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Emons, Günter
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Emons, Günter
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Emons, Günter
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Emons, Guenter
Emons, G.
Emons, Günther
Emons, Guenther
Emons, Gunther
Emons, Gunter
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2001Review [["dc.bibliographiccitation.firstpage","340"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.lastpage","345"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Krauss, T."],["dc.contributor.author","Nia, A. H."],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Emons, G."],["dc.date.accessioned","2018-11-07T08:50:17Z"],["dc.date.available","2018-11-07T08:50:17Z"],["dc.date.issued","2001"],["dc.description.abstract","Cervical cancer is world-wide the second most frequent cancer found in women and represents 12% of all female malignancies. In fact, it is the most common female cancer in developing countries. There is now sufficient evidence to recommend that women with locally advanced cervical cancer confined to the pelvis receive concurrent pelvic radiation and chemotherapy. New surgical techniques such as laparoscopically assisted radical vaginal hysterectomy and trachelectomy (a fertility-preserving radical operation technique) are being, established and have to be evaluated for their long-term safety. Causal treatment by developing multivalent antiviral drugs and vaccines is no longer a pure theoretical approach. Despite these improvements, the early diagnosis by colposcopy and gynaecological cytology remains the safest method to ensure early treatment avoiding death of cervical cancer."],["dc.identifier.doi","10.1159/000055105"],["dc.identifier.isi","000171132700004"],["dc.identifier.pmid","11574761"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21661"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","0378-584X"],["dc.title","New developments in the treatment of cervical cancer"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2002Journal Article [["dc.bibliographiccitation.firstpage","725"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cellular Biochemistry"],["dc.bibliographiccitation.lastpage","735"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Grundker, Carsten"],["dc.contributor.author","Blaschke, S."],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Hofbauer, L. C."],["dc.date.accessioned","2018-11-07T10:33:20Z"],["dc.date.available","2018-11-07T10:33:20Z"],["dc.date.issued","2002"],["dc.description.abstract","The anti-resorptive effects of estrogen on bone metabolism are thought to be mediated through modulation of paracrine factors produced by osteoblastic lineage cells that act on osteoclastic lineage cells. Receptor activator of nuclear factor-kappaB ligand (RANKL) is the essential factor for osteoclast formation and activation and enhances bone resorption. By contrast, osteoprotegerin (OPG), which is produced by osteoblastic lineage cells acts as a decoy receptor that neutralizes RANKL and prevents bone loss. Recently, 17beta-estradiol was found to stimulate OPG mRNA levels and protein secretion in a human osteoblastic cell line through activation of the estrogen receptor (ER)-alpha. In this study, we assessed the effects of the phytoestrogen genistein on OPG mRNA steady state levels (by semiquantitative RT-PCIR and Northern analysis) and protein production (by ELISA) in primary human trabecular osteoblasts (hOB) obtained from healthy donors. Genistein increased OPG mRNA levels and protein secretion by hOB cells by up to two- to six-fold in a dose- (P< 0.0001) and time-dependent (P< 0.0001) fashion with a maximum effect at 10(-7) M. Co-treatment with the pure ER antagonist ICI 182,780 completely abrogated the stimulatory effects of genistein on OPG protein secretion, indicating that these effects were specific and directly mediated through the ER. Pre-treatment with genistein partially prevented the inhibitory effects of the glucocorticoid dexamethasone on OPG mRNA and protein production. The stimulation of OPG mRNA levels by genistein was not affected by the protein synthesis inhibitor, cycloheximide and was shown to be due to enhancement of OPG gene transcription. In conclusion, our data suggest that the phytoestrogen genistein is capable of upregulating the production of OPG by human osteoblasts. Thus, dietary sources of phytoestrogens may help to prevent bone resorption and bone loss by enhanced osteoblastic production of OPG. (C) 2002 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jcb.10087"],["dc.identifier.isi","000173618800008"],["dc.identifier.pmid","11835398"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44583"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0730-2312"],["dc.title","Phytoestrogen genistein stimulates the production of osteoprotegerin by human trabecular osteoblasts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2004Journal