Emons, Günter

[["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Gruendker, Carsten"],["dc.contributor.author","Peick, D."],["dc.contributor.author","Fister, Stefanie"],["dc.contributor.author","Emons, G."],["dc.date.accessioned","2018-11-07T08:46:28Z"],["dc.date.available","2018-11-07T08:46:28Z"],["dc.date.issued","2010"],["dc.format.extent","36"],["dc.identifier.isi","000274745200095"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20699"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","Strengthening of GnRH-II antagonist-induced apoptosis via combined treatment of 40H-Tamoxifen in a case estrogen-receptor-positive breast cancer"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1223"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","International Journal of Oncology"],["dc.bibliographiccitation.lastpage","1229"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Eicke, Nicola"],["dc.contributor.author","Guenthert, Andreas R."],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T09:01:26Z"],["dc.date.available","2018-11-07T09:01:26Z"],["dc.date.issued","2006"],["dc.description.abstract","The majority of human endometrial and ovarian cancers express receptors for GnRH type I (GnRH-I). Their proliferation is time- and dose-dependently reduced by GnRH-I and its analogs. GnRH-I analogs activate a phosphotyrosine-phosphatase (PTP) and inhibit EGF-induced mitogenic signal transduction. Recently we found that GnRH type II (GnRH-II) and its agonist [D-Lys(6)]GnRH-II also have antiproliferative effects on these tumor cells which are significantly greater than those of GnRH-I agonists. In a more recent study, we showed that the antiproliferative activity of GnRH-II on human endometrial and ovarian cancer cell lines is not mediated through the GnRH-I receptor. The underlying signal transduction mechanisms of GnRH-III are still unknown. In this study we showed that the mitogenic effects of growth factors in endometrial and ovarian cancer cell lines were counteracted by GnRH-II agonist [D-LyS(6)]GnRH-II, indicating an interaction with the mitogenic signal transduction. We showed that [D-LyS6]GnRH-III reduces EGF-induced auto-tyrosine-phosphorylation of EGF-receptors via activation of a PTP and that EGF-induced activation of mitogen-activated protein kinase was blocked in cells treated with [D-Lys(6)]GnRH-H. Furthermore, EGF-induced expression of the immediate early gene c-fos was inhibited by treatment with [D-Lys(6)]GnRH-II. After knock-out of GnRH-I receptor expression, GnRH-H agonist [D-LyS(6)]GnRH-II still activated PTP and inhibited the EGF-induced mitogenic signal transduction. These data indicate, that the effects of GnRH-H are not due to a cross-reaction with the GnRH-I receptor. In conclusion these data suggest that the si naling of GnRH-II agonist [D-LyS(6)]GnRH-H is comparable to that of GnRH-I analogs."],["dc.identifier.isi","000241476100022"],["dc.identifier.pmid","17016655"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24424"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Professor D A Spandidos"],["dc.relation.issn","1019-6439"],["dc.title","GnRH-II agonist [D-Lys(6)]GnRH-II inhibits the EGF-induced mitogenic signal transduction in human endometrial and ovarian cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","988"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Journal of Cancer"],["dc.bibliographiccitation.lastpage","997"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Untch, Michael"],["dc.contributor.author","Eidtmann, H."],["dc.contributor.author","du Bois, Andreas"],["dc.contributor.author","Meerpohl, H. G."],["dc.contributor.author","Thomssen, C."],["dc.contributor.author","Ebert, Andreas"],["dc.contributor.author","Harbeck, N."],["dc.contributor.author","Jackisch, C."],["dc.contributor.author","Heilman, V."],["dc.contributor.author","Emons, G."],["dc.contributor.author","Wallwiener, D."],["dc.contributor.author","Wiese, W."],["dc.contributor.author","Blohmer, Jens-Uwe"],["dc.contributor.author","Hoffken, K."],["dc.contributor.author","Kuhn, W."],["dc.contributor.author","Reichardt, Peter"],["dc.contributor.author","Muscholl, M."],["dc.contributor.author","Pauschinger, M."],["dc.contributor.author","Langer, B."],["dc.contributor.author","Luck, H. J."],["dc.date.accessioned","2018-11-07T10:49:11Z"],["dc.date.available","2018-11-07T10:49:11Z"],["dc.date.issued","2004"],["dc.description.abstract","This