Abstract
The pituitary hormone corticotropin is occasionally produced by nonpituitary tumors, leading to the ectopic corticotropin syndrome. Whereas the ectopic corticotropin syndrome was classically seen as a discrete and homogenous condition, there is increasing evidence that it actually includes distinct pathologic entities. Various types of tumors, most often originating in the lung, can secrete corticotropin; among them are the well-differentiated and rather indolent carcinoids, and, by contrast, the highly aggressive small-cell cancers. The former tumors often respond in an unanticipated, pituitary-like manner to the modulators of corticotroph function. The recent cloning of the V3 vasopressin receptor and the demonstration of its close association with the corticotroph phenotype, offers a new molecular tool with which to explore corticotropin-secreting nonpituitary tumors. The high levels of V3 receptor gene expression in most carcinoids reveal that corticotropin production by these tumors is but one aspect of a wider program of corticotroph differentiation.
Published Version
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