Toxic Responses of the Adrenal Medulla☆

Tischler, A.S.; Nyska, A.; Elmore, S.A.

doi:10.1016/b978-0-12-801238-3.02146-2

Cited by 1 publication

(3 citation statements)

References 149 publications

(144 reference statements)

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“…Multiple microscopic adrenal medullary lesions that were cytologically identical to PCs but did not invade or compress the adrenal cortex were present in three irradiated and four non-irradiated animals. Although similar microscopic lesions would be classified as hyperplastic nodules in veterinary pathology literature (Tischler et al 2014), they are classified here as micro PCs in light of current understanding based on molecular studies of small adrenal medullary nodules in humans (Korpershoek et al 2014). Multiple pituitary adenomas were present in both groups of rats, as shown in Supplementary Table 3.…”

Section: Resultsmentioning

confidence: 97%

“…In contrast to mice and other species, rats have an unusual proclivity to develop PCs. The incidence of these tumors increases throughout life and is especially high in males compared to females, with a ratio up to 10:1 in some rat strains (Tischler et al 2014). Abdominal or head and neck PGs are also occasionally reported (van Zwieten et al 1979, Hall et al 1987.…”

Section: Introductionmentioning

confidence: 99%

“…In WT Sprague-Dawley rats, PCs begin to be detected at age 1-2 years, and the prevalence at 2 years is approximately 10% (Pace et al 2002). The incidence is further increased by a variety of agents including high calorie diet, radiation, drugs and hormones (Tischler et al 2004(Tischler et al , 2014. In view of their innate proclivity to develop PCCs, we hypothesized that rats would a priori be superior to mice as a potential Sdhb tumor model.…”

Section: Introductionmentioning

confidence: 99%

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A xenograft and cell line model of SDH-deficient pheochromocytoma derived from Sdhb+/− rats

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Cochran

Baleja

et al. 2020

Endocrine-Related Cancer

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Tumors caused by loss-of-function mutations in genes encoding TCA cycle enzymes have been recently discovered and are now of great interest. Mutations in succinate dehydrogenase (SDH) subunits cause pheochromocytoma/paraganglioma (PCPG) and syndromically associated tumors, which differ phenotypically and clinically from more common SDH-intact tumors of the same types. Consequences of SDH deficiency include rewired metabolism, pseudohypoxic signaling and altered redox balance. PCPG with SDHB mutations are particularly aggressive, and development of treatments has been hampered by lack of valid experimental models. Attempts to develop mouse models have been unsuccessful. Using a new strategy, we developed a xenograft and cell line model of SDH-deficient pheochromocytoma from rats with a heterozygous germline Sdhb mutation. The genome, transcriptome and metabolome of this model, called RS0, closely resemble those of SDHB-mutated human PCPGs, making it the most valid model now available. Strategies employed to develop RS0 may be broadly applicable to other SDH-deficient tumors.

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Section: Resultsmentioning

confidence: 97%