Article [["dc.bibliographiccitation.firstpage","277"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Ultrasound in Obstetrics and Gynecology"],["dc.bibliographiccitation.lastpage","283"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Pauer, H. U."],["dc.contributor.author","Bader, Werner"],["dc.contributor.author","Oppermann, Martin"],["dc.contributor.author","Hilgers, Ralf-Dieter"],["dc.contributor.author","Gauruder-Burmester, A."],["dc.contributor.author","Lange, Rainer"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Hackenberg, R."],["dc.contributor.author","Krauss, T."],["dc.date.accessioned","2018-11-07T10:51:05Z"],["dc.date.available","2018-11-07T10:51:05Z"],["dc.date.issued","2004"],["dc.description.abstract","Objective To assess the topography of the bladder neck by introital ultrasound before and after open colposuspension. Methods Three hundred and ten women with urodynamically proven stress urinary incontinence were included in this long-term study to investigate the position and function of the bladder neck at rest and during straining. Height (H), distance (D), and urethrovesical angle of the bladder neck (beta) were measured by means of preoperative and postoperative introital ultrasound. Women were followed up; 152 of them (49%) completed 48 months of follow-up. Results At the 6-month follow-up examination, 90.0% of the women were continent (279/310), 3.5% (11/310) showed voiding difficulties, 3.5% (11/310) had urgency, and 1.6% (5/310) bad developed de novo urge incontinence. At the 48-month follow-up, 76.8% of the patients were still continent. All postoperative measurements yielded significantly lower values for angle beta at rest and during straining compared with the preoperative results (P < 0.0001). The median linear movement of the bladder neck during straining decreased from 18.0 mm before surgery to 6.4 mm at the 48-month follow-up (P < 0.0001). The median level of ventrocranial elevation of the vesicourethral junction was 14.3 mm immediately after surgery, 9.9 mm after 6 months and 6.6 mm after 48 months. The degree of surgical bladder-neck elevation was associated with postoperative urgency/de novo urge incontinence (P < 0.0001) and voiding difficulty (P < 0.0001). Conclusions The colposuspension procedure reduces angle at rest and during straining, restricts linear movement with straining, and elevates the bladder neck. Perioperative introital ultrasound improves understanding of this surgical procedure and might help to prevent postoperative complications. Copyright (C) 2004 ISUOG. Published by John Wiley Sons, Ltd."],["dc.identifier.doi","10.1002/uog.982"],["dc.identifier.isi","000220287300014"],["dc.identifier.pmid","15027018"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48802"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","John Wiley & Sons Ltd"],["dc.relation.issn","0960-7692"],["dc.title","Introital ultrasound of the lower genital tract before and after colposuspension: a 4-year objective follow-up"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2004Journal Article [["dc.bibliographiccitation.firstpage","1136"],["dc.bibliographiccitation.issue","7-8"],["dc.bibliographiccitation.journal","TISSUE ENGINEERING"],["dc.bibliographiccitation.lastpage","1147"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Haase, Detlef"],["dc.contributor.author","Vehmeyer, K."],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Truemper, Lorenz H."],["dc.date.accessioned","2018-11-07T10:47:58Z"],["dc.date.available","2018-11-07T10:47:58Z"],["dc.date.issued","2004"],["dc.description.abstract","Progenitor cells with differentiation capacity along multiple mesengenic lineages are attractive tools for numerous purposes in regenerative medicine. Such mesengenic progenitor cells have been isolated from adult mammalian bone marrow, and we here report placental tissue as an alternative source for these cells. By means of dissection/proteinase digestion techniques, high numbers of viable mononuclear cells were harvested from human placenta at term, and a mesenchymal cell population with characteristic expression of CD9, CD29, and CD73 was obtained in culture. The in vitro growth behavior of such placenta-derived mesengenic cells was similar to that of human bone marrow mesengenic progenitor cells. After in vitro propagation for more than three passages the cells were exclusively of maternal origin. Differentiation experiments showed differentiation potential along osteogenic, chondrogenic, adipogenic, and myogenic lineages. In conclusion, we propose human term placenta as an easily accessible, ample source of multipotent mesengenic progenitor cells."],["dc.identifier.doi","10.1089/ten.2004.10.1136"],["dc.identifier.isi","000223851200017"],["dc.identifier.pmid","15363170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48088"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mary Ann Liebert Inc"],["dc.relation.issn","1076-3279"],["dc.title","Mesengenic