17 results on '"Céraline J"'
Search Results
2. Data sharing under the general data protection regulation: Time to harmonize law and research ethics?
- Author
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Vlahou, A. Hallinan, D. Apweiler, R. Argiles, A. Beige, J. Benigni, A. Bischoff, R. Black, P.C. Boehm, F. Céraline, J. Chrousos, G.P. Delles, C. Evenepoel, P. Fridolin, I. Glorieux, G. Van Gool, A.J. Heidegger, I. Ioannidis, J.P.A. Jankowski, J. Jankowski, V. Jeronimo, C. Kamat, A.M. Masereeuw, R. Mayer, G. Mischak, H. Ortiz, A. Remuzzi, G. Rossing, P. Schanstra, J.P. Schmitz-Dräger, B.J. Spasovski, G. Staessen, J.A. Stamatialis, D. Stenvinkel, P. Wanner, C. Williams, S.B. Zannad, F. Zoccali, C. Vanholder, R.
- Abstract
The General Data Protection Regulation (GDPR) became binding law in the European Union Member States in 2018, as a step toward harmonizing personal data protection legislation in the European Union. The Regulation governs almost all types of personal data processing, hence, also, those pertaining to biomedical research. The purpose of this article is to highlight the main practical issues related to data and biological sample sharing that biomedical researchers face regularly, and to specify how these are addressed in the context of GDPR, after consulting with ethics/legal experts. We identify areas in which clarifications of the GDPR are needed, particularly those related to consent requirements by study participants. Amendments should target the following: (1) restricting exceptions based on national laws and increasing harmonization, (2) confirming the concept of broad consent, and (3) defining a roadmap for secondary use of data. These changes will be achieved by acknowledged learned societies in the field taking the lead in preparing a document giving guidance for the optimal interpretation of the GDPR, which will be finalized following a period of commenting by a broad multistakeholder audience. In parallel, promoting engagement and education of the public in the relevant issues (such as different consent types or residual risk for re-identification), on both local/national and international levels, is considered critical for advancement. We hope that this article will open this broad discussion involving all major stakeholders, toward optimizing the GDPR and allowing a harmonized transnational research approach. © 2021 Lippincott Williams and Wilkins. All rights reserved.
- Published
- 2021
3. UP47 - Pathological activities of androgen receptor variants in cell plasticity in prostate cancer
- Author
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Erdmann, E., Fix, S., Cottard, F., Ye, T., Kieffer, B., and Ceraline, J.
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- 2023
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- View/download PDF
4. Data Sharing Under the General Data Protection Regulation: Time to Harmonize Law and Research Ethics?
- Author
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Vlahou, A., Hallinan, D., Apweiler, R., Argiles, A., Beige, J., Benigni, A., Bischoff, R., Black, P.C., Boehm, F., Céraline, J., Chrousos, G.P., Delles, C., Evenepoel, P., Fridolin, I., Glorieux, G., Gool, A.J. van, Heidegger, I., Ioannidis, J.P., Jankowski, J., Jankowski, V., Jeronimo, C., Kamat, A.M., Masereeuw, R., Mayer, G., Mischak, H., Ortiz, A., Remuzzi, G., Rossing, P., Schanstra, J.P., Schmitz-Dräger, B.J., Spasovski, G., Staessen, J.A., Stamatialis, D., Stenvinkel, P., Wanner, C., Williams, S.B., Zannad, F., Zoccali, C., Vanholder, R., Vlahou, A., Hallinan, D., Apweiler, R., Argiles, A., Beige, J., Benigni, A., Bischoff, R., Black, P.C., Boehm, F., Céraline, J., Chrousos, G.P., Delles, C., Evenepoel, P., Fridolin, I., Glorieux, G., Gool, A.J. van, Heidegger, I., Ioannidis, J.P., Jankowski, J., Jankowski, V., Jeronimo, C., Kamat, A.M., Masereeuw, R., Mayer, G., Mischak, H., Ortiz, A., Remuzzi, G., Rossing, P., Schanstra, J.P., Schmitz-Dräger, B.J., Spasovski, G., Staessen, J.A., Stamatialis, D., Stenvinkel, P., Wanner, C., Williams, S.B., Zannad, F., Zoccali, C., and Vanholder, R.
- Abstract
Contains fulltext : 235731.pdf (Publisher’s version ) (Open Access)
- Published
- 2021
5. Unfaithfulness and promiscuity of a mutant androgen receptor in a hormone-refractory prostate cancer
- Author
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Monge, A., Jagla, M., Lapouge, G., Sasorith, S., Cruchant, M., Wurtz, J.-M., Jacqmin, D., Bergerat, J.-P., and Céraline, J.
