PubMed · 6918114
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M Fischer. 1981. [Rectal polyps].. https://pubmed.ncbi.nlm.nih.gov/6918114/
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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.
The nonadenomatous parathyroid glands associated with parathyroid adenoma in patients with primary hyperparathyroidism (pHPT) are assumed to exhibit suppressed secretion of parathyroid hormone (PTH). Because the function of these glands is of clinical importance for calcium homeostasis after surgery for pHPT, we studied the decrease of serum levels associated with intact PTH (i-PTH) and amino-terminal PTH (N-PTH) after excision of a parathyroid adenoma. Blood samples were obtained from the cubital vein and the inferior thyroid vein in six patients with pHPT. The results show that the levels of both i-PTH and N-PTH decreased after removal of the parathyroid adenoma (p < 0.05 for both). Because the reduction was more pronounced for i-PTH than for N-PTH, the N/i ratio increased from 0.54 +/- 0.33 to 3.76 +/- 1.62 (p < 0.05). Furthermore, the levels of i-PTH and N-PTH were higher centrally than peripherally both before and after adenoma excision (p < 0.05). The results therefore suggest that the secretion of i-PTH and N-PTH in the remaining normal-size parathyroid glands is not completely suppressed. Furthermore, in these parathyroid glands the secretion of amino-terminal PTH fragments is relatively predominant when compared to the release of the intact PTH. The findings underscore the importance of the N-terminal PTH fragment for maintaining calcium homeostasis during the early postoperative period after surgery for pHPT and may explain the rarity of prolonged hypocalcemia after parathyroidectomy.
We recently isolated from differential displays and subsequently cloned a human alpha-intercrine (hIRH) whose mRNA is reduced in human hepatocellular carcinomas. We now report that on Northern blots its mRNA is absent from premalignant colonic adenomas and from all of 27 human malignant cell lines (including breast, cervix, colon, duodenal, gastric, leukemia, liver, lung, melanoma, and pancreatic lines). hIRH mRNA was present in most normal human and mouse tissues and fibroblast derived cell lines but absent from leukocytes and brain. Two mRNA signals, at approximately 2 Kb and approximately 3.5 Kb, had variation in signal strength or size between tissues and species.