Thelen, Paul

[["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","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.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","589"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","British Journal of Cancer"],["dc.bibliographiccitation.lastpage","598"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Soruri, Afsaneh"],["dc.contributor.author","Meschter, O."],["dc.contributor.author","Heintze, A."],["dc.contributor.author","Zschunke, F."],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Schlott, T."],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Fayyazi, Afshin"],["dc.date.accessioned","2018-11-07T10:46:28Z"],["dc.date.available","2018-11-07T10:46:28Z"],["dc.date.issued","2004"],["dc.description.abstract","Testicular germ cell tumours (TGCT) represent the most common malignancies in young males. Whereas in 1970s, the survival rate in patients with metastatic testicular tumours was only 5%, these days, 80% of the patients treated by modern chemotherapy will survive their disease. The drug that revolutionised the cure rate for patients with metastatic testicular tumours was cisdiamminedichloroplatinum ( cisplatin, CDDP). In vitro experiments on neoplastic germ cell lines showed that their exquisite sensitivity to CDDP could be attributed to p53-dependent and -independent pathways. Applying cDNA macroarray, semiquantitative RT-PCR and Western blot analyses, blocking experiments, caspase activity assays, and morphological methods, we sought here to define the p53-independent pathway(s) involved in the CDDP-induced apoptosis. For this purpose, we used the human TGCT cell line NCCIT, the mutated p53 of which is known to remain inactive during the course of CDDP-induced apoptosis. Our experiments showed that within hours of CDDP application, two prototype members of the 'mitogen-activated protein kinase' ( MAPK) family, designated 'MAPK ERK kinase' (MEK) and 'extracellular signal-regulated kinase' ( ERK), were dually phosphorylated and caspase-3 became active. Functional assays using MEK inhibitors demonstrated that the phosphorylation of MEK and ERK was required for the activation of caspase-3 as the executing caspase. Interestingly, experiments with the human malignant germ cell line NTERA, which is known to possess wild-type p53, revealed the same results. Thus, our data suggest that CDDP mediates its p53-independent apoptosis-inducing effect on the malignant human testicular germ cells - at least partially - through activation of the MEK - ERK signalling pathway."],["dc.identifier.doi","10.1038/sj.bjc.6601919"],["dc.identifier.isi","000222930400029"],["dc.identifier.pmid","15266324"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47752"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0007-0920"],["dc.title","Cisplatin-induced apoptosis in human malignant testicular germ cell lines depends on MEK/ERK activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","50"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","59"],["dc.bibliographiccitation.volume","202"],["dc.contributor.author","Grzmil, M."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T10:52:50Z"],["dc.date.available","2018-11-07T10:52:50Z"],["dc.date.issued","2004"],["dc.description.abstract","The type I insulin-like growth factor receptor (IGF-IR) is involved in tumour cell proliferation, invasion, and cancer cell survival. Several studies indicate that the IGF axis contributes to prostate cancer pathogenesis, but there is no consensus regarding the relative expression of the IGF-IR in benign and malignant prostate epithelium. In this study, endogenous IGF-IR gene expression was reduced in stably transfected PC-3 cells by employing an antisense RNA strategy which resulted in significant suppression of both PC3 cell invasion and proliferation in vitro. Furthermore, it was demonstrated that a direct correlation exists between the inhibition of IGF-IR gene expression and either up-regulation of IGF binding protein (BP)-3 or down-regulation of matrix metalloproteinase (MMP)2 expression in androgen-independent PC-3 cells. Moreover, inhibition of IGF-IR gene expression in transfected PC-3 cells leads to an enhanced rate of spontaneous apoptosis. In addition, expression analyses by quantitative RT-PCR on RNA from laser microdissected matched normal prostate and prostate tumour samples revealed that IGF-IR gene expression was up-regulated in nine of 12 prostate cancers, whereas IGFBP-3 gene expression was downregulated in all 12 prostate carcinomas analysed. These results indicate an important role for IGF-IR and IGFBP-3 in the homeostasis of prostate carcinoma cells and provide a further basis for targeting IGF-IR or IGFBP-3 gene expression in order to improve understanding of the IGF-IR-activated signalling pathways and as a potential treatment for prostate cancer. Copyright (C) 2003 John Wiley Sons, Ltd."],["dc.identifier.doi","10.1002/path.1492"],["dc.identifier.isi","000187668700007"],["dc.identifier.pmid","14694521"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49206"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","John Wiley & Sons Ltd"],["dc.relation.issn","0022-3417"],["dc.title","Blockade of the type IIGF receptor expression in human prostate cancer cells inhibits proliferation and invasion, up-regulates lGF binding protein-3, and suppresses MMP-2 expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1385"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","International Journal of Oncology"],["dc.bibliographiccitation.lastpage","1394"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Hasibeder, Astrid"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Schweyer, Stefan"],["dc.date.accessioned","2018-11-07T09:18:23Z"],["dc.date.available","2018-11-07T09:18:23Z"],["dc.date.issued","2013"],["dc.description.abstract","Phytoestrogens have been shown to exert antiproliferative effects on different cancer cells. In addition it could be demonstrated that inhibition of proliferation is associated with downregulation of the known stem cell factors NANOG, POU5F1 and SOX2 in tumor cells. We demonstrate the potential of Belamcanda chinensis extract (BCE) and tectorigenin as anticancer drugs in cell lines of malignant testicular germ cell tumor cells (TGCT) by inhibition of proliferation and regulating the expression of stem cell factors. The TGCT cell lines TCam-2 and NTera-2 were treated with BCE or tectorigenin and MTT assay was used to measure the proliferation of tumor cells. In addition, the expression of stem cell factors was analyzed by quantitative PCR and western blot analysis. Furthermore, global expression analysis was performed by microarray technique. BCE and tectorigenin inhibited proliferation and downregulated the stem cell factors NANOG and POU5F1 in TGCT cells. In addition, gene expression profiling revealed induction of genes important for the differentiation and inhibition of oncogenes. Utilizing connectivity map in an attempt to elucidate mechanism underlying BCE treatments we found highly positive association to histone deacetylase inhibitors (HDACi) amongst others. Causing no histone deacetylase inhibition, the effects of BCE on proliferation and stem cell factors may be based on histone-independent mechanisms such as direct hyperacetylation of transcription factors. Based on these findings, phytoestrogens may be useful as new agents in the treatment of TGCT."],["dc.identifier.doi","10.3892/ijo.2013.2060"],["dc.identifier.isi","000324982700007"],["dc.identifier.pmid","23969837"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28398"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Spandidos Publ Ltd"],["dc.relation.issn","1019-6439"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Phytoestrogens regulate the proliferation and expression of stem cell factors in cell lines of malignant testicular germ cell tumors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1115"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Carcinogenesis"],["dc.bibliographiccitation.lastpage","1124"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Witt, Daria"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","von Hardenberg, Sandra"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Neesen, Juergen"],["dc.contributor.author","Kaulfuss, Silke"],["dc.date.accessioned","2018-11-07T09:25:10Z"],["dc.date.available","2018-11-07T09:25:10Z"],["dc.date.issued","2013"],["dc.description.abstract","In this study, primary murine prostate cancer (PCa) cells were derived using the well-established TRAMP model. These PCa cells were treated with the histone deacetylase inhibitor, valproic acid (VPA), and we demonstrated that VPA treatment has an antimigrative, antiinvasive and antiproliferative effect on PCa cells. Using microarray analyses, we discovered several candidate genes that could contribute to the cellular effects we observed. In this study, we could demonstrate that VPA treatment of PCa cells causes the re-expression of cyclin D2, a known regulator that is frequently lost in PCa as we could show using immunohistochemical analyses on PCa specimens. We demonstrate that VPA specifically induces the re-expression of cyclin D2, one of the highly conserved D-type cyclin family members, in several cancer cell lines with weak or no cyclin D2 expression. Interestingly, VPA treatment had no effect in fibroblasts, which typically have high basal levels of cyclin D2 expression. The re-expression of cyclin D2 observed in PCa cells is activated by increased histone acetylation in the promoter region of the Ccnd2 gene and represents one underlying molecular mechanism of VPA treatment that inhibits the proliferation of cancer cells. Altogether, our results confirm that VPA is an anticancer therapeutic drug for the treatment of tumors with epigenetically repressed cyclin D2 expression."],["dc.identifier.doi","10.1093/carcin/bgt019"],["dc.identifier.isi","000318646000021"],["dc.identifier.pmid","23349020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30001"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0143-3334"],["dc.title","Valproic acid inhibits the proliferation of cancer cells by re-expressing cyclin D2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Urology Supplements"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Strauss, A."],["dc.contributor.author","Schweyer, Stefan"],["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","278"],["dc.identifier.doi","10.1016/S1569-9056(08)60826-X"],["dc.identifier.isi","000253839801229"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54839"],["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","Beneficial effects on LNCaP prostate cancer cells derived from histone deacetylase inhibitor treatments"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1271"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Der Urologe"],["dc.bibliographiccitation.lastpage","1274"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Wuttke, Wolfgang"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.date.accessioned","2018-11-07T10:59:29Z"],["dc.date.available","2018-11-07T10:59:29Z"],["dc.date.issued","2007"],["dc.description.abstract","Prostate cancer is more frequently diagnosed in men from Western countries than from Asian societies. Therefore, nutritional factors such as phyto-oestrogens from soya are considered to cause this prostate cancer prevention effect. As there is no curative therapy for hormone-refractory prostate cancer, new strategies are in demand which might include phyto-oestrogens or inhibitors of histone deacetylases. Both approaches have in common the potential to reduce the aberrant androgen receptor and IGF receptor signalling. Furthermore, invasiveness and acquired survival strategies of turnours can be diminished. Reduced tumour cell proliferation and PSA secretion coincide with altered gene expression in the aforementioned processes. In addition, selective knock-down of genes by RNA interference afforded functional analyses regarding impact and succession of expression events involved in the beneficial effects caused by phyto-oestrogens and histone deacetylase inhibitors."],["dc.identifier.doi","10.1007/s00120-007-1452-0"],["dc.identifier.isi","000250342100104"],["dc.identifier.pmid","17641866"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50711"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1433-0563"],["dc.title","Molecular principles of alternative treatment approaches for hormone-refractory prostate cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]