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Mol Cell Endocrinol. 2013 May 22;371(1-2):208-20. doi: 10.1016/j.mce.2013.01.015. Epub 2013 Feb 26.

cAMP/PKA signaling defects in tumors: genetics and tissue-specific pluripotential cell-derived lesions in human and mouse.

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Section on Genetics & Endocrinology (SEGEN), Program on Developmental Endocrinology & Genetics, NICHD, NIH, Bethesda MD 20892, USA.


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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