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- 2006
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6. P27 - Androgen receptor-mediated transcriptional repression targets cell plasticity in prostate cancer
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Erdmann, É., Ould Madi Berthélémy, P., Cottard, F., Angel, C.Z., Schreyer, E., Ye, T., Morlet, B., Negroni, L., Kieffer, B., and Céraline, J.
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- 2022
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7. Anti-angiogenic effects of the thienopyridine SR 25989 in vitro and in vivo in a murine pulmonary metastasis model
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Mah-Becherel, M C M, primary, Céraline, J, additional, Deplanque, G, additional, Chenard, M-P, additional, Bergerat, J-P, additional, Cazenave, J-P, additional, and Klein-Soyer, C, additional
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- 2002
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8. Androgen receptor-mediated transcriptional repression targets cell plasticity in prostate cancer.
- Author
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Erdmann É, Ould Madi Berthélémy P, Cottard F, Angel CZ, Schreyer E, Ye T, Morlet B, Negroni L, Kieffer B, and Céraline J
- Subjects
- Androgens, Cell Line, Tumor, Cell Plasticity, Gene Expression Regulation, Neoplastic, Humans, Male, Prostate metabolism, Prostatic Neoplasms, Castration-Resistant pathology, Receptors, Androgen metabolism
- Abstract
Androgen receptor (AR) signaling remains the key therapeutic target in the management of hormone-naïve-advanced prostate cancer (PCa) and castration-resistant PCa (CRPC). Recently, landmark molecular features have been reported for CRPC, including the expression of constitutively active AR variants that lack the ligand-binding domain. Besides their role in CRPC, AR variants lead to the expression of genes involved in tumor progression. However, little is known about the specificity of their mode of action compared with that of wild-type AR (AR-WT). We performed AR transcriptome analyses in an androgen-dependent PCa cell line as well as cross-analyses with publicly available RNA-seq datasets and established that transcriptional repression capacity that was marked for AR-WT was pathologically lost by AR variants. Functional enrichment analyses allowed us to associate AR-WT repressive function to a panel of genes involved in cell adhesion and epithelial-to-mesenchymal transition. So, we postulate that a less documented AR-WT normal function in prostate epithelial cells could be the repression of a panel of genes linked to cell plasticity and that this repressive function could be pathologically abrogated by AR variants in PCa., (© 2021 The Authors. Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.)
- Published
- 2022
- Full Text
- View/download PDF
9. Data Sharing Under the General Data Protection Regulation: Time to Harmonize Law and Research Ethics?
- Author
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Vlahou A, Hallinan D, Apweiler R, Argiles A, Beige J, Benigni A, Bischoff R, Black PC, Boehm F, Céraline J, Chrousos GP, Delles C, Evenepoel P, Fridolin I, Glorieux G, van Gool AJ, Heidegger I, Ioannidis JPA, Jankowski J, Jankowski V, Jeronimo C, Kamat AM, Masereeuw R, Mayer G, Mischak H, Ortiz A, Remuzzi G, Rossing P, Schanstra JP, Schmitz-Dräger BJ, Spasovski G, Staessen JA, Stamatialis D, Stenvinkel P, Wanner C, Williams SB, Zannad F, Zoccali C, and Vanholder R
- Subjects
- Europe, Humans, Biomedical Research ethics, Biomedical Research legislation & jurisprudence, Computer Security legislation & jurisprudence, Computer Security trends, Health Records, Personal ethics, Information Dissemination legislation & jurisprudence, Information Dissemination methods
- Abstract
The General Data Protection Regulation (GDPR) became binding law in the European Union Member States in 2018, as a step toward harmonizing personal data protection legislation in the European Union. The Regulation governs almost all types of personal data processing, hence, also, those pertaining to biomedical research. The purpose of this article is to highlight the main practical issues related to data and biological sample sharing that biomedical researchers face regularly, and to specify how these are addressed in the context of GDPR, after consulting with ethics/legal experts. We identify areas in which clarifications of the GDPR are needed, particularly those related to consent requirements by study participants. Amendments should target the following: (1) restricting exceptions based on national laws and increasing harmonization, (2) confirming the concept of broad consent, and (3) defining a roadmap for secondary use of data. These changes will be achieved by acknowledged learned societies in the field taking the lead in preparing a document giving guidance for the optimal interpretation of the GDPR, which will be finalized following a period of commenting by a broad multistakeholder audience. In parallel, promoting engagement and education of the public in the relevant issues (such as different consent types or residual risk for re-identification), on both local/national and international levels, is considered critical for advancement. We hope that this article will open this broad discussion involving all major stakeholders, toward optimizing the GDPR and allowing a harmonized transnational research approach.
