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Results for “PLACENTAL HORMONES”

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At least 271 records · Page 15Linked to original sources
PubMed1994

[Expression of human chorionic gonadotropin, human placental lactogen and pregnancy-specific 1-glycoprotein in malignant trophoblastic neoplasms].

The expression of placental hormones in 91 malignant trophoblastic neoplasms was studied immunohistochemically using a panel of antibodies against hCG, human placental lactogen (hPL) and pregnancy-specific 1-glycoprotein (SP). The results indicated that the expression of hCG in invasive moles was weaker than that in choriocarcinoma, but the expression of hPL and SP1 was stronger than those in choriocarcinoma. The expression of hPL and SP1 in the metastatic tumors of invasive moles was weaker than the expression at in the primary tumors, but the secretory capacity of hCG in metastatic choriocarcinomas was stronger than that in the primary neoplasms. In this study, the qualities of expression of the placental hormones in invasive moles and choriocarcinomas corresponded to the degree of tumor malignancy, the biological behaviour and the grading of trophoblastic cell differentiation. We believe that the detection of hCG, hPL and SP1, in malignant trophoblastic neoplasms was of value for establishing tumor diagnosis and typing and for judgement on prognosis.

Biomarkers, Tumor↗
PubMed2002

Autocrine human growth hormone inhibits placental transforming growth factor-beta gene transcription to prevent apoptosis and allow cell cycle progression of human mammary carcinoma cells.

Multiple cellular effects of human growth hormone (hGH) are mediated by an indirect mechanism requiring transcriptional activation of genes encoding protein effector molecules such as insulin-like growth factor-1. Such protein effector molecules then act directly to mediate the cellular functions of hGH. We report here that autocrine hGH production by mammary carcinoma cells specifically results in the transcriptional repression of the p53-regulated placental transforming growth factor-beta (PTGF-beta) gene. Transcriptional repression of the PTGF-beta gene does not require the p53-binding sites in the PTGF-beta promoter, and autocrine hGH also desensitized the response of the PTGF-beta promoter to p53 overexpression. Transcriptional repression of the PTGF-beta gene is accompanied by consequent decreases in its protein product, Smad-mediated transcription, and its cellular effects that include cell cycle arrest and apoptosis. PTGF-beta specifically inhibited the autocrine hGH-stimulated expression of cyclin D1 required for autocrine hGH-stimulated mammary carcinoma cell cycle progression. Thus, one mechanism by which autocrine hGH promotes an increase in mammary carcinoma cell number is by transcriptional repression of protein effector molecules that promote cell cycle arrest and apoptosis. Such transcriptional repression of negative regulatory factors, such as PTGF-beta, may also be requisite for direct stimulation of mammary carcinoma cell mitogenesis by hGH.

Apoptosis↗
PubMed1979

Processing in vitro of placental peptide hormones by smooth microsomes.

Rough and smooth microsomes were prepared from ascites tumor cells, rat liver, and bovine adrenal cortex. Proteolytic removal of the signal peptide in pre-placental lactogen and asparagine-linked glycosylation of the alpha subunit of chorionic gonadotropin by these fractions were examined in mRNA-dependent lysates from ascites cells. Both processing steps were performed by smooth microsomes, which was unexpected because it has been presumed that only rough microsomes contain components for ribosomal binding. Thus smooth microsomes are apparently capable of interacting with polysomes bearing secretory nascent chains, and cleavage and asparagine-linked glycosylation activities are present in both rough and smooth endoplasmic reticulum.

Adrenal Cortex↗
PubMed1983

The immunocytochemical demonstration of human placental lactogenic hormone (hPL): a parameter for the functional capacity of the trophoblast.

Forty-two placentae from pregnancies of 36 to 42 weeks' gestation were examined: the maternal serum human placental lactogen (hPL) values of the mothers during the last week of gestation ranged between 3 and 12 micrograms/ml. hPL was demonstrated by the indirect immunofluorescence technique and was present in all placentae. A significant regional difference in hPL concentration was not found, but within individual sections focal differences in intensity were apparent. Of intensity group I (weakly positive) 92 per cent correlated with maternal serum hPL values of 3 to 6 micrograms/ml; 78 per cent of group II/III (very strongly positive) with values above 6 micrograms/ml. In the four-field Chi-square test the probability of error was at 5%. In 32 cases trophoblast islands (Islands of Ortmann) were present, of which 20 were hPL positive. Their degree of intensity corresponded to group I of the syncytiotrophoblast. Of the placentae showing hPL-positive Islands of Ortmann, 95 per cent correlated with maternal serum hPL values below 6 micrograms/ml whilst 70 per cent of the hPL-negative trophoblast islands correlated with serum values above 8 micrograms/ml. It is suggested that maternal serum hPL values are determined by the rate of synthesis of hPL by the placenta and not by the rate of secretion. The focal differences in intensity indicates that the serum level does not only depend on the absolute surface area of the trophoblast, but that there also exist qualitative and functional differences between different areas of the syncytiotrophoblast. Heterotopic hPL synthesis in the Islands of Ortmann is considered to be independent of hPL synthesis by the syncytiotrophoblast.

Female↗