Thelen, Paul

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Urology Supplements"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Possner, Maria"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Strauss, A."],["dc.contributor.author","Schulz, W."],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2018-11-07T11:17:35Z"],["dc.date.available","2018-11-07T11:17:35Z"],["dc.date.issued","2008"],["dc.format.extent","173"],["dc.identifier.doi","10.1016/S1569-9056(08)60407-8"],["dc.identifier.isi","000253839800404"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54838"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.issn","1569-9056"],["dc.title","Functional analysis of NKX3.1 by RNA interference in LNCaP prostate 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","543"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","552"],["dc.bibliographiccitation.volume","163"],["dc.contributor.author","Grzmil, M."],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Voigt, S."],["dc.contributor.author","Mury, D."],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T10:37:03Z"],["dc.date.available","2018-11-07T10:37:03Z"],["dc.date.issued","2003"],["dc.description.abstract","To analyze differential gene expression of putative prostate tumor markers we compared the expression levels of more than 400 cancer-related genes using the cDNA array technique in a set of capsule-invasive prostate tumor and matched normal prostate tissue. The overexpression. of Bax inhibitor-1 (BI-1) in prostate carcinoma and prostate cancer cell lines was confirmed by using Northern blot and Western blot analyses. Quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) on intact RNAs from 17 paired laser-captured microdissected epithelial tissue samples confirmed up-regulated BI-1 expression in 11 of 17 prostate tumors. In addition, it was demonstrated that BI-1 expression is down-regulated in stromal cells as. compared to matched normal epithelial cells of the prostate. In situ hybridization experiments on prostate sections also revealed that BI-1 expression is mainly restricted to epithelial cells. Furthermore, quantitative RT-PCR on RNAs derived from five benign prostate hyperplasia (BPH) samples showed no significant difference in BI-1 expression as compared to normal epithelial prostate tissue. To determine the function of BI-1 in vitro, human PC-3, LNCaP, and DU-145 prostate carcinoma cells were transfected with small interfering double-strand RNA (siRNA) oligonucleotides against the BI-1 gene leading to a specific down-regulation of BI-1 expression. Furthermore, transfection of PC-3, LNCaP, and DU-145 cells with BI-1 sequence-specific siRNAs caused a significant increase in spontaneous apoptosis in all cell lines. Taken together, our results indicate that the human BI-1 gene contains the potential to serve as a prostate cancer expression marker and as a potential target for developing therapeutic strategies for prostate cancer."],["dc.identifier.doi","10.1016/S0002-9440(10)63682-6"],["dc.identifier.isi","000184366400016"],["dc.identifier.pmid","12875974"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45473"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Investigative Pathology, Inc"],["dc.relation.issn","0002-9440"],["dc.title","Bax inhibitor-1 is overexpressed in prostate cancer and its specific down-regulation by RNA interference leads to cell death in human prostate carcinoma cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","341"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Anticancer Research"],["dc.bibliographiccitation.lastpage","349"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Pottek, T."],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Schweyer, Stefan"],["dc.date.accessioned","2018-11-07T09:16:04Z"],["dc.date.available","2018-11-07T09:16:04Z"],["dc.date.issued","2012"],["dc.description.abstract","Testicular germ cell tumours (TGCTs) are the most common malignancy in young men aged 18-35 years. They are clinically and histologically subdivided into seminomas and non-seminomas. 1,25-Dihydroxyvitamin,25(OH)(2)D(3)) is the active form of vitamin D and exerts its actions via a specific intracellular vitamin D receptor (VDR). Several investigations in the recent years have revealed, in addition to a physiological occurrence of the VDR in various tissues, VDR expression in different human malignancies. Furthermore, 1,25(OH)(2)D(3) plays an important role in the regulation of cell proliferation and differentiation. In different normal and malignant cell types, antiproliferative and pro-differentiating effects of 1,25(OH)(2)D(3) are described. We investigated whether TGCT express the VDR, wether differences exist between the histological subtypes and if vitamin D has a function on the proliferation of tumour cells. Furthermore, we investigated the potential function of the vitamin D-regulated genes nuclear receptor co-repressor 1 (NCOR1), nuclear receptor co-repressor 2 (NCOR2), thyroid receptor interacting protein 15 (TRIP I 5), Growth Arrest and DNA Damage (GADD45), MAP kinase-activated protein kinase 2 (MAPKAPK2), Cytochmme P450, family 24, subfamily A, polypeptide 1 (C.YP24A1) and Cytochrome P450, family 27, subfamily B. polypeptide (CYP27B1) in the pathogenesis of TGCT. We demonstrate, for the first time, that primary TGCT as well as TGCT cell lines, express VDR mRNA and protein. Vitamin D and VDR may play a role in the pathogenesis of TGCTs. Furthermore, vitamin D inhibits proliferation of TGCT cell-lines, potentially via an increase in expression of GADD45. Our data suggest that vitamin D could play a role in antitumour therapy."],["dc.identifier.isi","000298780700017"],["dc.identifier.pmid","22213325"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27850"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Int Inst Anticancer Research"],["dc.relation.issn","0250-7005"],["dc.title","Expression and Function of the Vitamin D Receptor in Malignant Germ Cell Tumour of the Testis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1261"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Der Urologe"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","51"],["dc.contributor.author","Loertzer, Hagen"],["dc.contributor.author","Schneider, P."],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Strauss, A."],["dc.date.accessioned","2018-11-07T09:06:35Z"],["dc.date.available","2018-11-07T09:06:35Z"],["dc.date.issued","2012"],["dc.description.abstract","In prolapse surgery several surgical techniques are available. The different open, laparoscopic and vaginal approaches are distinguished by distinct success and relapse rates and operation-specific complications. A safe and optimal therapeutic pelvic floor surgery should be based on the three support levels according to DeLancy and be individually adjusted for every patient. The vaginal approach may be used for all kinds of female genital prolapse and is a comparatively less invasive technique with a short time of convalescence. Apart from stress incontinence there is no need for synthetic meshes in primary approaches and excellent results with low complication and relapse rates can be achieved. An uncritical application of synthetic material is to be avoided in vaginal repair at all times. Abdominal surgical techniques, both open and laparoscopic, present their strengths in the therapeutic approach to level 1 defects or stress incontinence. They provide excellent functional and anatomical corrections and low relapse rates. Abdominally inserted meshes have lower complication rates than vaginal ones."],["dc.identifier.doi","10.1007/s00120-012-2869-7"],["dc.identifier.isi","000308665900010"],["dc.identifier.pmid","22526180"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25592"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-2592"],["dc.title","Prolapse surgery. With abdominal or vaginal meshes?"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","339"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","International Journal of Molecular Medicine"],["dc.bibliographiccitation.lastpage","346"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Krahn, Lisa"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Brehm, Ralph"],["dc.contributor.author","Loertzer, Hagen"],["dc.date.accessioned","2018-11-07T09:28:47Z"],["dc.date.available","2018-11-07T09:28:47Z"],["dc.date.issued","2013"],["dc.description.abstract","The aim of this study was to elucidate whether the treatment of a prostate carcinoma cell line (LNCaP) and LNCaP-derived tumors with the histone deacetylase (HDAC) inhibitor valproate in combination with the mammalian target of rapamycin (mTOR) inhibitor temsirolimus resulted in synergistic effects on cell proliferation and tumor growth. LNCaP cells were treated with valproate, temsirolimus or a combination of both. The proliferation rates and the expression of key markers of tumorigenesis were evaluated. In in vivo experiments, LNCaP cells were implanted into immune-suppressed male nude mice. Mice were treated with valproate (per os), temsirolimus (intravenously) or with a combination of both. Tumor volumes were calculated and mRNA expression was quantified. The incubation of LNCaP cells with the combination of valproate and temsirolimus resulted in a decrease of cell proliferation with an additive effect of both drugs in comparison to the single treatment. In particular, the combined application of valproate and temsirolimus led to a significant upregulation of insulin-like growth factor-binding protein-3 (IGFBP-3), which mediates apoptosis and inhibits tumor cell proliferation. In the mouse model, we found no significant differences in tumor growth between the different treatment arms but immunohistological analyses showed that tumors treated with a combination of valproate and temsirolimus, but not with the single drugs alone, exhibited a significant lower proliferation capacity."],["dc.identifier.doi","10.3892/ijmm.2012.1221"],["dc.identifier.isi","000313858500009"],["dc.identifier.pmid","23292124"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30859"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Spandidos Publ Ltd"],["dc.relation.issn","1107-3756"],["dc.title","Synergistic effects of histone deacetylase inhibitor in combination with mTOR inhibitor in the treatment of prostate carcinoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","81"],["dc.bibliographiccitation.volume","213"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Bachem, A."],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Steinfelder, Hans Juergen"],["dc.contributor.author","Soruri, Afsaneh"],["dc.contributor.author","Wagner, W."],["dc.contributor.author","Pottek, T."],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Hopker, W. W."],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Fayyazi, Afshin"],["dc.date.accessioned","2018-11-07T10:59:10Z"],["dc.date.available","2018-11-07T10:59:10Z"],["dc.date.issued","2007"],["dc.description.abstract","Testicular germ cell tumours (TGCT) represent the most common malignancy in young males. We reported previously that two prototype members of the mitogen-activated protein kinase (MAPK) family, the MAPK ERK kinase (MEK) and extracellular signal-regulated kinase (ERK), are inactive in malignant testicular germ cells and become active after drug stimulation, leading to apoptosis of tumour cells. In this study, we asked whether the protein phosphatase PP2A, a known inhibitor of the MEK-ERK pathway, participates in the proliferation and/or apoptosis of primary TGCT (n = 48) as well as two TGCT cell lines (NTERA and NCCIT). Quantitative RT-PCR, immunohistochemistry, western blot analyses and phosphatase assay indicate that primary TGCT as well as TGCT cell lines express PP2A and that PP2A is active in TGCT cell lines. The inhibition of PP2A by application of two PP2A inhibitors, cantharidic acid (CA) and okadaic acid (OA), results in a significant increase in caspase-3-mediated apoptosis of TGCT cell lines. Thereby, PP2A inhibition was accompanied by phosphorylation and activation of MEK and ERK. Functional assays using the MEK inhibitor PD98059 demonstrated that the phosphorylation of NIEK and ERK was required for the induction of caspase-3-mediated apoptosis of malignant germ cells. Thus, our data suggest that inhibition of PP2A mediates its apoptosis-inducing effect on TGCT through activation of the MEK-ERK signalling pathway that leads to caspase-3-mediated apoptosis of tumour cells. In addition our results support previous observations that PP2A exerts an anti-apoptotic effect on malignant tumour cells. Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/path.2203"],["dc.identifier.isi","000249181800009"],["dc.identifier.pmid","17590861"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50636"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","John Wiley & Sons Ltd"],["dc.relation.issn","0022-3417"],["dc.title","Expression and function of protein phosphatase PP2A in malignant testicular germ cell tumours"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Walleck, Eiko"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Trojan, Lutz"],["dc.contributor.author","Strauss, Arne"],["dc.date.accessioned","2018-11-07T09:28:04Z"],["dc.date.available","2018-11-07T09:28:04Z"],["dc.date.issued","2013"],["dc.identifier.isi","000333679600131"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30688"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Oncology"],["dc.publisher.place","Alexandria"],["dc.relation.conference","Genitourinary Cancers Symposium of the Conquer-Cancer-Foundation of American-Society-of-Clinical-Oncology (ASCO)"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","1527-7755"],["dc.relation.issn","0732-183X"],["dc.title","Analysis of putative resistance mechanisms in recent treatments targeting the androgen receptor in castration-resistant prostate cancer (CRPC)"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","35"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","CANCER GENETICS AND CYTOGENETICS"],["dc.bibliographiccitation.lastpage","47"],["dc.bibliographiccitation.volume","176"],["dc.contributor.author","Schulten, Hans Juergen"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Polten, Andreas"],["dc.contributor.author","Borst, Christoph"],["dc.contributor.author","Gunawan, Bastian"],["dc.contributor.author","Nagel, Holger"],["dc.date.accessioned","2018-11-07T11:00:53Z"],["dc.date.available","2018-11-07T11:00:53Z"],["dc.date.issued","2007"],["dc.description.abstract","We describe two newly established malignant mesothelioma (MM) cell lines derived from a pleural effusion of a male. One cell line, designated as MM-Z03E, reveals an epithelioid cobblestone morphology, while the second one, designated as MM-Z03S and subcloned after in vivo selection, exhibits a sarcomatoid storiform growth pattern. Both cell lines showed the immunologic profile characteristic for MM (i.e., expression of cytokeratin, CK18, calretinin, and vimentin in both phenotypes). Cytogenetics, multicolor fluorescence in situ hybridization, comparative genomic hybridization, and oligonucleotide array CGH were performed on both cell lines. Aberrations shared by both cell lines included chromosomal losses of 1q34 similar to qter, 4, 9p, 10p, 13, 14, 16q, 18, and 22, as well as a complex structural aberration involving chromosome 17. Aberrations exclusive to MM-Z03E included gains of 3q11q27 and 5p, while gain of 9q and losses of 3q27qter, 11q, and 18 in MM-Z03S were