- Published
- 2021
- Full Text
- View/download PDF
10. ZMIZ1 Variants Cause a Syndromic Neurodevelopmental Disorder.
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Carapito R, Ivanova EL, Morlon A, Meng L, Molitor A, Erdmann E, Kieffer B, Pichot A, Naegely L, Kolmer A, Paul N, Hanauer A, Tran Mau-Them F, Jean-Marçais N, Hiatt SM, Cooper GM, Tvrdik T, Muir AM, Dimartino C, Chopra M, Amiel J, Gordon CT, Dutreux F, Garde A, Thauvin-Robinet C, Wang X, Leduc MS, Phillips M, Crawford HP, Kukolich MK, Hunt D, Harrison V, Kharbanda M, Smigiel R, Gold N, Hung CY, Viskochil DH, Dugan SL, Bayrak-Toydemir P, Joly-Helas G, Guerrot AM, Schluth-Bolard C, Rio M, Wentzensen IM, McWalter K, Schnur RE, Lewis AM, Lalani SR, Mensah-Bonsu N, Céraline J, Sun Z, Ploski R, Bacino CA, Mefford HC, Faivre L, Bodamer O, Chelly J, Isidor B, and Bahram S
- Published
- 2020
- Full Text
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11. ZMIZ1 Variants Cause a Syndromic Neurodevelopmental Disorder.
- Author
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Carapito R, Ivanova EL, Morlon A, Meng L, Molitor A, Erdmann E, Kieffer B, Pichot A, Naegely L, Kolmer A, Paul N, Hanauer A, Tran Mau-Them F, Jean-Marçais N, Hiatt SM, Cooper GM, Tvrdik T, Muir AM, Dimartino C, Chopra M, Amiel J, Gordon CT, Dutreux F, Garde A, Thauvin-Robinet C, Wang X, Leduc MS, Phillips M, Crawford HP, Kukolich MK, Hunt D, Harrison V, Kharbanda M, Smigiel R, Gold N, Hung CY, Viskochil DH, Dugan SL, Bayrak-Toydemir P, Joly-Helas G, Guerrot AM, Schluth-Bolard C, Rio M, Wentzensen IM, McWalter K, Schnur RE, Lewis AM, Lalani SR, Mensah-Bonsu N, Céraline J, Sun Z, Ploski R, Bacino CA, Mefford HC, Faivre L, Bodamer O, Chelly J, Isidor B, and Bahram S
- Subjects
- Alleles, Animals, Child, Child, Preschool, Developmental Disabilities pathology, Female, Humans, Infant, Intellectual Disability pathology, Male, Mice, Syndrome, Transcription Factors chemistry, Transcription Factors metabolism, Developmental Disabilities genetics, Intellectual Disability genetics, Point Mutation, Transcription Factors genetics
- Abstract
ZMIZ1 is a coactivator of several transcription factors, including p53, the androgen receptor, and NOTCH1. Here, we report 19 subjects with intellectual disability and developmental delay carrying variants in ZMIZ1. The associated features include growth failure, feeding difficulties, microcephaly, facial dysmorphism, and various other congenital malformations. Of these 19, 14 unrelated subjects carried de novo heterozygous single-nucleotide variants (SNVs) or single-base insertions/deletions, 3 siblings harbored a heterozygous single-base insertion, and 2 subjects had a balanced translocation disrupting ZMIZ1 or involving a regulatory region of ZMIZ1. In total, we identified 13 point mutations that affect key protein regions, including a SUMO acceptor site, a central disordered alanine-rich motif, a proline-rich domain, and a transactivation domain. All identified variants were absent from all available exome and genome databases. In vitro, ZMIZ1 showed impaired coactivation of the androgen receptor. In vivo, overexpression of ZMIZ1 mutant alleles in developing mouse brains using in utero electroporation resulted in abnormal pyramidal neuron morphology, polarization, and positioning, underscoring the importance of ZMIZ1 in neural development and supporting mutations in ZMIZ1 as the cause of a rare neurodevelopmental syndrome., (Copyright © 2018 American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.)
- Published
- 2019
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12. [Androgen receptor variants in prostate cancer].
