Kaulfuß, Silke

[["dc.bibliographiccitation.artnumber","55"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Breast Cancer Research"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Weber-Lassalle, Nana"],["dc.contributor.author","Borde, Julika"],["dc.contributor.author","Weber-Lassalle, Konstantin"],["dc.contributor.author","Horváth, Judit"],["dc.contributor.author","Niederacher, Dieter"],["dc.contributor.author","Arnold, Norbert"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Ernst, Corinna"],["dc.contributor.author","Paul, Victoria G."],["dc.contributor.author","Honisch, Ellen"],["dc.contributor.author","Klaschik, Kristina"],["dc.contributor.author","Volk, Alexander E."],["dc.contributor.author","Kubisch, Christian"],["dc.contributor.author","Rapp, Steffen"],["dc.contributor.author","Lichey, Nadine"],["dc.contributor.author","Altmüller, Janine"],["dc.contributor.author","Lepkes, Louisa"],["dc.contributor.author","Pohl-Rescigno, Esther"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Larsen, Mirjam"],["dc.contributor.author","Richters, Lisa"],["dc.contributor.author","Rhiem, Kerstin"],["dc.contributor.author","Wappenschmidt, Barbara"],["dc.contributor.author","Engel, Christoph"],["dc.contributor.author","Meindl, Alfons"],["dc.contributor.author","Schmutzler, Rita K."],["dc.contributor.author","Hahnen, Eric"],["dc.contributor.author","Hauke, Jan"],["dc.date.accessioned","2019-07-09T11:51:25Z"],["dc.date.available","2019-07-09T11:51:25Z"],["dc.date.issued","2019"],["dc.description.abstract","BACKGROUND: The role of the BARD1 gene in breast cancer (BC) and ovarian cancer (OC) predisposition remains elusive, as published case-control investigations have revealed controversial results. We aimed to assess the role of deleterious BARD1 germline variants in BC/OC predisposition in a sample of 4920 BRCA1/2-negative female BC/OC index patients of the German Consortium for Hereditary Breast and Ovarian Cancer (GC-HBOC). METHODS: A total of 4469 female index patients with BC, 451 index patients with OC, and 2767 geographically matched female control individuals were screened for loss-of-function (LoF) mutations and potentially damaging rare missense variants in BARD1. All patients met the inclusion criteria of the GC-HBOC for germline testing and reported at least one relative with BC or OC. Additional control datasets (Exome Aggregation Consortium, ExAC; Fabulous Ladies Over Seventy, FLOSSIES) were included for the calculation of odds ratios (ORs). RESULTS: We identified LoF variants in 23 of 4469 BC index patients (0.51%) and in 36 of 37,265 control individuals (0.10%), resulting in an OR of 5.35 (95% confidence interval [CI] = 3.17-9.04; P < 0.00001). BARD1-mutated BC index patients showed a significantly younger mean age at first diagnosis (AAD; 42.3 years, range 24-60 years) compared with the overall study sample (48.6 years, range 17-92 years; P = 0.00347). In the subgroup of BC index patients with an AAD < 40 years, an OR of 12.04 (95% CI = 5.78-25.08; P < 0.00001) was observed. An OR of 7.43 (95% CI = 4.26-12.98; P < 0.00001) was observed when stratified for an AAD < 50 years. LoF variants in BARD1 were not significantly associated with BC in the subgroup of index patients with an AAD ≥ 50 years (OR = 2.29; 95% CI = 0.82-6.45; P = 0.11217). Overall, rare and predicted damaging BARD1 missense variants were significantly more prevalent in BC index patients compared with control individuals (OR = 2.15; 95% CI = 1.26-3.67; P = 0.00723). Neither LoF variants nor predicted damaging rare missense variants in BARD1 were identified in 451 familial index patients with OC. CONCLUSIONS: Due to the significant association of germline LoF variants in BARD1 with early-onset BC, we suggest that intensified BC surveillance programs should be offered to women carrying pathogenic BARD1 gene variants."],["dc.identifier.doi","10.1186/s13058-019-1137-9"],["dc.identifier.pmid","31036035"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16123"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59944"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Germline loss-of-function variants in the BARD1 gene are associated with early-onset familial breast cancer but not ovarian cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0200343"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Blesinger, Hannah"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Aung, Thiha"],["dc.contributor.author","Schwoch, Sonja"],["dc.contributor.author","Prantl, Lukas"],["dc.contributor.author","Rößler, Jochen"],["dc.contributor.author","Wilting, Jörg"],["dc.contributor.author","Becker, Jürgen"],["dc.date.accessioned","2019-07-09T11:45:49Z"],["dc.date.available","2019-07-09T11:45:49Z"],["dc.date.issued","2018"],["dc.description.abstract","Lymphatic malformations (LM) are characterized by the overgrowth of lymphatic vessels during pre- and postnatal development. Macrocystic, microcystic and combined forms of LM are known. The cysts are lined by lymphatic endothelial cells (LECs). Resection and sclerotherapy are the most common treatment methods. Recent studies performed on LM specimens in the United States of America have identified activating mutations in the phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) gene