Hanf, Volker

[["dc.bibliographiccitation.firstpage","334"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","International Journal of Gynecological Cancer"],["dc.bibliographiccitation.lastpage","338"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T08:31:09Z"],["dc.date.available","2018-11-07T08:31:09Z"],["dc.date.issued","2009"],["dc.description.abstract","Effects of electromagnetic fields (EMFs) on the incidence of breast cancer (BC) have been proposed by a number of epidemiological studies. The molecular mechanism of the impact of EMFs on cells is not yet clear, although changes in gene expression have been reported in various cellular systems. In this investigation, the interference of low-frequency EMFs with the plasminogen activator system was examined in BC cells. MCF-7 BC cells from 2 different sources were exposed to highly homogeneous 50-Hz EMFs. Changes in gene expression were analyzed by reverse transcriptase-polymerase chain reaction. In MCF-7 cells exposed to 1.2 mu T ENT expression of the urokinase plasminogen activator gene and of plasminogen-activator inhibitor-1 was markedly increased. The expression of the receptor for urokinase plasminogen activator was only marginally increased in I of the 2 tested cell lines and expression of the tissue plasminogen activator was at least slightly down-regulated in BC cells exposed to EMFs. EMFs may be able to increase the metastatic potential of breast tumors. The use of our newly established exposure system for EMFs may allow us to study the signaling processes involved in the induction of a metastatic phenotype of breast cancer cells."],["dc.identifier.doi","10.1111/IGC.0b013e31819f53ec"],["dc.identifier.isi","000266976600006"],["dc.identifier.pmid","19407555"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17055"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1048-891X"],["dc.title","Exposure of MCF-7 Breast Cancer Cells to Electromagnetic Fields Up-Regulates the Plasminogen Activator System"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","169"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Bioelectromagnetics"],["dc.bibliographiccitation.lastpage","176"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Gruendker, Carsten"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Hanf, Volker"],["dc.date.accessioned","2018-11-07T11:16:21Z"],["dc.date.available","2018-11-07T11:16:21Z"],["dc.date.issued","2008"],["dc.description.abstract","Breast cancer is the most common malignancy of women in Western societies. The increasing exposure to electromagnetic fields has been suspected to contribute to the rising incidence of breast cancer in industrialized Countries. The majority of breast tumors is treated with the partial antiestrogen tamoxifen. Most tumors become resistant to tamoxifen in the course of treatment resulting in treatment failure. Electromagnetic fields reduce the efficacy of tamoxifen similar to tamoxifen resistance. In this study we investigated the mechanism by which electromagnetic fields influence the sensitivity to tamoxifen. In cells exposed to 1.2 mu T of a 50 Hz electromagnetic field gene expression of cofactors of the estrogen receptors was compared to sham exposed cells. Using a gene array technology several cofactors were found to be differentially expressed. The expression of the coactivators, SRC-I and AIB 1, and of two corepressors, N-Cor and SMRT, was quantified by RT-PCR. Both coactivators were expressed more strongly in the exposed cells while the expression of two corepressors decreased. The RNA analysis was confirmed by Western blots. The contradirectional changes in gene expression of coactivators and corepressors by electromagnetic fields results in a lower sensitivity to tamoxifen. Electromagnetic fields may contribute to the induction of tamoxifen resistance in vivo. Bioelectromagnetics 29:169-176, 2008. (C) 2007 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/bem.20387"],["dc.identifier.isi","000254479100002"],["dc.identifier.pmid","18027843"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54564"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0197-8462"],["dc.title","Electromagnetic fields alter the expression of estrogen receptor cofactors in breast 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","237"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Bioelectromagnetics"],["dc.bibliographiccitation.lastpage","245"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T08:44:20Z"],["dc.date.available","2018-11-07T08:44:20Z"],["dc.date.issued","2010"],["dc.description.abstract","The growth of estrogen-receptor positive breast cancer cells is inhibited by the pineal gland hormone, melatonin. Concern has been raised that power-line frequency and microwave electromagnetic fields (EMEs) could reduce the efficiency of melatonin on breast cancer cells. In this study we investigated the impact of EMIT's on the signal transduction of the high-affinity receptor MT1 M parental MCF-7 cells and MCF-7 cells transfected with the MT1 gene. The binding of the cAMP-responsive element binding (CREB) protein to a promoter sequence of BRCA-1 after stimulation with melatonin was analyzed by a gel-shift assay and the expression of four estrogen-responsive genes was measured in sham-exposed breast cancer cells and cells exposed to a sinusoidal 50Hz EMF of 1.2 mu T for 48 h. In sham-exposed cells, binding of CREB to the promoter of BRCA-1 was increased by estradiol and subsequently diminished by treatment with melatonin. In cells exposed to 1.2 mu T, 50Hz. EMF. binding of CREB was almost completely omitted. Expression of BRCA-1, p53, p21(WAF), and c-myc was increased by estradiol stimulation and subsequently decreased by melatonin treatment in both cell lines, except for p53 expression in the