Recent data suggest that individuals with recessive dystrophic epidermolysis bullosa (RDEB) only develop squamous-cell carcinoma (SCC) in the presence of the NC1 domain of type VII collagen. This conclusion was based on experimental work in which cryosections of SCCs from 10 people with RDEB all showed positive type VII collagen immunostaining and observations in a murine model of SCC development in which tumors only occurred using keratinocytes from RDEB subjects that expressed detectable levels of the NC1 domain of the type VII collagen protein. To assess whether the clinical interpretation was valid in another cohort of RDEB patients, we examined expression of type VII collagen in 17 SCC tumors excised from 11 patients. Indirect immunofluorescent staining of SCC cryosections and Western blotting of cultured keratinocyte lysates identified two RDEB individuals who did not express detectable levels of type VII collagen. Mutation analysis revealed that these two patients harbor compound heterozygous nonsense mutations within the region of the COL7A1 gene encoding the NC1 domain. These data suggest that individuals with RDEB can develop SCC regardless of type VII collagen expression and that additional factors have a role in explaining the high incidence of tumors complicating this genodermatosis.
The concentration of adrenocorticotrophic hormone in the blood of rats was estimated at various time intervals after the removal of the adrenal glands. The hormone was not detectable until 10 days after the operation. Its concentration rose to a maximum value 3 weeks after adrenalectomy and this high circulating level was maintained for at least another 2 weeks. There were no significant differences between the results obtained using hypophysectomized and hydrocortisone-treated rats for the bioassay procedures.Direct estimates of the concentration of adrenocorticotrophic hormone (ACTH) in the blood of adrenalectomized rats have produced conflicting results. Gemzell, Van Dyke, Tobias & Evans [1951] showed that bilateral adrenalectomy in the rat resulted in an immediate and progressive increase in the circulating level of ACTH. Sydnor & Sayers [1952, 1953, 1954] and Sydnor [1955] found that the level of ACTH in the blood of adrenalectomized rats was considerably greater than that of the intact animal. On the other hand, Barrett & Hodges [1956 a] were unable to demonstrate any difference in plasma ACTH concentration between normal and adrenalectomized rats 3, 6 and 12 days after the removal of the adrenal glands. The present investi¬ gation was performed in an attempt to explain the discrepancy between these findings.The results of experiments are described in which estimates of the blood ACTH con¬ centration in rats at various times after the removal of their adrenal glands were made by two different methods. METHODSAlbino Wistar rats were used. They were fed on 'rat cubes' (diet 41, Lane-Petter & Dyer [1952]) and water, and kept in a room at a constant temperature of 70°F. The animals weighed 120-160 g at the beginning of the experiments.Bilateral adrenalectomy was performed under ether anaesthesia and the adrenal¬ ectomized rats were maintained on the normal diet with 0-9% sodium chloride solution in place of drinking water.Hypophysectomy was performed under ether anaesthesia by the parapharyngeal approach as described by Smith [1927, 1930]. The hypophysectomized rats received the normal diet with the addition of 4 % glucose to the drinking water. These animals were used for the ACTH assays 24 hr after the removal of their pituitary glands. At the end of each experiment the completeness of hypophysectomy was checked macroscopically at autopsy.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.