prospective, parallel-group, dose-escalation study evaluated the cardiac safety of trastuzumab (Herceptin((R))) plus epirubicin/ cyclophosphamide (EC) in women with human epidermal growth factor receptor-2 (HER2)-positive metastatic breast cancer (MBC) and determined an epirubicin dose for further evaluation. HER2-positive patients received standard-dose trastuzumab plus epirubicin (60 or 90 mg/m(2))/cyclophosphamide (600 mg/m(2)) 3-weekly (EC60 + H, n = 26; EC90 + H, n = 25), for four to six cycles; 23 HER2-negative patients received EC alone (90/600 mg/m(2)) 3-weekly for six cycles (EC90). All patients underwent thorough cardiac evaluation. Two EC90 + H-treated patients experienced symptomatic congestive heart failure 4.5 and 6 months after the end of chemotherapy. One EC60 + H-treated patient experienced an asymptomatic decrease in left ventricular ejection fraction (LVEF) to < 50% 6 months after the end of chemotherapy. No such events occurred in control patients. Asymptomatic LVEF decreases of > 10% points were detected in 12 (48%), 14 (56%) and 5 (24%) patients treated with EC60 + H, EC90 + H, and EC90. Objective response rates with EC60 + H and EC90 + H were > 60%, and 26% for EC90 alone. These results indicate that trastuzumab may be combined with EC with manageable cardiotoxicity and promising efficacy. (C) 2004 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ejca.2004.01.011"],["dc.identifier.isi","000221467400017"],["dc.identifier.pmid","15093573"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48372"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0959-8049"],["dc.title","Cardiac safety of trastuzumab in combination with epirubicin and cyclophosphamide in women with metastatic breast cancer: results of a phase I trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Geburtshilfe und Frauenheilkunde"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Stein, W."],["dc.contributor.author","Brockhausen, S."],["dc.contributor.author","Bilgin, F."],["dc.contributor.author","de Lange, D."],["dc.contributor.author","Emons, G."],["dc.date.accessioned","2018-11-07T11:11:26Z"],["dc.date.available","2018-11-07T11:11:26Z"],["dc.date.issued","2008"],["dc.format.extent","S38"],["dc.identifier.isi","000259577500156"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53436"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.issn","0016-5751"],["dc.title","Subpartual asphyxia in infants with a weight over > 2500g in Mekane Hiwot Hospital in Eritrea, South Africa"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","436"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Geburtshilfe und Frauenheilkunde"],["dc.bibliographiccitation.lastpage","445"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Hadji, P."],["dc.contributor.author","Rabe, Tamara I."],["dc.contributor.author","Ortmann, Olaf"],["dc.contributor.author","Mueck, Alfred O."],["dc.contributor.author","von Holst, T."],["dc.contributor.author","Emons, G."],["dc.contributor.author","Schulz, Klaus-Dieter"],["dc.date.accessioned","2018-11-07T10:30:14Z"],["dc.date.available","2018-11-07T10:30:14Z"],["dc.date.issued","2002"],["dc.description.abstract","The multifactorial disease of osteoporosis is one of the most frequent diseases, affecting about 5 - 6 Mio. postmenopausal women in Germany, today. In spite of the introduction of new technologies of fracture risk assessment and new pharmacological opportunities the incidence of fracture is still increasing. Therefore, early identification of women at high risk as well as early and individualised preventive measures are essential in the prevention of osteoporosis. Changes of dietary habits as well as lifestyle including an increase in physical activity are of up most importance. In addition to Calcium and Vitamin D supplementation, hormone replacement therapy (HRT) is accepted as the first line and cost effective pharmacological treatment for the prevention of osteoporosis. Numerous cross sectional, case-control and prospective studies showing the effect of HRT on bone reabsorption and bone mineral density (BMD) have been published. HRT reduces bone turnover which is followed by an increase of BMD. A number of case-control and cohort studies as well as a