Strauß, Arne

[["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.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","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.artnumber","574"],["dc.bibliographiccitation.journal","SpringerPlus"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Trojan, Lutz"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2018-11-07T09:33:49Z"],["dc.date.available","2018-11-07T09:33:49Z"],["dc.date.issued","2014"],["dc.description.abstract","Recent breakthrough therapies targeting androgen receptor signalling in castration resistant prostate cancer (CRPC) involve multifunctional androgen receptor (AR) blockade and exhaustive androgen deprivation. Nevertheless, limitations to an enduring effectiveness of new drugs are anticipated in resistance mechanisms occurring under such treatments. In this study we used CRPC cell models VCaP and LNCaP as well as AR-negative PC-3- and non-neoplastic epithelial BPH-1-cells treated with 5, 10 or 25 mu mol/L abiraterone hydrolyzed from abiraterone acetate (AA). The origin of CYP17A1 up-regulation under AA treatment was investigated in CRPC cell models by qRT-PCR and western-blot procedures. AA treatments of AR positive CRPC cell models led to decreased expression of androgen regulated genes such as PSA. In these cells diminished expression of androgen regulated genes was accompanied by an up-regulation of CYP17A1 expression within short-term treatments. No such effects became evident in AR-negative PC-3 cells. AR directed siRNA (siAR) used in VCaP cells significantly reduced mRNA expression and AR protein abundance. Such interference with AR signalling in the absence of abiraterone acetate also caused a marked up-regulation of CYP17A1 expression. Down-regulation of androgen regulated genes occurs in spite of an elevated expression of CYP17A1, the very target enzyme for this drug. CYP17A1 up-regulation already takes place within such short treatments with AA and does not require adaptation events over several cell cycles. CYP17A1 is also up-regulated in the absence of AA when AR signalling is physically eliminated by siAR. These results reveal an immediate counter-regulation of CYP17A1 expression whenever AR-signalling is inhibited adequately but not a persisting adaptation yielding drug resistance."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG)"],["dc.identifier.doi","10.1186/2193-1801-3-574"],["dc.identifier.isi","000359105300002"],["dc.identifier.pmid","25332874"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11151"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32049"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","2193-1801"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Increased expression of CYP17A1 indicates an effective targeting of the androgen receptor axis in castration resistant prostate cancer (CRPC)"],["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","459"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","International Braz J Urol"],["dc.bibliographiccitation.lastpage","467"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Leitsmann, Conrad"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Schmid, Marianne"],["dc.contributor.author","Meller, Johannes"],["dc.contributor.author","Sahlmann, Carsten-Oliver"],["dc.contributor.author","Meller, Birgit"],["dc.contributor.author","Trojan, Lutz"],["dc.contributor.author","Strauss, Arne"],["dc.date.accessioned","2021-06-01T10:48:28Z"],["dc.date.available","2021-06-01T10:48:28Z"],["dc.date.issued","2019"],["dc.description.abstract","Purpose: 68Ga-PSMA PET/CT imaging is a promising modality for the staging of recurrent prostate cancer (PCa). Current evidence suggests limited diagnostic value of the 68Ga-PSMA PET/CT in PSA-levels ≤0.3ng/mL. Experimental data have demonstrated an increase in PSMA-expression in PCa metastases by androgen deprivation in vitro. The aim of the current study was to investigate a possible enhancing effect of PSMA with low-dose androgen deprivation in patients with BCR and low PSA-levels. Materials and Methods: Five patients with PCa and BCR, following radical prostatectomy, underwent 68Ga-PSMA PET/CT. A consecutive 68Ga-PSMA PET/CT was performed 6 to 11 days after injection of 80mg of Degarelix (Firmagon®). We recorded PSA and testosterone serum-levels and changes of PSMA-uptake in 68Ga-PSMA PET/CT images. Results: Median PSA prior 68Ga-PSMA PET/CT was 0.27ng/mL. All patients had a decrease in testosterone serum levels from median 2.95μg/l to 0.16μg/l following Degarelix injection. We observed an increase in the standardized uptake value (SUV) in PSMA-positive lymphogenous and osseous lesions in two patients following androgen deprivation. In another two patients, no PSMA positive signals were detected in either the first or the second scan. Conclusion: Our preliminary results of this feasibility assessment indicate a possible enhancing effect of PSMA-imaging induced by low-dose ADT. Despite several limitations and the small number of patients, this could be a new approach to improve staging by 68Ga-PSMA PET/CT in PCa patients with BCR after primary therapy. Further prospective studies with larger number of patients are needed to validate our findings."],["dc.identifier.doi","10.1590/s1677-5538.ibju.2018.0305"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85949"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.relation.eissn","1677-6119"],["dc.relation.issn","1677-5538"],["dc.title","Enhancing PSMA-uptake with androgen deprivation therapy – a new way to detect prostate cancer metastases?