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Hanf, Volker
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Hanf, Volker
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Hanf, Volker
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Hanf, V.
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2003Journal Article [["dc.bibliographiccitation.firstpage","440"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","NEUROENDOCRINOLOGY LETTERS"],["dc.bibliographiccitation.lastpage","444"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Bartsch, C."],["dc.contributor.author","Hill, S. M."],["dc.contributor.author","Kreienberg, Rolf"],["dc.contributor.author","Hanf, Volker"],["dc.date.accessioned","2018-11-07T10:34:30Z"],["dc.date.available","2018-11-07T10:34:30Z"],["dc.date.issued","2003"],["dc.description.abstract","OBJECTIVES: Detection of the antiestrogenic effect of melatonin on various breast cancer cell lines and its dependence of the differential expression of estrogen receptors (ERalpha and ERbeta) and melatonin receptors (mt1 and RZRalpha,). SETTING AND DESIGN: Dose-response curves of estradiol were determined in 6 different breast cancer cell lines using a colorimetric proliferation assay in the absence or presence of various melatonin concentrations. METHODS: In order to detect the minor growth inhibitory effect of melatonin, a simple yet novel approach was employed: instead of incubating cells at single estradiol-concentrations at increasing melatonin levels, breast cancer cells were grown in microwell-plates for 4 days at increasing concentrations of estradiol (10(-12) M - 10(-10) M) in the absence or presence of melatonin (10(-9) M - 10(-8) M). Cell number was determined using Alamar blue and colorimetry, RT-PCR was performed for the expression of ERalpha, ERbeta, RZRalpha and mt1. RESULTS: Melatonin at concentrations of 10(-9) M and 5x10(-9) M shifted the dose-response curves of estradiol to higher concentrations. Responsiveness to melatonin depended on expression of ERalpha but not on ERbeta. mRNA of ERbeta was not detectable in the breast cancer cell lines used. Only small amounts of mt1 transcripts were detectable in MCF-7 cells of one source. In MCF-7 cells transfected with the mt1 gene and in an ovarian cancer cell line mt1 was expressed at significant levels. RZRalpha was expressed in all tested cell lines at different amounts. CONCLUSION: The growth of all ERalpha-positive breast cancer cell lines can be inhibited by melatonin. The effect in most cell lines is weak yet clearly reproducible. RZRalpha clearly contributes to the growth inhibitory effect of melatonin."],["dc.identifier.isi","000187882100012"],["dc.identifier.pmid","15073572"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44887"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Maghira & Maas Publications"],["dc.relation.issn","0172-780X"],["dc.title","Tracking, the elusive antiestrogenic effect of melatonin: A new methodological approach"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details PMID PMC WOS2009Journal Article [["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"]]Details DOI PMID PMC WOS2018Journal Article [["dc.bibliographiccitation.firstpage","1089"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Geburtshilfe und Frauenheilkunde"],["dc.bibliographiccitation.lastpage","1109"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Emons, Günter"],["dc.contributor.author","Steiner, Eric"],["dc.contributor.author","Vordermark, Dirk"],["dc.contributor.author","Uleer, Christoph"],["dc.contributor.author","Bock, Nina"],["dc.contributor.author","Paradies, Kerstin"],["dc.contributor.author","Ortmann, Olaf"],["dc.contributor.author","Aretz, Stefan"],["dc.contributor.author","Mallmann, Peter"],["dc.contributor.author","Kurzeder, Christian"],["dc.contributor.author","Hagen, Volker"],["dc.contributor.author","van