Human chorionic gonadotropin in colorectal cancer and its relationship to prognosis
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Effects of artificially induced hyperprolactinemia in male DBA/2 mice were studied by transplanting four pituitary glands under the kidney capsules. After 52--57 days the animals were sacrificed, and tissue and plasma samples were obtained. Plasma concentrations of FSH and LH were significantly higher in pituitary-grafted mice than in sham-operated controls. Testicular LH/human chorionic gonadotropin (hCG) binding, measured via use of [125I]iodo-hCG, was significantly depressed both on a per milligram protein and per testes basis in hyperprolactinemic mice. Coincident with decreased hCG binding was a significantly diminished ability of decapsulated testes to produce testosterone in response to hCG in vitro. However, testosterone production by unstimulated hyperprolactinemic mouse testes was normal. Significantly increased body, seminal vesicle, and adrenal weights were also present in hyperprolactinemic mice. The data indicate that hyperprolactinemia in mice is associated with decreased testicular LH/hCG binding and a concomitant decrease in the responsiveness to hCG in vitro. These actions may be mediated by increased plasma LH concentrations.
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The time course of stress-induced testicular hyposensitivity to gonadotropins was studied in hypophysectomized or naloxone-treated rats exposed to various periods of immobilization. Blood was collected from a chronically indwelling intra-atrial catheter every hour for luteinizing hormone (LH) and testosterone (T) measurement. Eight hours of immobilization completely suppressed T secretion without significant effect on LH. Human chorionic gonadotropin (hCG, 5 IU/rat, i.m.) induced a marked increase in plasma T levels in normal control groups 3 h post-injection while in immobilized rats the response was completely abolished, even after only 30 min of stress. In hypophysectomized rats, as expected, plasma T levels were undetectable, but, contrary to results obtained in normal animals, hCG induced a similar increase of plasma T levels both in control and stressed rats. Immobilization stress failed to inhibit plasma T values in hypophysectomized rats pretreated for 4 days with human menopausal gonadotropin (hMG) + hCG, while it did so in similarly treated normal animals. Naloxone induced a rise of plasma LH and T levels in control rats, but did not antagonize the stress-induced fall of plasma T concentration. In all groups, steroid testicular content mimicked variations of plasma T values. In particular, in stressed animals the lack of accumulation of testicular 17-hydroxyprogesterone probably reflected a normal activity of 17-20 lyase. These results indicate that stress induces very rapidly a state of Leydig cell hyposensitivity to gonadotropins and a blockade of T biosynthesis. The causal relationship between the two effects is presently not clear but these events seem to be due to stress-induced release of an inhibitory factor of pituitary origin other that endorphin.
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Abstract Colorectal cancer, the third leading cause of cancer deaths in America, has a poor clinical outcome once the disease has progressed to stage IV metastatic cancer. Five-year survivorship of stage IV is only 10%, but survivorship of stage I is drastically higher at 90%. Therefore, understanding the early stages of colorectal cancer metastasis is critical to develop therapeutic strategies for treating and preventing stage IV colorectal cancer. Using an orthotopic model for colorectal cancer metastasis, we have observed that our highly metastatic cell line produces a pre-metastatic upregulation of Lipocalin-2 both in circulation and in the liver. Overexpression of Lipocalin-2 in our highly metastatic cell line led to an overall reduction of circulating iron. Lipocalin-2 is upregulated in many primary tumors of epithelial origin, but the role of Lipocalin-2 in metastasis remains unclear. The full effects and implications of Lipocalin-2 in colorectal cancer metastasis remain to be elucidated. Citation Format: Daniel Titus Hughes. The role of Lipocalin-2 in colorectal cancer metastasis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2097A. doi:10.1158/1538-7445.AM2014-2097A
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Decreased serum testosterone has been reported in old male rats, but in vivo studies have shown decreased gonadotropin levels and normal testis response to 120 min or more of gonadotropin stimulation, leaving doubt as to whether an aging defect exists in the Leydig cell per se. We compared the function of Leydig cells from old Wistar rats (22-25 months) with cells from mature rats (6-9 months) in vitro. The cells from old rats showed a 77% diminution in testosterone secretory response to hCG after incubation with various concentrations of hCG for 120 min. Cells from old animals reached a maximum response at a hCG concentration of 0.2 ng⁄ml, and cells from mature rats reached a maximum response at a hCG concentration of 0.5 ng⁄ml. Testosterone secretory response to 0.2 and 0.5 ng/ml hCG was also diminished in the old animals after incubations ranging from 60-180 min Leydig cells from old rats had 27% fewer gonadotropin receptors than mature rats (P < 0.001); however, total intracellular cAMP and protein-bound cAMP increases after hCG were not significantly different. Our findings point to the development of an intrinsic Leydig cell defect with age in the strain of rats studied, not reversible by hCG stimulation up to 3 h in vitro. They also suggest that the alteration responsible for the testosterone secretory hyporesponsiveness of Leydig cells from old rats is probably not attributable to a reduction in gonadotropin receptors or deficient cAMP production.