progenitor cells derived from human placenta"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2005Journal Article [["dc.bibliographiccitation.firstpage","574"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Prenatal Diagnosis"],["dc.bibliographiccitation.lastpage","576"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Schluter, G."],["dc.contributor.author","Steckel, M."],["dc.contributor.author","Schiffmann, H."],["dc.contributor.author","Harms, K."],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Pauer, H. U."],["dc.date.accessioned","2018-11-07T09:39:50Z"],["dc.date.available","2018-11-07T09:39:50Z"],["dc.date.issued","2005"],["dc.description.abstract","Prenatal molecular genetic diagnosis for Noonan syndrome I is reported. Noonan syndrome was suspected because of large cystic hygroma colli, massive pleural effusion and ascites at 23 weeks of gestation and normal karyotype (46,XX). DNA was prepared from amnion cells and screened for mutations in the PTPN11 gene. In exon 8, a missense mutation (S285F) was found. Delivery was induced at 33 weeks of gestation because of silent cardiotocography (CTG). Despite immediate drainage of the hydrothorax, mechanical ventilation was insufficient and the child died 9 h after birth due to severe pulmonary hypoplasia. Pleural punctate was enriched for small lymphocytes and thus was characterized as chylus. Prenatal ultrasound findings in Noonan syndrome usually are unspecific and rarely lead to a diagnosis. However, with the combination of cystic hygroma, pleural effusion, ascites and normal karyotype Noonan syndrome should be considered and DNA testing for PTPN11 mutations may be appropriate. Malformations of lymphatic vessels and/or chylothorax in Noonan syndrome seem to be more frequent than usually anticipated. Copyright (c) 2005 John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/pd.1189"],["dc.identifier.isi","000230969000008"],["dc.identifier.pmid","16032767"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33379"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","John Wiley & Sons Ltd"],["dc.relation.issn","0197-3851"],["dc.title","Prenatal DNA diagnosis of Noonan syndrome in a fetus with massive hygroma colli, pleural effusion and ascites"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2003Journal Article [["dc.bibliographiccitation.firstpage","86"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","GYNAKOLOGE"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Gunthert, Andreas R."],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Hanf, Volker"],["dc.date.accessioned","2018-11-07T10:41:18Z"],["dc.date.available","2018-11-07T10:41:18Z"],["dc.date.issued","2003"],["dc.description.abstract","Endometrial cancer is, apart from breast cancer, the most common gynecologic malignancy in western industrialized countries with a mortality. rate of ca 20-25%. Estrogen-associated endometrial cancer (type 1) has a favourable prognosis; but the non-estrogen-related type 2 tends to have a poor outcome. Endometrial hyperplasias without atypia can be safely treated with endocrine interventions. Conservative treatment of atypical endometrial hyperplasias should be reserved for women who wish to preserve their fertility, provided a thorough histological follow-up is possible. The cornerstone of the treatment of invasive endometrial cancer is radical surgery including complete pelvic and para-aortic lymphonodectomy in tumors larger than stage 1a or with other risk factors. The routine use of adjuvant teletherapy is not indicated when correct surgical staging as been performed. There are no evidence based recommendations for adjuvant hormonal or chemotherapy. In patients with disseminated endometrial cancer, endo-crine therapy is a reasonable initial approach. Palliative chemotherapy is indicated after the failure of an endocrine treatment, in patients. with receptor-negative tumors, or when life threatening tumor manifestations require a fast response."],["dc.identifier.doi","10.1007/s00129-002-1321-2"],["dc.identifier.isi","000181666600002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46500"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0017-5994"],["dc.title","Endocrine therapy of endometrial cancer and endometrial hyperplasia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI WOS2003Journal Article [["dc.bibliographiccitation.firstpage","58"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.lastpage","60"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Pauer, H. U."],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Krauss, T."],["dc.date.accessioned","2018-11-07T10:41:27Z"],["dc.date.available","2018-11-07T10:41:27Z"],["dc.date.issued","2003"],["dc.description.abstract","Background: Metastasis of distant malignancies to the cervix uteri is a rare occurrence and the frequency is approximately 4% for all tumours. However, the frequency of cervical metastasis of breast cancer is much lower and is estimated to range