Oorschot, Birgitt"],["dc.contributor.author","Höcht, Stefan"],["dc.contributor.author","Feyer, Petra"],["dc.contributor.author","Egerer, Gerlinde"],["dc.contributor.author","Friedrich, Michael"],["dc.contributor.author","Cremer, Wolfgang"],["dc.contributor.author","Prott, Franz-Josef"],["dc.contributor.author","Horn, Lars-Christian"],["dc.contributor.author","Prömpeler, Heinrich"],["dc.contributor.author","Langrehr, Jan"],["dc.contributor.author","Leinung, Steffen"],["dc.contributor.author","Beckmann, Matthias"],["dc.contributor.author","Kimmig, Rainer"],["dc.contributor.author","Letsch, Anne"],["dc.contributor.author","Reinhardt, Michael"],["dc.contributor.author","Alt-Epping, Bernd"],["dc.contributor.author","Kiesel, Ludwig"],["dc.contributor.author","Menke, Jan"],["dc.contributor.author","Gebhardt, Marion"],["dc.contributor.author","Steinke-Lange, Verena"],["dc.contributor.author","Rahner, Nils"],["dc.contributor.author","Lichtenegger, Werner"],["dc.contributor.author","Zeimet, Alain"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Weis, Joachim"],["dc.contributor.author","Mueller, Michael"],["dc.contributor.author","Henscher, Ulla"],["dc.contributor.author","Schmutzler, Rita"],["dc.contributor.author","Meindl, Alfons"],["dc.contributor.author","Hilpert, Felix"],["dc.contributor.author","Panke, Joan"],["dc.contributor.author","Strnad, Vratislav"],["dc.contributor.author","Niehues, Christiane"],["dc.contributor.author","Dauelsberg, Timm"],["dc.contributor.author","Niehoff, Peter"],["dc.contributor.author","Mayr, Doris"],["dc.contributor.author","Grab, Dieter"],["dc.contributor.author","Kreißl, Michael"],["dc.contributor.author","Witteler, Ralf"],["dc.contributor.author","Schorsch, Annemarie"],["dc.contributor.author","Mustea, Alexander"],["dc.contributor.author","Petru, Edgar"],["dc.contributor.author","Hübner, Jutta"],["dc.contributor.author","Rose, Anne"],["dc.contributor.author","Wight, Edward"],["dc.contributor.author","Tholen, Reina"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Fleisch, Markus"],["dc.contributor.author","Juhasz-Boess, Ingolf"],["dc.contributor.author","Lax, Sigurd"],["dc.contributor.author","Runnebaum, Ingo"],["dc.contributor.author","Tempfer, Clemens"],["dc.contributor.author","Nothacker, Monika"],["dc.contributor.author","Blödt, Susanne"],["dc.contributor.author","Follmann, Markus"],["dc.contributor.author","Langer, Thomas"],["dc.contributor.author","Raatz, Heike"],["dc.contributor.author","Wesselmann, Simone"],["dc.contributor.author","Erdogan, Saskia"],["dc.date.accessioned","2020-12-10T18:12:05Z"],["dc.date.available","2020-12-10T18:12:05Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1055/a-0715-2964"],["dc.identifier.eissn","1438-8804"],["dc.identifier.issn","0016-5751"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74238"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Interdisciplinary Diagnosis, Therapy and Follow-up of Patients with Endometrial Cancer. Guideline (S3-Level, AWMF Registry Number 032/034-OL, April 2018) – Part 2 with Recommendations on the Therapy and Follow-up of Endometrial Cancer, Palliative Care, Psycho-oncological/Psychosocial Care/Rehabilitation/Patient Information and Healthcare Facilities"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2003Journal 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 WOS2004Conference Abstract [["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","EJC SUPPLEMENTS"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Schimming, H."],["dc.contributor.author","Kreienberg, Rolf"],["dc.contributor.author","Girgert, Rainer"],["dc.date.accessioned","2018-11-07T10:50:33Z"],["dc.date.available","2018-11-07T10:50:33Z"],["dc.date.issued","2004"],["dc.format.extent","109"],["dc.identifier.doi","10.1016/S1359-6349(04)90796-3"],["dc.identifier.isi","000202990100211"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48684"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.issn","1359-6349"],["dc.title","Antiproliferative activity of tamoxifen on MCF-7 breast cancer cells is modulated by weak electromagnetic field exposure"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI WOS2004Journal Article [["dc.bibliographiccitation.firstpage","1719"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","American Journal of Obstetrics and Gynecology"],["dc.bibliographiccitation.lastpage","1720"],["dc.bibliographiccitation.volume","191"],["dc.contributor.author","Gunthert, Andreas R."],["dc.contributor.author","Hinney, Bernd"],["dc.contributor.author","Nesselhut, K."],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Emons, G."],["dc.date.accessioned","2018-11-07T10:44:01Z"],["dc.date.available","2018-11-07T10:44:01Z"],["dc.date.issued","2004"],["dc.description.abstract","We report the case of a patient with voluminous unilateral hypertrophy