in LM. However, whole tissue but not isolated cell types were studied. Here, we studied LM tissues resected at the University Hospitals Freiburg and Regensburg, Germany. We isolated LECs and fibroblasts separately, and sequenced the commonly affected exons 8, 10, and 21 of the PIK3CA gene. We confirm typical monoallelic mutations in 4 out of 6 LM-derived LEC lines, and describe two new mutations i.) in exon 10 (c.1636C>A; p.Gln546Lys), and ii.) a 3bp in-frame deletion of GAA (Glu109del). LM-derived fibroblasts did not possess such mutations, showing cell-type specificity of the gene defect. High activity of the PIK3CA-AKT- mTOR pathway was demonstrated by hyperphosphorylation of AKT-Ser473 in all LM-derived LECs (including the ones with newly identified mutations), as compared to normal LECs. Additionally, hyperphosphorylation of ERK was seen in all LM-derived LECs, except for the one with Glu109del. In vitro, the small molecule kinase inhibitors Buparlisib/BKM-120, Wortmannin, and Ly294002, (all inhibitors of PIK3CA), CAL-101 (inhibitor of PIK3CD), MK-2206 (AKT inhibitor), Sorafenib (multiple kinases inhibitor), and rapamycin (mTOR inhibitor) significantly blocked proliferation of LM-derived LECs in a concentration-dependent manner, but also blocked proliferation of normal LECs. However, MK-2206 appeared to be more specific for mutated LECs, except in case of Glu109 deletion. In sum, children that are, or will be, treated with kinase inhibitors must be monitored closely."],["dc.identifier.doi","10.1371/journal.pone.0200343"],["dc.identifier.pmid","29985963"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15320"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59313"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","PIK3CA mutations are specifically localized to lymphatic endothelial cells of lymphatic malformations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1557"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Human Mutation"],["dc.bibliographiccitation.lastpage","1578"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Parsons, Michael T."],["dc.contributor.author","Tudini, Emma"],["dc.contributor.author","Li, Hongyan"],["dc.contributor.author","Hahnen, Eric"],["dc.contributor.author","Wappenschmidt, Barbara"],["dc.contributor.author","Feliubadaló, Lidia"],["dc.contributor.author","Aalfs, Cora M."],["dc.contributor.author","Agata, Simona"],["dc.contributor.author","Aittomäki, Kristiina"],["dc.contributor.author","Alducci, Elisa"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Engel, Christoph"],["dc.contributor.author","Spurdle, Amanda B."],["dc.date.accessioned","2019-12-02T14:12:29Z"],["dc.date.accessioned","2021-10-27T13:21:42Z"],["dc.date.available","2019-12-02T14:12:29Z"],["dc.date.available","2021-10-27T13:21:42Z"],["dc.date.issued","2019"],["dc.description.abstract","The multifactorial likelihood analysis method has demonstrated utility for quantitative assessment of variant pathogenicity for multiple cancer syndrome genes. Independent data types currently incorporated in the model for assessing BRCA1 and BRCA2 variants include clinically calibrated prior probability of pathogenicity based on variant location and bioinformatic prediction of variant effect, co-segregation, family cancer history profile, co-occurrence with a pathogenic variant in the same gene, breast tumor pathology, and case-control information. Research and clinical data for multifactorial likelihood analysis were collated for 1,395 BRCA1/2 predominantly intronic and missense variants, enabling classification based on posterior probability of pathogenicity for 734 variants: 447 variants were classified as (likely) benign, and 94 as (likely) pathogenic; and 248 classifications were new or considerably altered relative to ClinVar submissions. Classifications were compared with information not yet included in the likelihood model, and evidence strengths aligned to those recommended for ACMG/AMP classification codes. Altered mRNA splicing or function relative to known nonpathogenic variant controls were moderately to strongly predictive of variant pathogenicity. Variant absence in population datasets provided supporting evidence for variant pathogenicity. These findings have direct relevance for BRCA1 and BRCA2 variant evaluation, and justify the need for gene-specific calibration of evidence types used for variant classification."],["dc.identifier.doi","10.1002/humu.23818"],["dc.identifier.eissn","1098-1004"],["dc.identifier.issn","1059-7794"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16801"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92041"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1098-1004"],["dc.relation.issn","1059-7794"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Large scale multifactorial likelihood quantitative analysis of BRCA1 and BRCA2 variants: An ENIGMA resource to support clinical variant