few recent prospective studies have been investigating the effect of HRT on osteoporosis related fracture. These studies confirm that HRT leads to a significant decrease of osteoporosis related fracture (Hip fracture by > 25 %). However, randomised, prospective studies are needed to underline the effect on osteoporosis related fracture. Although the effect of HRT on BMD is independent of both, the age at which treatment is started and the route of administration, a dose-response relation as well as a greater response in patients with a lower initial BMD has been reported. Since bone is lost rapidly when treatment is stopped, the duration of treatment is clinically important in evaluating the effect of HRT on BMD. Hereby, a duration of 10 years and more seems desirable. Since the ongoing controversial discussion on the duration dependent increase of the incidence of breast cancer and the discussion on secondary prevention of cardiovascular disease, any therapy decision must be individually evaluated. The following article gives a systematical review on the recent literature regarding the influence of HRT on BMD and osteoporosis related fracture."],["dc.identifier.doi","10.1055/s-2002-32281"],["dc.identifier.isi","000176216100002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43820"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0016-5751"],["dc.title","The possible role of estrogens and progestagens in the prevention of osteoporosis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Miller, David S."],["dc.contributor.author","Gabra, Hani"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","McMeekin, D. Scott"],["dc.contributor.author","Oza, Amit M."],["dc.contributor.author","Temkin, Sarah Madhu"],["dc.contributor.author","Vergote, Ignace"],["dc.date.accessioned","2018-11-07T09:40:07Z"],["dc.date.available","2018-11-07T09:40:07Z"],["dc.date.issued","2014"],["dc.identifier.isi","358613202168"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33440"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Oncology"],["dc.publisher.place","Alexandria"],["dc.relation.conference","50th Annual Meeting of the American-Society-of-Clinical-Oncology"],["dc.relation.eventlocation","Chicago, IL"],["dc.relation.issn","1527-7755"],["dc.relation.issn","0732-183X"],["dc.title","ZuptEC: Phase III study or zuptarelin doxorubicin (AEZS-108) te platinum-taxane pretreated endontetrial cancer (Study AEZS-108-050)"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1334"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","The Journal of Obstetrics and Gynaecology Research"],["dc.bibliographiccitation.lastpage","1342"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Gründker, Carsten"],["dc.contributor.author","Wokoun, Ulrike"],["dc.contributor.author","Hellriegel, Martin"],["dc.contributor.author","Emons, Günter"],["dc.date.accessioned","2020-12-10T18:29:03Z"],["dc.date.available","2020-12-10T18:29:03Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1111/jog.13980"],["dc.identifier.eissn","1447-0756"],["dc.identifier.issn","1341-8076"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76505"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Inhibition of aerobic glycolysis enhances the anti‐tumor efficacy of Zoptarelin Doxorubicin in triple‐negative breast cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Hellinger, Johanna W."],["dc.contributor.author","Schömel, Franziska"],["dc.contributor.author","Buse, Judith V."],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Emons, Günter"],["dc.contributor.author","Gründker, Carsten"],["dc.date.accessioned","2021-04-14T08:31:47Z"],["dc.date.available","2021-04-14T08:31:47Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1038/s41598-020-74838-8"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17824"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83712"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2045-2322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Identification of drivers of breast cancer invasion by secretome analysis: insight into CTGF signaling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","65"],["dc.bibliographiccitation.journal","Reproductive biology and