between 0.8 and 1.7%. With the exception of ovarian metastases, secondary tumours of the female genital tract are rather uncommon. Therefore, these conditions pose diagnostic problems for the clinician. Patient: A 40-year-old woman with the diagnosis of invasive ductal cell carcinoma of the right breast underwent mastectomy with dissection of axillary lymph nodes in 1998. Subsequently, the patient received 6 cycles of chemotherapy with cyclophosphamide, methotrexate and fluorouracil. The initial tumour stage was pT2, pN0 (0/13), M0, G2. The oestrogen and progesterone receptors were positive and expression of the C-erb-B2 coding oncogene was negative. Gynaecological and ultrasonographic examination revealed a normal cervix without evident lesions. Exfoliative cytology was negative. 14 months after treatment the patient presented with an axillary relapse and surgery, second-line chemotherapy with doxorubicine and radiation therapy of the chest wall and the axilla were performed. The patient developed liver metastases 14 months later and at this time ultrasonographic pelvic examination revealed a 2.2 cm tumour of the cervix with good vascularisation. The patient had no clinical symptoms, i.e. no vaginal bleeding or discharge. Sonomorphologically this tumour appeared as a leiomyoma of the cervix. Cervical biopsies and curettage, however, revealed metastatic carcinoma expressing oestrogen and progesterone receptors consistent with the primary breast cancer. Under palliative chemotherapy with docetaxel progression of liver metastases and cervical metastasis occurred and the patient died 9 months later. Conclusion: Metastatic involvement of the cervix should be considered in women with a history of breast cancer who present with vaginal bleeding or suspicious changes of the cervix on transvaginal ultrasound. Therefore, gynaecological and ultrasonographic examination of the pelvis represent an important part of the follow-up investigations in women with primary breast cancer."],["dc.identifier.doi","10.1159/000069865"],["dc.identifier.isi","000181695300008"],["dc.identifier.pmid","12624519"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46534"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","0378-584X"],["dc.title","Uterine cervical metastasis of breast cancer: A rare complication that may be overlooked"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2004Conference Abstract [["dc.bibliographiccitation.journal","Journal of Bone and Mineral Research"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Grundker, Carsten"],["dc.contributor.author","Blaschke, S."],["dc.contributor.author","Frosch, Karl-Heinz"],["dc.contributor.author","Schoppet, M."],["dc.contributor.author","Emons, G."],["dc.contributor.author","Hofbauer, L. C."],["dc.date.accessioned","2018-11-07T10:45:17Z"],["dc.date.available","2018-11-07T10:45:17Z"],["dc.date.issued","2004"],["dc.format.extent","S143"],["dc.identifier.isi","000224326800562"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47470"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Bone & Mineral Res"],["dc.publisher.place","Washington"],["dc.relation.conference","26th Annual Meeting of the American-Society-for-Bone-and-Mineral-Research"],["dc.relation.eventlocation","Seattle, WA"],["dc.relation.issn","0884-0431"],["dc.title","An isopropanolic extract of Cimicifuga racemosa (black cohosh) stimulates osteoprotegerin production by primary human osteoblasts."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2003Journal Article [["dc.bibliographiccitation.firstpage","4206"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","The Journal of Clinical Endocrinology & Metabolism"],["dc.bibliographiccitation.lastpage","4213"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Grundker, Carsten"],["dc.contributor.author","Blaschke, S."],["dc.contributor.author","Niederkleine, B."],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Frosch, Karl-Heinz"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Hofbauer, L. C."],["dc.date.accessioned","2018-11-07T10:36:37Z"],["dc.date.available","2018-11-07T10:36:37Z"],["dc.date.issued","2003"],["dc.description.abstract","Raloxifene reduces bone loss and prevents vertebral fractures in postmenopausal women. Its skeletal effects are mediated by estrogen receptors ( ER) and their modulation of paracrine osteoblastic factors. Receptor activator of nuclear factor-kappaB ligand is essential for osteoclasts and enhances bone resorption, whereas osteoprotegerin (OPG) neutralizes receptor activator of nuclear factor-kappaB ligand. Here, we assessed the effects of raloxifene on OPG production in human osteoblasts (hOB). Raloxifene enhanced gene expression of ER-alpha and progesterone receptor. Moreover, raloxifene increased OPG mRNA levels and protein secretion by hOB in a dose- and time-dependent fashion by 2- to 4-fold with a maximum effect at 10(-7) M and after 72 h ( P < 0.001). Treatment with the ER antagonist ICI 182,780 abrogated