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Abstract
Detection of recurrence from medullary thyroid carcinoma (MTC) remains a diagnostic problem, especially when increased serum tumour marker levels suggest recurrence and conventional imaging techniques are non-diagnostic. In this study, we performed 111In-octreotide and 99mTc(V)-dimercaptosuccinic acid (DMSA) scans in a series of eleven patients with MTC presenting with elevated serum tumour markers after surgery.
111In-octreotide whole body studies detected tumour in six of the eleven patients studied and detected nine tumoral localizations. 99mTc(V)-DMSA whole body studies detected tumour in five of the eleven patients studied and eight tumoral localizations. 111In-octreotide and 99mTc(V)-DMSA studies detected recurrence in all four patients with basal calcitonin levels above 1000 ng/l. We conclude that 111In-octreotide and 99mTc(V)-DMSA studies have limited sensitivity to detect recurrence in patients with MTC, although their sensitivity may improve with high serum calcitonin levels. These radionuclide imaging techniques should be employed when conventional imaging techniques are negative or inconclusive or, in the case of 111In-octreotide studies, should be employed when we want to investigate the presence of somatostatin receptors that provide the basis for treatment with somatostatin analogues.
Journal of Endocrinology (1995) 144, 339–345
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Interest in epigenetics has gained substantial momentum as a result of their identified role in the regulation of tumor progression as well as their ability to pharmacologically target genes. Pituitary neuroendocrine tumors (PitNETs) tend to be inactivated via epigenetic modification, and although emerging evidence has suggested a role for epigenetic factors in PitNET tumorigenesis, the degree to which these factors may be targeted by new therapeutic strategies still remains poorly understood. The objective of the present study was to examine the participation of the EZH2/H3K27me3 axis in the proliferation of lactotroph tumor cells. We demonstrated that the levels of EZH2 and H3K27me3 were increased in murine experimental prolactin (PRL) tumors with respect to a control pituitary, in contrast with the low p21 mRNA levels encountered, with an H3K27me3 enrichment being observed in its promoter region in a GH3 tumor cell. Furthermore, specific EZH2/H3K27me3 axis inhibition blocked the proliferation of primary tumor cell culture and GH3 cells, thereby making it an attractive therapeutic target for PRL PitNETs.