endocrinology"],["dc.bibliographiccitation.lastpage","7"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Gründker, Carsten"],["dc.contributor.author","Emons, Günter"],["dc.date.accessioned","2019-07-09T11:41:55Z"],["dc.date.available","2019-07-09T11:41:55Z"],["dc.date.issued","2003"],["dc.description.abstract","The expression of GnRH (GnRH-I, LHRH) and its receptor as a part of an autocrine regulatory system of cell proliferation has been demonstrated in a number of human malignant tumors, including cancers of the ovary. The proliferation of human ovarian cancer cell lines is time- and dose-dependently reduced by GnRH and its superagonistic analogs. The classical GnRH receptor signal-transduction mechanisms, known to operate in the pituitary, are not involved in the mediation of antiproliferative effects of GnRH analogs in these cancer cells. The GnRH receptor rather interacts with the mitogenic signal transduction of growth-factor receptors and related oncogene products associated with tyrosine kinase activity via activation of a phosphotyrosine phosphatase resulting in downregulation of cancer cell proliferation. In addition GnRH activates nucleus factor ?B (NF?B) and protects the cancer cells from apoptosis. Furthermore GnRH induces activation of the c-Jun N-terminal kinase/activator protein-1 (JNK/AP-1) pathway independent of the known AP-1 activators, protein kinase (PKC) or mitogen activated protein kinase (MAPK/ERK). Recently it was shown that human ovarian cancer cells express a putative second GnRH receptor specific for GnRH type II (GnRH-II). The proliferation of these cells is dose- and time-dependently reduced by GnRH-II in a greater extent than by GnRH-I (GnRH, LHRH) superagonists..."],["dc.identifier.doi","10.1186/1477-7827-1-65"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/1258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58547"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","616.99"],["dc.subject.ddc","618.1"],["dc.title","Role of gonadotropin-releasing hormone (GnRH) in ovarian cancer ; Review"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","549"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Oncology Reports"],["dc.bibliographiccitation.lastpage","554"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Ziegler, Elke"],["dc.contributor.author","Olbrich, Teresa"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T09:28:41Z"],["dc.date.available","2018-11-07T09:28:41Z"],["dc.date.issued","2013"],["dc.description.abstract","Kisspeptins are peptides derived from the metastasis suppressor gene KISS1 interacting with GPR54 as their corresponding receptor. The KISS1/GPR54 system is one regulator of cellular motility mechanisms leading to decreased migration and invasion. Its role in cell proliferation processes is not clearly understood. In this study, breast cancer cell lines, T47D, ZR75-1, MDA-MB-231, MDA-MB-435s, MDA-MB-453, HCC 70, HCC 1806, HCC 1937 and MCF-7, were investigated for their endogenous GPR54 expression by immunocytochemistry, RT-PCR and western blot analysis. The effect of kisspeptin-10 on proliferation was measured in MDA-MB-231, MDA-MB-435s, HCC 1806 and MCF-7 cells. Further experiments on proliferation were carried out with cells transfected with GPR54. All of the tested breast cancer cell lines expressed GPR54 in different amounts. No effects on proliferation were detected in the breast cancer cells expressing the receptor endogenously. In transfected neuronal cells overexpressing GPR54, proliferation was significantly inhibited by kisspeptin-10. The results indicate that the antiproliferative action of kisspeptin depends on the nature of GPR54 expression. The effect was detected in an artificial system of cells transfected with GPR54 and not in cells expressing the receptor endogenously. Thus, the antiproliferative action of kisspeptin seems not to be important for pathophysiological processes."],["dc.description.sponsorship","Deutsche Krebshilfe, Dr Mildred Scheel Stiftung"],["dc.identifier.doi","10.3892/or.2012.2135"],["dc.identifier.isi","000313605100021"],["dc.identifier.pmid","23152107"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30839"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Spandidos Publ Ltd"],["dc.relation.issn","1021-335X"],["dc.title","Antiproliferative effects of kisspeptin-10 depend on artificial GPR54 (KISS1R) expression levels"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]