In the sellar region most tumors of our collection (n = 1937) are pituitary adenomas, followed by craniopharyngiomas, chordomas and meningiomas. Difficulties in morphological differential diagnosis by light microscopy may occur in meningiomas, plasmacytomas, chordomas and germinomas. In these cases, immunohistological investigations and sometimes even electron microscopy are helpful in solving the problems. Meningiomas can sometimes resemble pituitary adenomas. Of diagnostic value in these cases is the expression of vimentin and S-100-protein in the meningioma cells. Plasmacytomas may also mimic pituitary adenomas. In these cases, the positive reaction with antibodies against LCA and immunoglobulins or against kappa-light-chains and lambda-light-chains leads to the diagnosis. Chordomas, too, can sometimes be hardly distinguished from pituitary adenomas. In these cases, the expression of S-100-protein, vimentin and CEA by the chordoma cells and the typical electron microscopic features of chordomas are helpful for the differential diagnosis. Germinomas may sometimes be indistinguishable from lymphocytic hypophysitis. Of diagnostic importance are here the expression of HCG and placental alkaline phosphatase by germinoma cells. In the above mentioned cases, it is also important to perform immunohistochemical examinations for pituitary hormones including alpha-subunit. All these tumors do not express these hormones.
Pro-opiomelanocortin (POMC) mRNA was demonstrated in pituitary adenomas from 16 patients with Cushing's disease and 10 with Nelson's syndrome. The intensity of signal was significantly greater in Nelson's syndrome than in Cushing's disease and there was a trend towards a greater proportion of positive cells. This probably reflects inhibition of POMC gene expression by the high circulating levels of cortisol in Cushing's disease. In the para-adenomatous gland, the intensity of signal was variable in cells showing Crooke's hyaline change, ranging from negative to strongly positive, in keeping with the functional heterogeneity of corticotrophs. In one case, junctional corticotrophs were present and these were more intensely stained than anterior lobe corticotrophs in the same gland. This supports the concept that these cells are subject to different regulatory influences from corticotrophs in the anterior lobe. Whether this is related to differences in embryological origins or to local factors is at present unclear.
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