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Schreyer E, Barthélémy P, Cottard F, Ould Madi-Berthélémy P, Schaff-Wendling F, Kurtz JE, and Céraline J
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- Castration, Disease Progression, Drug Resistance, Neoplasm genetics, Humans, Male, Prostatic Neoplasms epidemiology, Prostatic Neoplasms pathology, Prostatic Neoplasms therapy, Prostatic Neoplasms, Castration-Resistant genetics, Prostatic Neoplasms, Castration-Resistant pathology, Prostatic Neoplasms, Castration-Resistant therapy, Signal Transduction genetics, Polymorphism, Genetic, Prostatic Neoplasms genetics, Receptors, Androgen genetics
- Abstract
Prostate cancer is a public health concern as it currently represents the most frequent malignancy in men in Europe. Progression of this hormone-dependent cancer is driven by androgens. Thus, the most common treatment for patients with advanced prostate cancer consists in an androgen ablation by castration therapy. However, the majority of patients relapses and develops a castration-resistant prostate cancer. This failure of androgen deprivation is related to the emergence of mutant and splice variants of the androgen receptor. Indeed, androgen receptor variants are ligand-independent, constitutively active and thus able to induce resistance to castration. This review focuses on AR variants signaling pathways and their role in resistance to castration and prostate cancer progression., (© 2017 médecine/sciences – Inserm.)
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- 2017
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13. Dual effects of constitutively active androgen receptor and full-length androgen receptor for N-cadherin regulation in prostate cancer.
- Author
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Cottard F, Madi-Berthélémy PO, Erdmann E, Schaff-Wendling F, Keime C, Ye T, Kurtz JE, and Céraline J
- Abstract
Constitutively active androgen receptor (AR) variants have been involved in the expression of mesenchymal markers such as N-cadherin in prostate cancer (PCa). However, the underlying molecular mechanisms remain elusive. It remains unclear, whether N-cadherin gene (CDH2) is a direct transcriptional target of AR variants or whether the observed upregulation is due to indirect effects through additional regulatory factors. Moreover, the specific contribution of full-length AR and AR variants in N-cadherin regulation in PCa has never been explored deeply. To investigate this, we artificially mimicked the co-expression of AR variants together with a full-length AR and performed miRNA-seq, RNA-seq and ChIP assays. Our results were in favor of a direct AR variants action on CDH2. Our data also revealed a distinctive mode of action between full-length AR and AR variants to regulate N-cadherin expression. Both wild type AR and AR variants could interact with a regulatory element in intron 1 of CDH2. However, a higher histone H4 acetylation in this genomic region was only observed with AR variants. This suggests that full-length AR may play an occluding function to impede CDH2 upregulation. Our data further highlighted a negative effect of AR variants on the expression of the endogenous full-length AR in LNCaP. These differences in the mode of action of AR variants and full-length AR for the control of one key gene for prostate cancer progression could be worth considering for targeting AR variants in PCa., Competing Interests: CONFLICTS OF INTEREST The authors report no conflicts of interest.
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- 2017
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14. Implication of NPM1 phosphorylation and preclinical evaluation of the nucleoprotein antagonist N6L in prostate cancer.
- Author
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Destouches D, Sader M, Terry S, Marchand C, Maillé P, Soyeux P, Carpentier G, Semprez F, Céraline J, Allory Y, Courty J, De La Taille A, and Vacherot F
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- Animals, Antineoplastic Agents pharmacology, Cell Line, Tumor, Docetaxel, Humans, Male, Mice, Nude, Nucleophosmin, Nucleoproteins metabolism, Peptides metabolism, Phosphorylation drug effects, Prostatic Neoplasms metabolism, Prostatic Neoplasms pathology, Prostatic Neoplasms, Castration-Resistant drug therapy, Prostatic Neoplasms, Castration-Resistant metabolism, Prostatic Neoplasms, Castration-Resistant pathology, Protein Binding, Receptors, Androgen metabolism, Taxoids pharmacology, Threonine metabolism, Tumor Burden drug effects, Nuclear Proteins metabolism, Nucleoproteins antagonists & inhibitors, Peptides pharmacology, Prostatic Neoplasms drug therapy, Xenograft Model Antitumor Assays
- Abstract
Despite the advent of several new treatment options over the past years, advanced/metastatic prostate carcinoma (PCa) still remains incurable, which justifies the search for novel targets and therapeutic molecules. Nucleophosmin (NPM1) is a shuttling nucleoprotein involved in tumor growth and its targeting could be a potential approach for cancer therapy. We previously demonstrated that the multivalent pseudopeptide N6L binds to NPM1 potently affecting in vitro and in vivo tumor cell growth of various tumor types as well as angiogenesis. Furthermore, NPM1 binds to androgen receptor (AR) and modulate its activity. In this study, we first investigated the implication of the NPM1 and its Thr199 and Thr234/237 phosphorylated forms in PCa. We showed that phosphorylated forms of NPM1 interact with androgen receptor (AR) in nucleoplasm. N6L treatment of prostate tumor cells led to inhibition of NPM1 phosphorylation in conjunction with inhibition of AR activity. We also found that total and phosphorylated NPM1 were overexpressed in castration-resistant PCa. Assessment of the potential therapeutic role of N6L in PCa indicated that N6L inhibited tumor growth both in vitro and in vivo when used either alone or in combination with the standard-of-care first- (hormonotherapy) and second-line (docetaxel) treatments for advanced PCa. Our findings reveal the role of Thr199 and Thr234/237 phosphorylated NPM1 in PCa progression and define N6L as a new drug candidate for PCa therapy.