the effects of raloxifene on OPG production. Moreover, raloxifene enhanced osteoblastic differentiation markers, type 1 collagen secretion, and alkaline phosphatase activity by 3- and 2-fold, respectively ( P < 0.001). In addition, raloxifene inhibited expression of the bone-resorbing cytokine IL-6 by 25 - 45% ( P < 0.001). In conclusion, our data suggest that raloxifene stimulates OPG production and inhibits IL-6 production by hOB. Because OPG production increases with osteoblastic maturation, enhancement of OPG production by raloxifene could be related to its stimulatory effects on osteoblastic differentiation."],["dc.identifier.doi","10.1210/jc.2002-021877"],["dc.identifier.isi","000185258700031"],["dc.identifier.pmid","12970288"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45369"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Endocrine Soc"],["dc.relation.issn","0021-972X"],["dc.title","Raloxifene concurrently stimulates osteoprotegerin and inhibits interleukin-6 production by human trabecular osteoblasts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2001Journal Article [["dc.bibliographiccitation.firstpage","651"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Journal of Endocrinology"],["dc.bibliographiccitation.lastpage","658"],["dc.bibliographiccitation.volume","145"],["dc.contributor.author","Grundker, Carsten"],["dc.contributor.author","Schlotawa, Lars"],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Emons, G."],["dc.date.accessioned","2018-11-07T08:28:12Z"],["dc.date.available","2018-11-07T08:28:12Z"],["dc.date.issued","2001"],["dc.description.abstract","Objective: The expression of luteinizing hormone-releasing hormone (LHRH) and its receptor as a part of an autocrine regulatory system of cell proliferation has been demonstrated in a number of human malignant tumours, including cancers of the endometrium. The signalling pathway through which LHRH acts in endometrial cancer is distinct from that in pituitary gonadotrophs. The LHRH receptor interacts with the mitogenic signal transduction of growth factor receptors via activation of a phosphotyrosine phosphatase, resulting in down-regulation of cancer cell proliferation. In addition, LHRH activates nucleus factor kappaB (NF kappaB) and protects the cancer cells from apoptosis. This study was conducted to investigate additional signalling mechanisms of the LHRH receptor cooperating with NF kappaB in endometrial cancer cells. Design: The LHRH agonist triptorelin-induced activator protein-1 (AP-1) activation was analysed using a pAP-1-SEAP reporter gene assay, Expression of c-jun mRNA was quantified using quantitative reverse transcription (RT)-PCR. c-Jun N-terminal kinase (JNK) activity was measured by quantification of phosphorylated c-Jun protein. Results: Treatment of Ishikawa and Eec-IA human endometrial cancer cells with 100 nM triptorelin resulted in a 3.1-fold and 3.5-fold activation of AP-1 respectively (P < 0.05). If the cells had been made quiescent, treatment with triptorelin (100 nM) resulted in a 41.7-fold and 48.6-fold increase of AP-1 activation respectively (P < 0.001). This effect was completely blocked by simultaneous treatment with pertussis toxin (PTX). A 17.6-fold and 17.3-fold increase of c-jun mRNA expression respectively (P < 0.001) was obtained after 20 min of stimulation with triptorelin (100 nM). Treatment with 1 nM triptorelin resulted in a 12.5-fold or an 11.9-fold increase, and treatment with 10 pM triptorelin resulted in a 6.5-fold or a 5.2-fold increase of maximal e-jun mRNA expression respectively (P < 0.001). Maximal c-Jun phosphorylation (68.5-fold and 60.2-fold, respectively, P < 0.001) was obtained after 90 min incubation with triptorelin (100 nM). Conclusions: These results suggest that the LHRH agonist triptorelin stimulates the activity of AP-1 in human endometrial cancer cells mediated through PTX-sensitive G-protein alpha (i). In addition, triptorelin activates JNK, known to activate AP-1. In earlier investigations we have shown that triptorelin does not activate phospholipase and protein kinase C (PKC) in endometrial cancer cells, In addition, it has been demonstrated that triptorelin inhibits growth factor-induced mitogen activated protein kinase (MAPK, ERK) activity. Thus triptorelin-induced activation of the JNK/AP-1 pathway in endometrial cancer cells is independent of the known AP-1 activators, PKC or MAPK (ERK)."],["dc.identifier.doi","10.1530/eje.0.1450651"],["dc.identifier.isi","000172217700015"],["dc.identifier.pmid","11720885"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16368"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bio Scientifica Ltd"],["dc.relation.issn","0804-4643"],["dc.title","Protein kinase C-independent stimulation of activator protein-1 and c-Jun N-terminal kinase activity in human endometrial cancer cells by the LHRH agonist triptorelin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS
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