Clinically nonfunctioning pituitary tumors are monoclonal in origin.

J M Alexander; B M Biller; H Bikkal; N T Zervas; A Arnold; A Klibanski

doi:10.1172/JCI114705

Division of Medicine, Massachusetts General Hospital, Boston 02114.

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Published in Volume 86, Issue 1 on July 1, 1990
J Clin Invest. 1990;86(1):336–340. https://doi.org/10.1172/JCI114705.
© 1990 The American Society for Clinical Investigation

Published July 1, 1990 - Version history

Clinically nonfunctioning pituitary adenomas are benign neoplasms comprising approximately 25-30% of pituitary tumors. Little is known about the pathogenesis of pituitary neoplasia. Clonal analysis allows one to make the important distinction between a polyclonal proliferation in response to a stimulatory factor versus a monoclonal expansion of a genetically aberrant cell. We investigated the clonal origin of pituitary tumors using X-linked restriction fragment length polymorphisms at the phosphoglycerate kinase and hypoxanthine phosphoribosyl-transferase genes. Restriction enzymes were used to distinguish maternal and paternal X-chromosomes, and combined with a methylation-sensitive restriction enzyme to analyze allelic X-inactivation patterns in six pituitary adenomas. All six tumors showed a monoclonal pattern of X-inactivation. These data indicate that nonfunctioning pituitary adenomas are unicellular in origin, a result consistent with the hypothesis that this tumor type is due to somatic mutation.

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