PubMed · 6170021
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H Munemitsu, M Matsuda, O Hirai, T Fukumitsu, J Kawamura. 1981. Intrasellar chondroma.. https://doi.org/10.2176/nmc.21.775
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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.
This study was designed to assess the diagnostic value of an immunochemical fecal occult blood test for small colorectal adenomas. In a screening program based comparative study, 60 colorectal adenomas under 1 cm (small polyp group), 60 colorectal adenomas 1 cm or larger (large polyp group) and 60 colorectal cancers (cancer group) detected by occult blood screening, and 120 healthy controls (control group), served as subjects. Moreover, 50 small adenomas, 50 large adenomas and 50 cancers detected in out-patient clinics, and 100 controls, served as subjects of a hospital based comparative study. Each of these subjects was tested by an immunochemical occult blood with 3 consecutive days, after removal of these colorectal neoplasms in a screening program based study and before as well as after removal in a hospital based study, and the positivity rate of this test was evaluated among these four groups in the two comparative studies. The positivity rate in a screening program based study was 23% for small polyp group, 8% for large polyp group, 5% for cancer group and 6% for control group, respectively. Significant difference was noted between small polyp and cancer as well as control groups (p <0.01), and between small polyp and large polyp groups (p <0.05). In a hospital based study, however, there was no significant difference in the positivity rate among four groups. These results suggest that high proportion of small polyps detected by fecal occult blood test screening may not be associated with bleeding from adenomas but probably from another gastrointestinal pathology.
Mice heterozygous for the ApcMin (Min) mutation develop adenomas throughout the intestinal tract. Apc is believed to be involved in cell migration, adhesion, and polarity. Adenoma multiplicity and growth rate are modulated by an unlinked modifier locus, Mom1. The secretory phospholipase Pla2g2a is a candidate for Mom1. Here, we investigate the range of action of Apc and Mom1. Analysis of chimeric Min mice indicates that the actions of both Apc and Mom1 are localized within the cell lineage that gives rise to intestinal tumors.