classification"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","11778"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","11791"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Keitel, Ulrike"],["dc.contributor.author","Scheel, Andreas"],["dc.contributor.author","Thomale, Jürgen"],["dc.contributor.author","Halpape, Rovena"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Scheel, Christina"],["dc.contributor.author","Dobbelstein, Matthias"],["dc.date.accessioned","2022-03-01T11:44:20Z"],["dc.date.available","2022-03-01T11:44:20Z"],["dc.date.issued","2014"],["dc.description.abstract","The transition from an epithelial to a mesenchymal phenotype (EMT) confers increased invasiveness and clonogenic potential to tumor cells. We used a breast epithelium-derived cell culture model to evaluate the impact of EMT on the cellular sensitivity towards chemotherapeutics and apoptotic stimuli. Cells that had passed through an EMT acquired resistance towards chemotherapeutics and death ligands. Mechanistically, we found that the levels of the apoptosis inhibitor Bcl-xL were strongly enhanced in mesenchymal versus epithelial cells, whereas the pro-apoptotic proteins Bim and Puma were diminished. Clinical samples from breast cancer showed enhanced Bcl-xL staining in cells that had dispersed into the desmoplastic stroma, as compared to cells that were part of large tumor cell aggregates, suggesting increased Bcl-xL expression when cells invade the stroma. Bcl-xL was necessary for apoptotic resistance in mesenchymal cells, and its expression was sufficient to confer such resistance to epithelial cells. To antagonize Bcl-xL, BH3-mimetics were used. They successfully interfered with the proliferation and survival of mesenchymal cells, and also inhibited the growth of xenograft tumors raised from the mesenchymal subpopulation. We conclude that enhanced Bcl-xL levels confer resistance to cells upon EMT, and that Bcl-xL represents a promising target for therapy directed against invasive cancer cells."],["dc.format.extent","14"],["dc.identifier.doi","10.18632/oncotarget.2634"],["dc.identifier.fs","610572"],["dc.identifier.pii","2634"],["dc.identifier.pmid","25473892"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11133"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102995"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1949-2553"],["dc.relation.issn","1949-2553"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.ddc","610"],["dc.title","Bcl-xL mediates therapeutic resistance of a mesenchymal breast cancer cell subpopulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1037"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","1049"],["dc.bibliographiccitation.volume","4"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Seemann, Henning"],["dc.contributor.author","Kampe, Rovena"],["dc.contributor.author","Meyer, Julia"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","König, Britta"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2019-07-09T11:54:26Z"],["dc.date.available","2019-07-09T11:54:26Z"],["dc.date.issued","2013"],["dc.description.abstract","Among the family of receptor tyrosine kinases (RTKs), platelet-derived growth factor receptor (PDGFR) has attracted increasing attention as a potential target of anti-tumor therapy in colorectal cancer (CRC). To study the function of PDGFRβ in CRC cell lines, SW480, DLD-1 and Caco-2 cells showing high PDGFRβ expression were used for receptor down-regulation by small interfering RNA (siRNA) and using the pharmacological inhibitor of PDGFRβ Ki11502. Blockade of PDGFRβ using both approaches led to moderate inhibition of proliferation and diminished activation of the downstream PI3K-signaling pathway in all three cell lines. Surprisingly, incubation with Ki11502 resulted in an arrest of SW480 cells in the G2 phase of the cell cycle, whereas the siRNA approach did not result in this effect. To address this difference, we analyzed the involvement of the PDGFRβ family member c-KIT in Ki11502 effectiveness, but siRNA and proliferation studies in SW480 and DLD-1 cells could not prove the involvement of c-KIT inactivation during Ki11502 treatment. Hence, an RTK activation antibody array on SW480 cells led us to the identification of the non-receptor tyrosine kinase SRC, which is inactivated after Ki11502 treatment but not after the siRNA approach. Further studies using the SRC-specific inhibitor PP2 showed that SRC inhibition upon treatment with the inhibitor Ki11502 is responsible for the observed effects of Ki11502 in SW480 and DLD-1 CRC cells. In summary, our results demonstrate that the inhibition of PDGFRβ alone using siRNA has only moderate cellular effects in CRC cell lines; however, the multi-target inhibition of PDGFRβ, c-KIT and SRC, e.g., using Ki11502, represents a promising therapeutic intervention for the treatment of CRC."],["dc.identifier.doi","10.18632/oncotarget.1085"],["dc.identifier.fs","598153"],["dc.identifier.pmid","23900414"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9173"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60657"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.ddc","610"],["dc.title","Blockade of the PDGFR family together with SRC leads to diminished proliferation of colorectal cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","877"],["dc.bibliographiccitation.journal","INTERNATIONAL JOURNAL OF