PubMed · 4188774
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M Linquette, J P May. 1969-11-15. [Simple goiter].. https://pubmed.ncbi.nlm.nih.gov/4188774/
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The high mobility group As (HMGAs) belong to a family of nonhistone nuclear proteins that orchestrate the assembly of nucleoprotein complexes. Through a complex network of protein-DNA and protein-protein interaction, they play important roles in gene transcription, recombination, and chromatin structure. This protein family is involved, through different mechanisms, in both benign and malignant neoplasias. We have recently reported that transgenic mice carrying the Hmga1 or Hmga2 genes under transcriptional control of the cytomegalovirus promoter develop pituitary adenomas secreting prolactin and growth hormone. We have shown that the mechanism of the HMGA2-induced pituitary adenoma is based on the increased E2F1 activity. The expression profile of mouse normal pituitary glands and adenomas induced in HMGA transgenic mice revealed an increased expression of the ccnb2 gene, coding for the cyclin B2 protein, in the neoplastic tissues compared with the normal pituitary gland. Here, we show, by electrophoretic mobility shift assay and chromatin immunoprecipitation, a direct binding of HMGA proteins to the promoter of ccnb2 gene, whereas luciferase assays showed that HMGAs are able to up-regulate ccnb2 promoter activity. Finally, we report an increased CCNB2 expression in human pituitary adenomas of different histotypes that is directly correlated with HMGA1 and HMGA2 expression. Because cyclin B2 is involved in the regulation of the cell cycle, these results taken together indicate that HMGA-induced cyclin B2 overexpression gives an important contribution to experimental and human pituitary tumorigenesis.
In order to examine modifying effects of simultaneous treatment with large amounts of vitamin A (VA) and thiourea (TU) on the thyroid tumorigenesis in rats, male F344 rats were initiated with N-bis(2-hydroxypropyl)nitrosamine (2800 mg/kg body weight, single s.c. injection), and starting 1 week later received diet containing 0.1% VA (VA group), drinking water containing 0.2% TU (TU group), 0.2% TU + 0.1% VA (TU + VA group) or tap water/basal diet (control group) for 19 weeks. Serum T3 and T4 in the TU and TU + VA groups were significantly decreased as compared to the control group, while serum TSH levels were remarkably increased. The ratios of T3 and T4 decrease and TSH increase in the TU + VA group were remarkably more pronounced than in the TU group. Thyroid neoplastic lesions were only induced in the TU and TU + VA groups. The multiplicity of intracapsular follicular cell proliferative foci in the TU + VA group was significantly increased as compared to the TU group value. Cell proliferation of hypertrophic and subcapsular follicular cells, as well as in hyperplasias, and neoplasias with adenomatous growth pattern was significantly higher in the combined treatment case than after TU alone. In the liver, centrilobular hypertrophy of hepatocytes was seen in the TU and TU + VA groups, this being especially marked in the latter group. In the combined group case the affected cells were strongly positive for GST-P antibody binding. The results of the present study suggest that cell proliferation of thyroid follicular cell proliferative lesions in rats is enhanced by strong TSH stimulation with simultaneous treatment of TU and large amounts of VA.
AIM OF STUDY: To define in a prospective study the prevalence and manifestations of subclinical hypercortisolism in a sizeable group of patients with incidentally detected adrenal adenoma. Such tumour - although usually clinically silent - may cause discrete endocrine dysfunctions. PATIENTS AND METHODS: Between 1990 and 1994, 85 consecutive patients with incidentally discovered adrenal adenoma were investigated (54 women, 31 men; mean age 54.1 +/- 13 [24-81] years). In addition to history and clinical examination all patients had a low-dose dexamethasone suppression test (2mg) and their morning basal plasma ACTH concentration was measured. The diagnosis of subclinical hypercortisolism was made if there was inadequate suppression of cortisol after dexamethasone administration, plasma ACTH level was decreased and there were no clinical signs of Cushing's syndrome. RESULTS: Five of the patients fulfilled the criteria of subclinical hypercortisolism (prevalence of 6%). One of them had oligomenorrhoea, another arterial hypertension, and three had mild histological proof of adrenal adenoma. Postoperatively the patient with oligomenorrhoea had normal menstrual cycles, while in all others with subclinical hypercortisolism excision of the tumour had no influence of their clinical state. CONCLUSIONS: Subclinical hypercortisolism is rare, but is one of the most common endocrine disorders in patients with incidental adrenal adenoma. It can be diagnosed only by hormonal analysis. Once the latent cortisol excess has been eliminated, those symptoms which are due to hormonal abnormality may regress, but nonspecific signs, such as obesity or hypertension, may not necessarily improve.