A non -isotopic in situ hybridization method with biotin-labelled oligonucleotide probes was used to examine growth hormone (GH) and prolactin (PRL) gene expression in 32 patients with pituitary adenomas; 13 were prolactinomas, 8 GH secreting
adenomas,
and 11 mixed GH and PRL secreting adenomas.
Positive immunostaining for GH was found in all patients with GH secreting adenomas, and mixed GH and PRL secreting adenomas. Positive immunostaining for PRL was found in all patients with prolactinomas and 9(81.8%) of 11 mixed GH and PRL
secreting
adenomas, 5(62.5%) of 8 GH secreting adenomas. Immunohistochemistry revealed that 13 were Lactotrope adenomas, 5 somatotrope adenoma, and 14 GH and PRL cell adenomas.
In situ hybridization revealed that GH mRNA expression was found in all the patients with somatotrope adenoma and GH and PRL cell adenomas, and 6(46.1%) of 13 lactotrope adenomas. PRL mRNA expression was 100% in lactotrope and GH and PRL cell
adenomas,
and 4 (80.0%) of 5 somatotrope adenomas.
The patients with clinical diagnosis of acromegaly had detectable PRL mRNA in their neoplasm and it is suggested that the PRL cells in the adenomas did not result from dedifferentiation, but from the neoplastic stimulus for some mixed tumors
probably
occurred in cells previously committed to produce PRL and GH. In lactotrope adenomas, the PRL cells of the patients without expression of GH mRNA mlay be arised from cells programmed to secrete PRL or precussor PRL cells rather than from mixed
GH-PRL
cells. The finding that some patients produced mRNA detectable by in situ hybridization, but no hormone detectable by immunohistochemistry within tumor was suggested of a silent adenoma. These observations indicated that in situ hybridization
studies
may improve the classification of pituitary adenomas and may provide a precise knowledge of the biology of these neoplasms.(J Kor Soc Endocrinol 9:82~92, 1994)
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