ONCOLOGY"],["dc.bibliographiccitation.lastpage","884"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Possner, Maria"],["dc.contributor.author","Heuser, Markus"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Schulz, Wolfgang"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2019-07-10T08:13:32Z"],["dc.date.available","2019-07-10T08:13:32Z"],["dc.date.issued","2008"],["dc.description.abstract","The function of the androgen-regulated homeobox protein NKX3.1 in prostate cancer is controversial. NKX3.1 is necessary for correct prostate development and undergoes frequent allelic loss in prostate cancer. However, no mutations occur in the coding region and some particularly aggressive cancers over-express the protein. Nevertheless NKX3.1 is often referred to as candidate tumor suppressor gene. Recent findings suggest a function in protection against oxidative damage involved in prostate carcinogenesis. Thus NKX3.1 may act differently at various stages of prostate cancer. Unlike a classical tumor suppressor NKX3.1 is up-regulated by androgens and down-regulated by phytoestrogens. In this study we performed RNAi based functional analysis by knocking down NKX3.1 expression in LNCaP prostate cancer cells and analyzing the impact of NKX3.1 on gene expression and cell proliferation. Knockdown of NKX3.1 evoked a massive down-regulation of NKX3.1 expression, followed by reduction in mRNA expression of the androdrogen receptor (AR) and the insulinlike growth factor receptor (IGF-1R). Western blot analysis showed strong decreases of NKX3.1, AR, and IGF-1R protein expression. Concomitantly, cell proliferation decreased and expression of prostate-specific antigen (PSA) mRNA and its secretion were diminished, whereas expression of IGF binding protein 3 (IGFBP-3) and MMP tissue inhibitor 3 (TIMP-3) was up-regulated. In tumor cells not deprived of NKX3.1 expression this gene still has a function which might differ from its role in prostate development and carcinogenesis. NKX3.1 knock-down altered the expression of genes highly relevant in prostate cancer cell proliferation and apoptosis. In LNCaP NKX3.1 most probably plays the role of an androgenregulated transcription factor whose down-regulation is paralleled by anti-proliferative and pro-apoptotic effects. Since NKX3.1 can regulate AR expression it may become a target for interference in hormone refractory prostate carcinoma."],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6151"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61271"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.rights.access","closedAccess"],["dc.subject","NKX3.1; prostate cancer; tumor suppressor; RNA interference"],["dc.subject.ddc","610"],["dc.title","Functional analysis of NKX3.1 in LNCaP prostate cancer cells by RNA interference"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","16951"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","16961"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Unterkircher, Valerie"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2019-07-09T11:45:18Z"],["dc.date.available","2019-07-09T11:45:18Z"],["dc.date.issued","2018"],["dc.description.abstract","Novel treatments for castration-resistant prostate cancer (CRPC) such as abiraterone acetate (AA) or enzalutamide effectively target the androgen pathway to arrest aberrant signalling and cell proliferation. Testosterone is able to inhibit tumour cell growth in CRPC. Estrogen receptor-beta (ERβ) binds the testosteronemetabolites 3β-androstanediol and 3α-androstanediol in parallel to the canonical estradiol. In the prostate it is widely accepted that ERβ regulates estrogen signalling, mediating anti-proliferative effects. We used the prostate cancer cell lines LNCaP, PC-3, VCaP, and the non-neoplastic BPH-1. VCaP cells were treated with 1 nmol/L testosterone over 20 passages, yielding the cell line VCaPrev, sensitive to hormone therapies. In contrast, LNCaP cells were grown for more than 100 passages yielding a high passage therapy resistant cell line (hiPLNCaP). VCaP and hiPLNCaP cell lines were treated with 5 μmol/L AA for more than 20 passages, respectively, generating the AAtolerant- subtypes VCaPAA and hiPLNCaPAA. Cell lines were treated with testosterone, dihydrotestosterone (DHT), R1881, and the androgen-metabolites 3β-androstanediol and 3α-androstanediol. 3β-androstanediol or 3α-androstanediol significantly reduced proliferation in all cell lines except the BPH-1 and androgen receptor-negative PC-3 and markedly downregulated AR and estrogen receptor alpha (ERα). Whereas ERβ expression was increased in all cell lines except BPH-1 or PC-3. In summary, 3β-adiol or 3α-adiol, as well as DHT and R1881, significantly reduced tumour cell growth in CRPC cells. Thus, these compounds represent novel potential therapeutic approaches to overcome drug-resistance in CRPC, especially with regard to AR-V7 function in therapy resistance. Furthermore, these data confirm the tumour suppressor properties of ERβ in CRPC."],["dc.identifier.doi","10.18632/oncotarget.24763"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15104"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59207"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.ddc","610"],["dc.title","Testosterone metabolites inhibit proliferation of castration- and therapy-resistant prostate cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]