cAMP Production by GHRH in GH-Producing Pituitary Adenoma Cells

Nakagawa, Kiyomasa; Ishizuka, Tatsuo; Shimizu, Chisato; Y, Matsuura; Wada, Nobuhiro; Kijima, Hiromichi; Ito, Yasufumi; Aida, T; Abe, Hiromi

doi:10.1055/s-2007-1003356

Cited by 4 publications

(2 citation statements)

References 3 publications

(3 reference statements)

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“…Group 1 shows a high cyclic adenosine 3',5'-monophosphate (cAMP) response to GHRH and has a normal Gs a. gene, while group 2 has an elevated basal cAMP level, a lower response to GHRH and a mutant Gs a gene. However, the dispersed cells of GH adenomas obtained from Japanese patients are reported to show a 1.4-fold or greater increase in cAMP levels after GHRH stimulation in almost all cases (28,29), and this seems compatible with the low frequency of Gs a gene mutations that we found. Some racial differences have been reported with regard to the genetic events that contribute to tumorigenesis.…”

Section: Discussionsupporting

confidence: 88%

Analysis of the Gs α gene in growth hormone-secreting pituitary adenomas by the polymerase chain reaction-direct sequencing method using paraffin-embedded tissues

Hosoi

Yokogoshi²,

Horie³

et al. 1993

Acta Endocrinologica

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of the Gs a gene in growthhormone-secreting pituitary adenomas by the polymerase chain reaction-direct sequencing method using paraffin-embedded tissues. Acta Endocrinol 1993;129:301-6. ISSN 0001-5598 We investigated the prevalence of Gs \ g=a\gene mutations in growth hormone (GH) secreting pituitary adenomas from Japanese patients with acromegaly. Forty-five GH-secreting adenomas were examined for the presence of point mutations in codons 201 or 227 of the Gs \ g=a\gene using the polymerase chain reaction-direct sequencing method and deoxyribonucleic acid extracted from paraffin-embedded tumor specimens. Mutation of codon 227 of the Gs \g=a\gene was not observed in any of the tumors, but a mis-sense mutation of codon 201 was identified in two tumors (4.4%). One lesion was a densely granulated GH cell adenoma in a patient with adenomatous goiter and breast cancer. The other was a mixed GH cell-prolactin cell adenoma in a patient with multiple endocrine neoplasia type 1 associated with parathyroid hyperplasia and a pancreatic islet cell tumor. The Gs \g=a\gene detected in parathyroid tissue and pancreatic tumor tissue was of the wild type in this second patient, and the mutation was specific to the pituitary tumor. These results suggest that point mutations of codons 201 or 227 of the Gs \g=a\gene may not be important mediators of oncogenesis for GH-secreting pituitary adenomas in Japan.

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Section: Discussionsupporting

confidence: 88%

Analysis of the Gs α gene in growth hormone-secreting pituitary adenomas by the polymerase chain reaction-direct sequencing method using paraffin-embedded tissues

Hosoi

Yokogoshi²,

Horie³

et al. 1993

Acta Endocrinologica

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show abstract

“…In an experimental setting, VIP stimulated the invasiveness of PC-3 cells [5], which as shown in the present paper, express mRNA for VPAC 1 receptors. VPAC 1 and GHRH receptors are coupled to adenylate cyclase and have similar signal transduction pathways to mitogenic stimuli comprising protein kinase A (PKA), the Ras/Raf kinases complex, and mitogen-activated protein kinase (MAP) [31][32][33][34]. Activation of PKA by neuropeptides stimulates protein kinase C, a downstream element of the androgen receptors pathway, and initiates transcription of androgen-responsive genes [35].…”

Section: Discussionmentioning

confidence: 99%

Potentiation of the inhibitory effect of growth hormone-releasing hormone antagonists on PC-3 human prostate cancer by bombesin antagonists indicative of interference with both IGF and EGF pathways

et al. 2000

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BACKGROUND In view of the involvement of various neuropeptides and growth factors in the progression of androgen‐independent prostate cancer, we investigated the effects of antagonists of growth hormone‐releasing hormone (GHRH) alone or in combination with an antagonist of bombesin/gastrin‐releasing peptide (BN/GRP) on PC‐3 human prostate cancers. METHODS Nude mice implanted with PC‐3 tumors received GHRH antagonists MZ‐5‐156 or JV‐1‐38, each at 20 μg/day s.c. In experiment 2, treatment consisted of daily injections of JV‐1‐38 (20 μg), BN/GRP antagonist RC‐3940‐II (10 μg), or a combination of JV‐1‐38 and RC‐3940‐II. Serum IGF‐I levels, expression of mRNA for IGF‐II, and characteristics of BN/GRP and EGF receptors in tumor tissue were investigated. RESULTS JV‐1‐38 induced a greater inhibition of tumor growth and suppression of IGF‐II mRNA than MZ‐5‐156, both compounds causing a similar decrease in serum IGF‐I. In experiment 2, JV‐1‐38 and RC‐3940‐II produced a comparable reduction in tumor volume (65% and 61%, respectively), but a combination of both antagonists augmented tumor inhibition to 75%. Combined treatment with JV‐1‐38 and RC‐3940‐II also led to a greater suppression of IGF‐II mRNA (92%), as compared with JV‐1‐38 (72%) or RC‐3940‐II (77%). Serum IGF‐I concentration was lowered only in mice treated with JV‐1‐38, while the downregulation of BN/GRP and EGF receptors was specific for groups receiving RC‐3940‐II. CONCLUSIONS The inhibitory effects of GHRH antagonists on PC‐3 human androgen‐independent prostate cancer can be potentiated by concomitant use of BN/GRP antagonists. The combination of both types of analogs apparently interferes with both IGF and bombesin/EGF pathways, and might be clinically useful for the management of androgen‐independent prostate cancer. Prostate 44:172–180, 2000. © 2000 Wiley‐Liss, Inc.

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Inhibition of human androgen-independent PC-3 and DU-145 prostate cancers by antagonists of bombesin and growth hormone releasing hormone is linked to PKC, MAPK and c-jun intracellular signalling

Stangelberger¹,

Schally²,

Varga³

et al. 2005

European Journal of Cancer

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cAMP Production by GHRH in GH-Producing Pituitary Adenoma Cells

Cited by 4 publications

References 3 publications

Analysis of the Gs α gene in growth hormone-secreting pituitary adenomas by the polymerase chain reaction-direct sequencing method using paraffin-embedded tissues

Analysis of the Gs α gene in growth hormone-secreting pituitary adenomas by the polymerase chain reaction-direct sequencing method using paraffin-embedded tissues

Potentiation of the inhibitory effect of growth hormone-releasing hormone antagonists on PC-3 human prostate cancer by bombesin antagonists indicative of interference with both IGF and EGF pathways

Inhibition of human androgen-independent PC-3 and DU-145 prostate cancers by antagonists of bombesin and growth hormone releasing hormone is linked to PKC, MAPK and c-jun intracellular signalling

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