Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The paper deals with a comparison of basal levels of secretion of total testosterone (T) and estradiol-17 beta (E2), their free and albumin and sex-steroid-binding globulin fractions as well as LH, FSH, prolactin and STH in blood serum of 60 normal height and 60 tall healthy adolescents and those with primary osteogenic sarcoma of bones at different stages of puberty. The study established a significantly higher level of testosterone and free androgen index and a lowered concentration of sex-steroid-binding globulin in blood serum of both normal and tall adolescent patients with osteogenic sarcoma at different stages of puberty. No significant differences were found in said indexes of estrogens between sarcoma patients and a specific group chosen for comparison, as far as physical status is concerned. The role of sex steroid hormones and, particularly, that of androgens in the pathogenetical mechanisms of osteogenic sarcoma growth is discussed.
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PMID:[Sex and pituitary hormone secretion in normal-height and tall adolescents with primary osteogenic sarcoma]. 130 Jul 19

Basal levels of secretion of total testosterone, estradiol-17 beta, their free, albumin-binding and sex steroid-binding globulin (SSBG)--binding fractions, luteinizing hormone, follicle-stimulating hormone, prolactin and somatotropic hormone were measured in blood serum in the following groups of adolescents: (1) healthy, (2) suffering primary osteogenic sarcoma of the bone, (3) osteogenic sarcoma patients with pubertal retardation, and (4) pubertal retardation. A significant increase in total testosterone fraction, free androgen index and a decrease in blood SSBG level were established in osteogenic sarcoma patients as compared to corresponding controls, irrespective of pubertal status. No difference in the above indexes for estrogens was established between osteogenic sarcoma patients and controls in both pubertal status subgroups. The role of sex steroid hormones, particularly, androgens in the pathogenesis of osteogenic sarcoma is discussed.
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PMID:[Sex and pituitary hormone secretion in adolescents with osteogenic sarcoma and retarded sexual development]. 130 Jul 36

The expression of prolactin receptor (PRL-R) mRNA was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR) combined with Southern analysis in total RNA extracts from two human osteosarcoma cell lines (MG-63 and Saos-2). The level of PRL-R transcript was significantly enhanced in cells cultured in the presence of 1,25-(OH)2 vitaminD3 (10(-7)M) and to a lesser extent in the presence of dexamethasone (10(-6)M). This first demonstration of PRL-R gene expression in osteoblast-like cells supports the hypothesis of a direct action of prolactin in bone cells, which is further strongly suggested by the stimulatory effect of 1,25-(OH)2 vitaminD3 and dexamethasone on PRL-R mRNA level in these cells.
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PMID:Expression of prolactin receptors in human osteosarcoma cells. 895 26

Based on their content of prolactin receptors, osteosarcoma cells were predicted to be responsive to prolactin (PRL), but whether PRL would be beneficial or contribute to pathogenesis was unclear. 1,25(OH)(2) vitamin D(3) [1alpha,25(OH)(2)D(3)] has antiproliferative effects on osteosarcoma cells, and a complex interregulatory situation exists between PRL and 1alpha,25(OH)(2)D(3). Using osteosarcoma cells, Western blot, real time RT-PCR, and promoter-luciferase assays, we have examined the interaction between PRL and 1alpha,25(OH)(2)D(3) and demonstrated that physiological concentrations of PRL block increased osteocalcin and vitamin D receptor (VDR) expression in response to 1alpha,25(OH)(2)D(3.) This blockade was shown to be the result of lack of nuclear accumulation of the VDR in response to 1alpha,25(OH)(2)D(3). Although inhibition of proteasomic degradation with MG132 had no effect on the VDR itself in a 30-min time frame, it relieved the blockade by PRL. Analysis of ubiquitinated proteins brought down by immunoprecipitation with anti-VDR showed PRL regulation of a 250-kDa protein-VDR complex. P250 was identified as the breast cancer tumor suppressor gene product, BRCA1, by Western blot of the VDR immunoprecipitate and confirmed by immunoprecipitation with anti-BRCA1 and blotting for the VDR in the absence and presence of PRL. Knockdown of BRCA1 inhibited nuclear translocation of the VDR and the ability of 1alpha,25(OH)(2)D(3) to induce the VDR. This, to our knowledge, is the first demonstration of a role for BRCA1 in nuclear accumulation of a steroid hormone and the first demonstration that PRL has the potential to affect the cell cycle through effects on BRCA1.
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PMID:Prolactin blocks nuclear translocation of VDR by regulating its interaction with BRCA1 in osteosarcoma cells. 1907 49

Hyperprolactinemia is one of the risk factor of decrease in bone mass which has been believed to be mediated by hypogonadism. However, the presence of prolactin receptor in human osteosarcoma cell line and primary bone cell culture from mouse calvariae supported the hypothesis of a direct prolactin (PRL) action on bone cells. Therefore, the aim of this study was to investigate the role of PRL and its signal transduction pathway in the regulation of bone metabolism via osteoblast differentiation. Human pre-osteoblasts (SV-HFO) that differentiate in a 3-week period from proliferating pre-osteoblasts (days 2-7) to extracellular matrix producing cells (days 7-14) which is eventually mineralized (days 14-21) were used. Concentration of PRL mimicked a lactating period (100 ng/ml) was used to incubate SV-HFO for 21 days in osteogenic medium. Human prolactin receptor mRNA and protein are expressed in SV-HFO. PRL significantly decreased osteoblast number (DNA content) which was due to a decrease in proliferation. PRL increased osteogenic markers, RUNX2 and ALP in early stage of osteoblast differentiation while decreasing it later suggesting a bi-directional effect. Calcium measurement and Alizarin red staining showed a reduction of mineralization by PRL while having neither an effect on osteoblast activity nor RANKL/OPG mRNA ratio. We also demonstrated that PRL action on mineralization was not via PI-3 kinase pathway. The present study provides evidence of a direct effect of prolactin on osteoblast differentiation and in vitro mineralization.
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PMID:Evidence for direct effects of prolactin on human osteoblasts: Inhibition of cell growth and mineralization. 1936 11