of vulvar labia and pseudocondylomata in the fossa navicularis associated with intestinal Crohn's disease. No fistulas were observed. The patient has had Crohn's disease for 8 years. Interrelationship of genital alterations and Crohn's disease are discussed. (C) 2004 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.ajog.2004.03.013"],["dc.identifier.isi","000225337500033"],["dc.identifier.pmid","15547549"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47180"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mosby, Inc"],["dc.relation.issn","0002-9378"],["dc.title","Vulvitis granulomatosa and unilateral hypertrophy of the vulva related to Crohn's disease: A case report"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2005Review [["dc.bibliographiccitation.firstpage","139"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Journal of Obstetrics & Gynecology and Reproductive Biology"],["dc.bibliographiccitation.lastpage","149"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Gonder, U."],["dc.date.accessioned","2018-11-07T10:53:49Z"],["dc.date.available","2018-11-07T10:53:49Z"],["dc.date.issued","2005"],["dc.description.abstract","Worldwide, each year approximately one million women are newly diagnosed with breast cancer (BC), in Germany 65 new cases per 100,000 inhabitants are registered, yearly. The fact that incidence has been rising in parallel with economic development indicates that environmental factors might play a role in the causation of BC. Migrational data have pointed to nutrition as one of the more relevant external factors involved. Preventive dietary advice often includes a reduction of alcohol, red meat and animal fat and increasing the intake of vegetables, fruit and fibre and lately, phytoestrogens from various sources. Clearly, the scientific basis for these recommendations appears sparse. The available prospective data from epidemiological studies and interventional trials do not support the overall hypothesis that higher fat-intakes are a relevant risk factor for BC development, more important seems the relative distribution of various fatty acids. A non-vegetarian eating habit (consumption of animal products) per se does not elevate BC risk, while consumption of broiled or deep fried meats cannot be ruled out as a risk factor in genetically susceptible individuals. It appears prudent to abstain from regular and increased alcohol consumption. This should be particularly true for pubescent girls, in whom glandular breast tissue is particularly vulnerable. In general, if alcohol is consumed on a regular basis, a sufficient supply of fresh vegetables and fruit is essential. While there is no overall protective effect of a high fruit and vegetable consumption speculation remains over possible beneficial effects of certain subcategories, especially brassica vegetables like broccoli, cauliflower and cabbage. In essence, regional differences in BC incidence are probably partially attributable to life long dietary habits. There is no need to adopt a foreign dietary plan in order to protect oneself against BC. Traditional western diets also have their beneficial ingredients that should be regular constituents in our meals. Lignans from traditionally made sourdough rye bread, linseed/flaxseed and berries are local sources of potentially canceroprotective phyto-estrogens. Furthermore, indole-3-carbinol rich cabbage species might contribute to BC protection by diet. Nevertheless, clear cut recommendations for or against single nutrients or secondary plant metabolites are not yet possible, lacking sufficient data on individual bioavailability, safety and long term outcome. BC prevention by dietary means therefore relies on an individually tailored mixed diet, rich in basic foods and traditional manufacturing and cooking methods. (c) 2005 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ejogrb.2005.05.011"],["dc.identifier.isi","000234101900002"],["dc.identifier.pmid","16316809"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49427"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0301-2115"],["dc.title","Nutrition and primary prevention of breast cancer: Foods, nutrients and breast cancer risk"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2008Journal Article [["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"]]Details DOI PMID PMC WOS2017Journal