transfected cell line, thereby proving the antiestrogenic effect of melatonin at molecular level. In contrast, in breast cancer cells transfected with MT1 exposed to 1.2 mu T of the 50Hz EMF, the expression of p53 and c-myc increased significantly after melatonin treatment but for p21(WAF). the increase was not significant. These results convincingly prove the negative effect of EMF on the antiestrogenic effect of melatonin in breast cancer cells. Bioelectromagnetics 31:237-245, 2010. (C) 2009 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/bem.20554"],["dc.identifier.isi","000276052600008"],["dc.identifier.pmid","19882681"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20177"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0197-8462"],["dc.title","Signal Transduction of the Melatonin Receptor MT1 Is Disrupted in Breast Cancer Cells by Electromagnetic Fields"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S74"],["dc.bibliographiccitation.journal","Experimental and Clinical Endocrinology & Diabetes"],["dc.bibliographiccitation.lastpage","S75"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T11:05:16Z"],["dc.date.available","2018-11-07T11:05:16Z"],["dc.date.issued","2007"],["dc.identifier.isi","000244865600280"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52028"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Johann Ambrosius Barth Verlag Medizinverlage Heidelberg Gmbh"],["dc.publisher.place","Stuttgart"],["dc.relation.issn","0947-7349"],["dc.title","GnRH agonist Triptorelin reverts increased expression of the cofactors A1B1 and SRC-1 in breast cancer cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","182"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","GYNAKOLOGE"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Grundker, Carsten"],["dc.contributor.author","Hanf, Volker"],["dc.date.accessioned","2018-11-07T10:40:22Z"],["dc.date.available","2018-11-07T10:40:22Z"],["dc.date.issued","2003"],["dc.description.abstract","Unopposed estrogens increase the risk of developing endometrial cancer. A relationship between estrogen exposure and the risk for breast cancer is very probable, an association of long-term estrogen substitution and ovarian cancer risk has been postulated recently. Estrogens have been considered as typical tumor promotors. Due to their estrogen-receptor-mediated mitogenic activity, these steroids were supposed to increase the statistical probability of spontaneous mutations. Recent experimental findings, however, suggest that estrogen metabolites, in particular 4-hydroxyes trogens are capable of inducing DNA-damage and transforming mutations.The clinical relevance of these genotoxic properties remains to be established. First molecular-epidemiologic studies suggest that some women might produce relevant amounts of mutagenic estrogen metabolites, increasing their risk for breast-, endometrial- or ovarian cancer. These findings might result in novel preventive strategies. The present data do not justify to abandon hormone replacement therapy. It seems to be wise, however, to restrict hormone replacement therapy to symptomatic women with a clear indication and according to the actual trend to limit it temporarily."],["dc.identifier.doi","10.1007/S00129-003-1332-7"],["dc.identifier.isi","000182463300002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46289"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0017-5994"],["dc.title","Are estrogens carcinogens?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","23"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Pineal Research"],["dc.bibliographiccitation.lastpage","31"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T08:27:21Z"],["dc.date.available","2018-11-07T08:27:21Z"],["dc.date.issued","2009"],["dc.description.abstract","Melatonin possesses anti-estrogenic effects on estrogen receptor expressing (ER+) breast cancer cells in culture by reducing cell cycle progression and cell proliferation. There is increasing agreement that on a cellular level the effects of melatonin are primarily induced by the membrane-bound receptor MT1. The participation of a second, nuclear receptor of the group of ligand-dependent transcription factors, called RZR alpha, is under debate. In this study we used a number of breast cancer cell lines differing in their expression of the estrogen receptor and the two known melatonin receptors. In MCF-7 breast cancer cells transfected with a vector carrying the MT1 gene (MCF-7Mel1a) binding of CREB-protein to the cAMP-responsive element of the breast cancer suppressing gene BRCA-1 was more strongly reduced by treatment with melatonin than in the parental cells. Expression of estrogen responsive genes was determined in serum-starved cells, cells stimulated for 16 hr with estradiol and cells subsequently treated with melatonin. Expression of BRCA-1, p53, p21(WAF) and c-myc were up-regulated by estradiol. Treatment of the stimulated cells with melatonin counteracted the increase induced by estradiol almost completely. The more MT1 a cell line expressed, the stronger was the reduction of the expression of the estradiol-induced genes. There was no correlation between the expression of the nuclear receptor RZR alpha and the effects of melatonin on these genes."],["dc.identifier.doi","10.1111/j.1600-079X.2009.00684.x"],["dc.identifier.isi","000267706300004"],["dc.identifier.pmid","19522736"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6112"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16188"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.relation.issn","0742-3098"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Membrane-bound melatonin receptor MT1 down-regulates estrogen responsive genes in breast cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]