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","19"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Clinical Pathology"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.date.accessioned","2019-07-09T11:54:07Z"],["dc.date.available","2019-07-09T11:54:07Z"],["dc.date.issued","2012"],["dc.description.abstract","Background 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. Cadherins are calcium-dependent transmembrane proteins of the group of adhesion proteins. They play a role in the stabilization of cell-cell contacts, the embryonic morphogenesis, in the maintenance of cell polarity and signal transduction. N-cadherin (CDH2), the neuronal cadherin, stimulates cell-cell contacts during migration and invasion of cells and is able to suppress tumour cell growth. Methods Tumour tissues were acquired from 113 male patients and investigated by immunohistochemistry, as were the three TGCT cell lines NCCIT, NTERA-2 and Tcam2. A monoclonal antibody against N-cadherin was used. Results Tumour-free testis and intratubular germ cell neoplasias (unclassified) (IGCNU) strongly expressed N-cadherin within the cytoplasm. In all seminomas investigated, N-cadherin expression displayed a membrane-bound location. In addition, the teratomas and yolk sac tumours investigated also differentially expressed N-cadherin. In contrast, no N-cadherin could be detected in any of the embryonal carcinomas and chorionic carcinomas examined. This expression pattern was also seen in the investigated mixed tumours consisting of seminomas, teratomas, and embryonal carcinoma. Conclusions N-cadherin expression can be used to differentiate embryonal carcinomas and chorionic carcinomas from other histological subtypes of TGCT."],["dc.identifier.doi","10.1186/1472-6890-12-19"],["dc.identifier.fs","593171"],["dc.identifier.pmid","23066729"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8499"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60578"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","N-cadherin expression in malignant germ cell tumours of the testis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1257"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","The Prostate"],["dc.bibliographiccitation.lastpage","1269"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Payne, Shannon R."],["dc.contributor.author","Serth, Juergen"],["dc.contributor.author","Schostak, Martin"],["dc.contributor.author","Kamradt, Jorn"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Model, Fabian"],["dc.contributor.author","Day, J. Kevin"],["dc.contributor.author","Liebenberg, Volker"],["dc.contributor.author","Morotti, Andrew"],["dc.contributor.author","Yamamura, S. U."],["dc.contributor.author","Lograsso, Joe"],["dc.contributor.author","Sledziewski, Andrew"],["dc.contributor.author","Semjonow, Axel"],["dc.date.accessioned","2018-11-07T11:25:26Z"],["dc.date.available","2018-11-07T11:25:26Z"],["dc.date.issued","2009"],["dc.description.abstract","BACKGROUND. A prostate cancer (PCa) biomarker with improved specificity relative to PSA is a public health priority. Hypermethylated DNA can be detected in body fluids from PCa patients and may be a useful biomarker, although clinical performance varies between studies. We investigated the performance of candidate PCa DNA methylation biomarkers identified through a genome-wide search. METHODS. Real-time PCR was used to measure four DNA methylation biomarkers: GSTP1 and three previously unreported candidates associated with the genes RASSF2, HIST1H4K, and TFAP2E in sodium bisulfite-modified DNA. Matched plasma and urine collected prospectively from 142 patients referred for prostate biopsy and 50 young asymptomatic males were analyzed. RESULTS. Analysis of all biomarkers in urine DNA significantly discriminated PCa from biopsy negative patients. The biomarkers discriminated PCa from biopsy negative patients with AUCs ranging from 0.64 for HIST1H4K (95% CI 0.55-0.72, P < 0.00001) to 0.69 for GSTPI (95% CI 0.60-0.77, P < 0.00001). All biomarkers showed minimal correlation with PSA. Multivariate analysis did not yield a panel that significantly improved performance over that of single biomarkers. All biomarkers showed greater sensitivity for PCa in urine than in plasma DNA. CONCLUSIONS. Analysis of the biomarkers in urine DNA significantly discriminated PCa from biopsy negative patients. The