Article [["dc.bibliographiccitation.artnumber","112"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Breast Cancer Research"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Bernhardt, Stephan"],["dc.contributor.author","Bayerlová, Michaela"],["dc.contributor.author","Vetter, Martina"],["dc.contributor.author","Wachter, Astrid"],["dc.contributor.author","Mitra, Devina"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Lantzsch, Tilmann"],["dc.contributor.author","Uleer, Christoph"],["dc.contributor.author","Peschel, Susanne"],["dc.contributor.author","John, Jutta"],["dc.contributor.author","Buchmann, Jörg"],["dc.contributor.author","Weigert, Edith"],["dc.contributor.author","Bürrig, Karl-Friedrich"],["dc.contributor.author","Thomssen, Christoph"],["dc.contributor.author","Korf, Ulrike"],["dc.contributor.author","Beissbarth, Tim"],["dc.contributor.author","Wiemann, Stefan"],["dc.contributor.author","Kantelhardt, Eva Johanna"],["dc.date.accessioned","2020-12-10T18:39:04Z"],["dc.date.available","2020-12-10T18:39:04Z"],["dc.date.issued","2017"],["dc.description.abstract","Abstract Background Breast cancer tumors are known to be highly heterogeneous and differences in their metabolic phenotypes, especially at protein level, are less well-understood. Profiling of metabolism-related proteins harbors the potential to establish new patient stratification regimes and biomarkers promoting individualized therapy. In our study, we aimed to examine the relationship between metabolism-associated protein expression profiles and clinicopathological characteristics in a large cohort of breast cancer patients. Methods Breast cancer specimens from 801 consecutive patients, diagnosed between 2009 and 2011, were investigated using reverse phase protein arrays (RPPA). Patients were treated in accordance with national guidelines in five certified German breast centers. To obtain quantitative expression data, 37 antibodies detecting proteins relevant to cancer metabolism, were applied. Hierarchical cluster analysis and individual target characterization were performed. Clustering results and individual protein expression patterns were associated with clinical data. The Kaplan-Meier method was used to estimate survival functions. Univariate and multivariate Cox regression models were applied to assess the impact of protein expression and other clinicopathological features on survival. Results We identified three metabolic clusters of breast cancer, which do not reflect the receptor-defined subtypes, but are significantly correlated with overall survival (OS, p ≤ 0.03) and recurrence-free survival (RFS, p ≤ 0.01). Furthermore, univariate and multivariate analysis of individual protein expression profiles demonstrated the central role of serine hydroxymethyltransferase 2 (SHMT2) and amino acid transporter ASCT2 (SLC1A5) as independent prognostic factors in breast cancer patients. High SHMT2 protein expression was significantly correlated with poor OS (hazard ratio (HR) = 1.53, 95% confidence interval (CI) = 1.10–2.12, p ≤ 0.01) and RFS (HR = 1.54, 95% CI = 1.16–2.04, p ≤ 0.01). High protein expression of ASCT2 was significantly correlated with poor RFS (HR = 1.31, 95% CI = 1.01–1.71, p ≤ 0.05). Conclusions Our data confirm the heterogeneity of breast tumors at a functional proteomic level and dissects the relationship between metabolism-related proteins, pathological features and patient survival. These observations highlight the importance of SHMT2 and ASCT2 as valuable individual prognostic markers and potential targets for personalized breast cancer therapy. Trial registration ClinicalTrials.gov, NCT01592825 . Registered on 3 May 2012."],["dc.identifier.doi","10.1186/s13058-017-0905-7"],["dc.identifier.eissn","1465-542X"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15161"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77532"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/16987 but duplicate"],["dc.publisher","BioMed Central"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)."],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Proteomic profiling of breast cancer metabolism identifies SHMT2 and ASCT2 as prognostic factors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2010Journal Article [["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"]]Details DOI PMID PMC WOS