Conclusion

With the exception of the gsp oncogene, which is implicated in the induction of a minority of somatotroph adenomas, the pathogenesis of pituitary adenomas remains unknown. Because removal of normal tissue from an adjacent corticotroph adenoma is sometimes curative and because pituitary adenomas may resolve without treatment, exogenous factors must be implicated in tumor propagation and are likely to be required for tumor initiation as well. Without clear information about trophic activity and clonal architecture in the normal pituitary, the presence of monoclonality cannot necessarily be taken to imply proto-oncogene activation and inexorable clonal expansion from a single cell. Equally, apparent loss of heterozygosity at various chromosomal regions cannot necessarily be implicated in pituitary adenoma formation without information about the ploidy of normal pituitary parenchymal cell clones.

It remains to be seen whether loss of heterozygosity or clonal expansion causes quantitative rather than qualitative abnormalities of gene products and somehow affects the ability of pituitary cells to correctly interpret their identities and functions, leading them to excessively exuberant trophic responses to recurrent physiologic stimuli and the development of the typical pituitary adenoma phenotype. In any case, given the strange and sometimes paradoxical behavior of these fascinating lesions, whichever mechanisms are adduced for pituitary adenoma induction and propagation must include an assessment of biologic plausibility in their evaluations of their causality.

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