exclusive to MM-Z03E. Both cell lines were able to develop solid transplant tumors in nude mice within 16 weeks, and immunophenotyping of tumor xenografts revealed an overall retained expression profile of the markers used. Remarkably, one xenograft from MM-Z03E revealed overexpression of p53 and widely invasive growth. In conclusion, both cell lines are useful in vivo and in vitro model systems to study the underlying genetic mechanisms of biphasic differentiation in MM, which can be of certain value considering the increasing relevance of assessing MM tumor biology for the clinical management of this disease. (c) 2007 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.cancergencyto.2007.03.005"],["dc.identifier.isi","000247710100004"],["dc.identifier.pmid","17574962"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51027"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0165-4608"],["dc.title","Establishment and characterization of two distinct malignant mesothelioma cell lines with common clonal origin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2626"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecular Cancer Therapeutics"],["dc.bibliographiccitation.lastpage","2633"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Stettner, Mark"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2018-11-07T10:58:18Z"],["dc.date.available","2018-11-07T10:58:18Z"],["dc.date.issued","2007"],["dc.description.abstract","In the prostate, estrogen receptor beta (ER beta), the preferred receptor for phytoestrogens, has features of a tumor suppressor. To investigate the mechanisms underlying the beneficial effects on prostate cancer of histone deacetylase inhibitor valproic acid (VPA) and phytoestrogen tectorigenin, we analyzed the expression of ER after tectorigenin or VPA treatment. For further functional analysis, we knocked down ER beta expression by RNA interference. LNCaP prostate cancer cells were treated with 5 mmol/L VPA or 100 mu mol/L tectorigenin and transfected with small interfering RNA (siRNA) against ER beta. Control transfections were done with luciferase (LUC) siRNA. Expression of ER beta was assessed by Western blot. mRNA expression was quantitated by real-time reverse transcription-PCR. Expression of ER beta mRNA and protein markedly increased after VPA or tectorigenin treatment. When ER beta was knocked down by siRNA, the expression of prostate-derived Ets factor, prostate-specific antigen, prostate cancer-specific indicator gene DD3(PCA3), insulin-like growth factor-1 receptor, the catalytic subunit of the telomerase, and ER beta was up-regulated and the tectorigenin effects were abrogated. ER beta levels were diminished in prostate cancer and loss of ER beta was associated with proliferation. Here, we show that siRNA-mediated knockdown of ER beta increases the expression of genes highly relevant to tumor cell proliferation. In addition, we show that one prominent result of treatment with VPA or tectorigenin is the up-regulation of ER beta resulting in antiproliferative effects. Thus, these drugs, by restoring the regulatory function of ER in tumor cells, could become useful in the intervention of prostate cancer."],["dc.identifier.doi","10.1158/1535-7163.MCT-07-0197"],["dc.identifier.isi","000250252100003"],["dc.identifier.pmid","17913855"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50445"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1535-7163"],["dc.title","The relevance of estrogen receptor-beta expression to the antiproliferative effects observed with histone deacetylase inhibitors and phytoestrogens in prostate cancer treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1240"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Der Urologe"],["dc.bibliographiccitation.lastpage","1245"],["dc.bibliographiccitation.volume","51"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Loertzer, Hagen"],["dc.contributor.author","Strauss, A."],["dc.date.accessioned","2018-11-07T09:06:34Z"],["dc.date.available","2018-11-07T09:06:34Z"],["dc.date.issued","2012"],["dc.description.abstract","Androgen deprivation is the predominant therapy for advanced prostate cancer. There is accumulating evidence that phases of intermission in androgen deprivation may have benefits regarding side effects, albeit there is as yet no general recommendation for intermittent androgen deprivation therapy. Recent systematic reviews at least substantiate a benefit from such regimens for general quality of life without therapy compromisation. In addition, preclinical data revealed further potential strategies for intermittent androgen deprivation therapy. Future studies must prove, however, that such approaches can be implemented in the clinical situation."],["dc.identifier.doi","10.1007/s00120-012-2870-1"],["dc.identifier.isi","000308665900007"],["dc.identifier.pmid","22526181"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25591"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1433-0563"],["dc.relation.issn","0340-2592"],["dc.title","Intermittent androgen deprivation as therapy for androgen-sensitive prostate cancer. Sense or nonsense?"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]