiated epidermoid carcinomas. No differences in the nature of the cellular patterns of the carcinomas in control and vitamin E groups were revealed by electron microscopic studies.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

Two-phase carcinogenesis in hamster buccal pouch.

A two-phase mechanism of chemical carcinogenesis in hamster buccal pouch has been demonstrated. Painting of buccal pouches three times weekly with a 0.1 percent solution of 7,12-dimethylbenz(a)anthracene (DMBA) in mineral oil for 10 weeks resulted in no visible tumors nor any microscopic evidence of dysplasia after the animals had been maintained for a 20 week period (Group 1 animals). Painting with 0.1 percent DMBA for 10 weeks, no treatment for a following 6 week period, and painting with 0.5 percent DMBA for a subsequent 4 weeks resulted in epidermoid carcinomas (Group 2 animals). Painting with 0.5 percent DMBA for 4 weeks in animals without prior treatment resulted in no tumors (Group 3 animals). It is postulated that the early treatment in Group 2 may serve for initiation and the later treatment for promotion.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

Delay in hamster buccal pouch carcinogenesis by aspirin and indomethacin.

Aspirin and indomethacin, administered systemically by oral route, were found to delay the development of hamster buccal pouch epidermoid carcinomas induced by thrice weekly topical applications of a 0.5 percent solution of 7,12-dimethylbenz(a)anthracene (DMBA) in mineral oil. Forty male and female Syrian hamsters (Mesocricetus auratus) were divided into four equal groups. In Group 1 animals the left buccal pouch was painted thrice weekly with DMBA. Group 2 animals were painted thrice weekly with DMBA and received 12 mg. aspirin daily by oral route. Group 3 animals were painted thrice weekly with DMBA and received 1 mg. indomethacin daily by oral route. Group 4 animals were maintained as untreated controls. Two animals in each of the four groups were killed with ether at 8, 10, 12, 13, and 14 weeks after the start of the experiment. At the time of sacrifice the buccal pouches were photographed and the average number of tumors and the average size of tumors in each group were noted. The left and right buccal pouches were dissected, fixed in 10 percent formalin, sectioned in paraffin, and stained with hematoxylin and eosin. Autopsies were also performed on each animal. Both left and right buccal pouches and major organs were studied histologically. Both aspirin and indomethacin in the dosages used were found to delay DMBA buccal pouch carcinogenesis. A suggested mechanism of action is the inhibition of prostaglandin synthesis by the role of both aspirin and indomethacin as inhibitors of prostaglandin synthetase. Indomethacin appeared to exert a greater tumor-inhibiting effect than aspirin in the dosages used.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

A transplantable anaplastic oral cancer model.

A stable model has been developed for oral mucosal anaplastic epidermoid carcinoma. This model more closely resembles the biologic characteristics of human oral carcinoma than previous models, such as primary epidermoid carcinomas induced in hamster buccal pouches or tongue by chemical carcinogens. This anaplastic oral cancer model was developed by serial abdominal transplantation in neonatal hamsters of original DMBA-induced primary epidermoid carcinomas of hamster buccal pouch. After the second generation, the tumors became stable, maintained an anaplastic appearance histologically, and were biologically aggressive, with rapid growth and metastatic potential. The original DMBA-induced buccal pouch tumors from 42 adult hamsters were transplanted abdominally through five generations in 151 neonatal hamsters. Immunosuppression was crucial in the initial transplantation but became unnecessary in the later serial transplantations. This model can serve as the basis for a variety of future immunologic and biologic studies dealing with oral cancer.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

Rapid induction of gamma-glutamyl transpeptidase-rich intraepithelial clones in 7,12-dimethylbenz(a)anthracene-treated hamster buccal pouch.

Individual gamma-glutamyl transpeptidase (GGT)-stained cells and cell doublets were rapidly induced in the epithelium of hamster buccal pouch treated with biweekly topical applications of 0.5%, 7,12-dimethylbenz(a)anthracene (DMBA) in mineral oil. The cells were detected histochemically in whole mounts of pouch epithelium harvested as early as 3 days after the first application of this carcinogen. During 3 consecutive weeks of DMBA treatment, progressively larger GGT-stained epithelial cell populations (plaques) up to 0.5 mm in diameter were encountered. Similar GGT-stained lesions were not detected in whole mounts of untreated epithelium and were rarely seen in GGT-stained whole mounts prepared from mineral oil-treated pouch epithelium. In an experiment designed to assess the stability of the GGT-staining pattern, very few plaques could be detected 12 weeks after a 3-week regimen of six DMBA applications. However, data are presented suggesting that a brief series of three DMBA applications reinduced GGT histochemical activity in occult intraepithelial plaques, which had los enzyme activity but had persisted over an 11-week treatment-free interval. The clonal nature of the GGT-stained plaques for their apparent ability to persist in an occult form for several weeks or months lend further support to the hypothesis that these carcinogen-altered cell populations may be potential precursors for the development of squamous epithelial neoplasia.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

Oral mucosal carcinogenesis in hamsters: inhibition by vitamin E.

