期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 371, 期 1-2, 页码 208-220出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2013.01.015
关键词
Adrenal glands; cAMP signaling pathway; Adrenocortical hyperplasia; PRKAR1A gene; Tumor
资金
- Intramural NIH HHS [ZIA HD008920-01] Funding Source: Medline
In the last few years, bench and clinical studies led to significant new insight into how cyclic adenosine monophosphate (cAMP) signaling, the molecular pathway that had been identified in the early 2000s as the one involved in most benign cortisol-producing adrenal hyperplasias, affects adrenocortical growth and development, as well as tumor formation. A major discovery was the identification of tissue-specific pluripotential cells (TSPCs) as the culprit behind tumor formation not only in the adrenal, but also in bone. Discoveries in animal studies complemented a number of clinical observations in patients. Gene identification continued in parallel with mouse and other studies on the cAMP signaling and other pathways.
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