biomarkers provided information independent of PSA and may warrant inclusion in nomograms for predicting prostate biopsy outcome. The biomarkers' PCa sensitivity was greater for urine than plasma DNA. The biomarker performances in urine DNA should next be validated in formal training and test studies. Prostate 69:1257-1269, 2009. (C) 2009 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/pros.20967"],["dc.identifier.isi","000269176600001"],["dc.identifier.pmid","19459176"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6152"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56620"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0045"],["dc.relation.issn","0270-4137"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","DNA Methylation Biomarkers of Prostate Cancer: Confirmation of Candidates and Evidence Urine is the Most Sensitive Body Fluid for Non-Invasive Detection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Loertzer, Hagen"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2018-11-07T09:10:22Z"],["dc.date.available","2018-11-07T09:10:22Z"],["dc.date.issued","2012"],["dc.identifier.isi","000318009803054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26474"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Oncology"],["dc.publisher.place","Alexandria"],["dc.relation.conference","48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)"],["dc.relation.eventlocation","Chicago, IL"],["dc.relation.issn","0732-183X"],["dc.title","Antitumor effects of zoledronic acid in combination with histone deacetylase inhibitor valproic acid"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Strauss, Arne"],["dc.date.accessioned","2018-11-07T09:10:23Z"],["dc.date.available","2018-11-07T09:10:23Z"],["dc.date.issued","2012"],["dc.identifier.isi","000318009802848"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26477"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Oncology"],["dc.publisher.place","Alexandria"],["dc.relation.conference","48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)"],["dc.relation.eventlocation","Chicago, IL"],["dc.relation.issn","0732-183X"],["dc.title","Histone deacetylase inhibitor (HDACi) LBH589 interference with androgen receptor expression transcriptional activity in 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","1699"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","The Prostate"],["dc.bibliographiccitation.lastpage","1709"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Heinrich, Elmar"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Trojan, Lutz"],["dc.contributor.author","Strauss, Arne"],["dc.date.accessioned","2018-11-07T09:18:22Z"],["dc.date.available","2018-11-07T09:18:22Z"],["dc.date.issued","2013"],["dc.description.abstract","BACKGROUNDThe primary therapeutic target for non-organ-confined prostate cancer is the androgen receptor (AR). Main strategies to ablate AR function are androgen depletion and direct receptor blockade by AR antagonists. However, incurable castration resistant prostate cancer (CRPC) develops resistance mechanisms to cope with trace amounts of androgen including AR overexpression and mutation in the AR ligand binding domain. METHODSThe CRPC cell model VCaP derivative of a prostate cancer bone metastasis was used in vitro and in nude mice in vivo to examine the effects of immediate testosterone boost on CRPC cells. In addition, a testosterone tolerant cell model was established by incremental acclimatization of VCaP cells to 1nM testosterone. The effects of androgen withdrawal and testosterone boosts on gene expression were assessed by quantitative real-time polymerase chain reaction, ELISA, and Western blots. Tumor cell proliferation was evaluated with a BrdU test. RESULTSTestosterone boosts on CRPC VCaP cells eliminate tumor cells to a higher extent than androgen withdrawal in androgen tolerant cells. The pronounced decrease of tumor cell proliferation was accompanied by a marked downregulation of AR expression regarding full-length AR and splice variant AR V7. CONCLUSIONSAcquiring castration resistance of prostate cancer cells by AR overexpression and amplification obviously sensitizes such cells to testosterone concentrations as low as physiological values. This introduces novel therapeutic means to treat CRPC with non-toxic measures and may find clinical implementation in intermittent androgen deprivation regimens. Prostate 73: 1699-1709, 2013. (c) 2013 Wiley Periodicals, Inc."],["dc.description.sponsorship","Deutsche Krebshilfe"],["dc.identifier.doi","10.1002/pros.22711"],["dc.identifier.isi","000324923400010"],["dc.identifier.pmid","23868789"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28396"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0045"],["dc.relation.issn","0270-4137"],["dc.title","Testosterone Boosts for Treatment of Castration Resistant Prostate Cancer: An Experimental Implementation of Intermittent Androgen Deprivation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]