Eighty young adult male and female Syrian golden hamsters (Mesocricetus auratus) were divided into 4 equal experimental groups. In group I animals the left buccal pouch was painted three times weekly with a 0.5% solution of 7,12-dimethylbenz[a]anthracene (DMBA) in heavy mineral oil. In group 2 animals the left buccal pouch was similarly painted with DMBA, but the animals also received orally 10 mg vitamin E (dl-alpha-tocopherol) in peanut oil twice weekly on alternate days with DMBA painting. Group 1 animals received a similar amount of peanut oil vehicle, group 3 animals received only vitamin E (vitamin E controls) in peanut oil, and group 4 animals served as untreated controls receiving only peanut oil. Four animals in each group (2 males and 2 females) were killed at 8, 10, 12, 14, and 16 weeks. Buccal pouches were photographed and excised, and tumors were noted and measured in the left buccal pouches. In group 2 animals receiving vitamin E, tumor formation was significantly delayed, so that by 14-16 weeks there were fewer tumors and their average size was smaller than that of tumors in group 1 animals that were painted with DMBA but received no vitamin E supplement. In group 2 there was also less invasion of underlying tissues and less surface necrosis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1981

Anaplastic carcinoma in the buccal pouches of hamsters as a model of oral cancer.

An anaplastic model of oral cancer has been developed by abdominal transplantation of carcinomas induced in buccal pouches of hamsters by DMBA. The transplanted tumors were replanted abdominally through five generations. The original carcinomas of the buccal pouch became stable in the abdomen after two generations of such transplantations and could thereafter be retransplanted intraperitoneally with 100% of success, as well as being transferable again to the buccal pouches of hamsters, where they were capable of being maintained as an oral model for anaplastic epidermoid carcinoma.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1980

Strength and biocompatibility of polymethacrylate-silica composite dental implant materials.

A study was made of the strength properties of several composite dental implant materials composed of silica microspheres (6%, 24%, and 48% by weight) and PMMA. Prepared specimens of the materials were tested for compressive strength and tensile strength as a function of the curing methods. Compressive strength was reduced only slightly when the 6% mixture was used, as compared to 100% PMMA, but the compressive strengths of the 12% and 24% mixtures were reduced by approximately 30% when compared to 100% PMMA. The compressive strengths of these materials were reduced even further after curing in a microwave oven, and the tensile strengths decreased to a greater degree. The 6% mixture was reduced by 38% in the heat-cured specimens and was reduced by 27% in the microwave-cured specimens. Tooth replica implants were placed in baboons and the peri-implant tissues were studied histologically after 6 months. Inflammation was minimal. Peri-implant alveolar bone was viable and active, and both connective tissue and epithelial attachment to the implant surface was evident.

Alveolar Process↗
PubMed1980

Retinoid inhibition of lingual carcinogenesis.

Sixty-four male and female Syrian hamsters, 3 months of age and weighing 90 to 120 grams, were divided into four equal experimental groups. In animals of Groups 1 and 2 the right posterior lateral border of the tongue was painted three times weekly with a 0.5 percent solution of DMBA in acetone. Group 2 animals also received 10 mg. of 13-cis-retinoic acid in peanut oil administered orally twice weekly by pipette. Carcinogen and retinoid were administered on alternate days. Group 3 animals received only 13-cis-retinoic acid. Group 4 animals served as untreated controls. Four animals in each group were killed at 12, 14, 16, and 18 weeks. The Group 2 animals, receiving 13-cis-retinoic acid, exhibited a significant delay in the development of lingual tumors, both grossly and microscopically. At 14 weeks carcinomas were found in the DMBA animals, but only dysplasia and areas of carcinoma in situ were found in the DMBA-retinoid animals. After 18 weeks the DMBA animals exhibited large lingual tumors with surfacenecrosis, while the DMBA-retinoid animals presented smaller tumors with less invasion of underlying tissue.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1980

Inhibition of hamster buccal pouch carcinogenesis by 13-cis-retinoic acid.

Sixty-four male and female Syrian hamsters, 3 months of age and weighing 90 to 120 grams, were divided into four equal experimental groups. In animals of Groups 1 and 2 the left buccal pouch was painted three times weekly with a 0.5% solution of DMBA in heavy mineral oil. Group 2 animals also received 10 mg. of 13-cis-retinoic acid in peanut oil administered orally twice a week by pipette. Carcinogen retinoid were administered on alternate days. Group 3 animals served as controls, receiving only 13-cis-retinoic acid. Group 4 animals served as untreated controls. Four animals in each group (two males and two females) were killed at 10, 12, 14, and 16 weeks. The Group 2 animals, which received 13-cis-retinoic acid, exhibited a significant delay in DMBA carcinogenesis of buccal pouch mucosa, as studied both grossly and histologically. Both groups eventually demonstrated well-differentiated epidermoid carcinomas, but the tumors were smaller in the DMBA-retinoid animals.

Animals↗
PubMed1980

Retinoid inhibition of experimental lingual carcinogenesis: ultrastructural observations.

Sixty-four male and female Syrian golden hamsters (Mesocricetus auratus) were divided into 4 equal groups. Group 1 animals had the posterior lateral borders of their tongues painted three times weekly with a 0.5% solution of 7,12-dimethylbenz[a]anthracene (DMBA) in acetone. Group 2 animals were painted with DMBA and also received 10 mg of 13-cis-retinoic acid in peanut oil administered orally by pipette twice weekly. Group 3 animals received only retinoid, and group 4 animals were untreated controls. Four animals in each group were killed at 12, 14, 16, and 18 weeks. In the DMBA-painted animals receiving 13-cis-retinoic acid, the leukoplakia and epidermoid carcinomas developed more slowly and were better differentiated microscopically. The better degree of differentiation was demonstrated by ultrastructural studies. Less cellular separation and fewer microvilli-like structures were evident. No tubular mitochondria were observed. Less dispersion of heterochromatin occurred throughout nuclei, and the basal lamina tended to be regular and continuous.

9,10-Dimethyl-1,2-benzanthracene↗