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The enzyme 3β-hydroxysteroid dehydrogenase/ Δ5-Δ4 isomerase (3β-HSD) catalyzes an obligatory step in the conversion of pregnenolone and other 5-ene-3β-hydroxysteroids into progesterone as well as precursors of all androgens and estrogens in the ovary. Since 3β-HSD is likely to be an important target for regulation by pituitary hormones, we have studied the effect of chronic treatment with LH (hCG), FSH, and PRL on ovarian 3β-HSD expression and activity in hypophysectomized adult female rats. Human CG (hCG) [10 IU, twice a day (bid)], ovine FSH (0.5 μg, bid), and ovine PRL (1 mg, bid) were administered, singly or in combination, for a period of 10 days starting 15 days after hypophysectomy. In hypophysectomized rats, PRL exerted a potent inhibitory effect on all the parameters studied. In fact, PRL caused a 81% decrease in ovarian 3β-HSD mRNA content accompanied by a similar decrease in 3β-HSD activity and protein levels. In addition, ovarian weight decreased by 40% whereas serum progesterone fell dramatically from 1.92 nmol/liter to undetectable levels after treatment with PRL. Whereas hCG alone had only slight stimulatory effects on 30- HSD mRNA, protein content and activity levels, treatment with the gonadotropin partially or completely reversed the potent inhibitory effects of oPRL on all the parameters measured. FSH, on the other hand, had no significant effect on 3β-HSD expression and activity. In situ hybridization experiments using the 35S-labeled rat ovary 30-HSD cDNA probe show that the inhibitory effect of PRL is exerted primarily on luteal cell 3β-HSD expression and activity. On the other hand, it can be seen that hCG stimulates 3/8-HSD mRNA accumulation in interstitial cells. The present data show that hCG and PRL exert potent and opposite cell-specific effects on ovarian 3j8-HSD expression, activity, and content in the rat ovary. Moreover, the present study could suggest that female infertility associated with hyperprolactinemia in women could well be related, at least in part, to the potent inhibitory effect of PRL on ovarian 3β-HSD expression and activity. (Endocrinology127: 2726–2737,1990)
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An isolated deficiency of pituitary gonadotropins was demonstrated in six 46 XY males, 22 to 36 years of age, with and without anosmia. Undetectable or low levels of serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) clearly separated hypogonadotropic from normal adult males. Chronic (8-12 wk) administration of clomiphene citrate caused no increase in serum FSH or LH in gonadotropin-deficient subjects. However, the administration of synthetic luteinizing hormone releasing factor (LRF) resulted in the appearance of serum LH and, to a lesser degree, serum FSH in three subjects tested. While levels of plasma testosterone were significantly lower in gonadotropin-deficient subjects, plasma androstenedione and dehydroepiandrosterone were in a range similar to that of age-matched normal men. Treatment with human chorionic gonadotropin (HCG) increased levels of plasma testosterone to normal adult male values in all gonadotropin-deficient subjects. Cessation of treatment with HCG resulted in the return of plasma testosterone to low, pretreatment levels. That HCG therapy with resultant normal levels of plasma testosterone may somehow stimulate endogenous gonadotropin secretion in gonadotropin-deficient subjects was not evident. The adult male levels of serum FSH and LH after LRF, and plasma testosterone after HCG, confirm pituitary and Leydig cell responsiveness in these subjects.
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Abstract. This study investigates the ability of the testis in the cryptorchid state to bind luteinizing hormone (LH) and prolactin (Prl). For this purpose, rats were made bilaterally cryptorchid at 21 days of age; sham-operated rats were used as controls. At 56 days, the animals were injected with saline or with increasing doses of human chorionic gonadotropin (hCG: 1, 10 or 100 IU) and killed 8 or 24 h after injection. Cryptorchidism and injection of hCG did not alter plasma Prl levels. In cryptorchid rats, both LH and Prl binding expressed in pmol/testis were lower than in shamoperated controls (about 75% and 65%, respectively), but unchanged (LH binding) or increased (Prl binding) when expressed in pmol/g testis. In controls, 100 IU hCG induced a significant decrease in LH binding at 24 h. Prl binding was also significantly lower in controls injected with 100 IU hCG than in those injected with 1 or 10 IU hCG, at 8 h. In cryptorchid rats injected with 100 IU hCG, the LH binding fell 8 h and 24 h after injection; at 24 h, hCG reduced Prl binding. In conclusion, there was a considerable decrease in LH and Prl receptors in the abdominal testes. The negative regulation of these receptors in response to hCG was maintained, but at times and for doses which differed from those observed in scrotal testes.
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