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- 2016
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15. Constitutively active androgen receptor variants upregulate expression of mesenchymal markers in prostate cancer cells.
- Author
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Cottard F, Asmane I, Erdmann E, Bergerat JP, Kurtz JE, and Céraline J
- Subjects
- Cadherins genetics, Cell Line, Tumor, Disease Progression, Homeodomain Proteins genetics, Humans, Male, Transcription Factors genetics, Vimentin genetics, Zinc Finger E-box-Binding Homeobox 1, Biomarkers, Tumor genetics, Genetic Variation, Mesoderm metabolism, Prostatic Neoplasms pathology, Receptors, Androgen genetics, Up-Regulation
- Abstract
Androgen receptor (AR) signaling pathway remains the foremost target of novel therapeutics for castration-resistant prostate cancer (CRPC). However, the expression of constitutively active AR variants lacking the carboxy-terminal region in CRPC may lead to therapy inefficacy. These AR variants are supposed to support PCa cell growth in an androgen-depleted environment, but their mode of action still remains unresolved. Moreover, recent studies indicate that constitutively active AR variants are expressed in primary prostate tumors and may contribute to tumor progression. The aim of this study was to investigate the impact of constitutively active AR variants on the expression of tumor progression markers. N-cadherin expression was analyzed in LNCaP cells overexpressing the wild type AR or a constitutively active AR variant by qRT-PCR, Western blot and immunofluorescence. We showed here for the first time that N-cadherin expression was increased in the presence of constitutively active AR variants. These results were confirmed in C4-2B cells overexpressing these AR variants. Although N-cadherin expression is often associated with a downregulation of E-cadherin, this phenomenon was not observed in our model. Nevertheless, in addition to the increased expression of N-cadherin, an upregulation of other mesenchymal markers expression such as VIMENTIN, SNAIL and ZEB1 was observed in the presence of constitutively active variants. In conclusion, our findings highlight novel consequences of constitutively active AR variants on the regulation of mesenchymal markers in prostate cancer.
- Published
- 2013
- Full Text
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16. Risk of hormone escape in a human prostate cancer model depends on therapy modalities and can be reduced by tyrosine kinase inhibitors.
- Author
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Guyader C, Céraline J, Gravier E, Morin A, Michel S, Erdmann E, de Pinieux G, Cabon F, Bergerat JP, Poupon MF, and Oudard S
- Subjects
- Androgens deficiency, Animals, Base Sequence, Castration, Cluster Analysis, Combined Modality Therapy, Disease-Free Survival, Gene Dosage genetics, Humans, Male, Mice, Mutation genetics, Prostatic Neoplasms genetics, Prostatic Neoplasms pathology, Protein-Tyrosine Kinases metabolism, Receptor, ErbB-2 genetics, Receptors, Androgen genetics, Androgens therapeutic use, Prostatic Neoplasms drug therapy, Prostatic Neoplasms enzymology, Protein Kinase Inhibitors pharmacology, Protein Kinase Inhibitors therapeutic use, Protein-Tyrosine Kinases antagonists & inhibitors, Xenograft Model Antitumor Assays
- Abstract
Almost all prostate cancers respond to androgen deprivation treatment but many recur. We postulated that risk of hormone escape--frequency and delay--are influenced by hormone therapy modalities. More, hormone therapies induce crucial biological changes involving androgen receptors; some might be targets for escape prevention. We investigated the relationship between the androgen deprivation treatment and the risk of recurrence using nude mice bearing the high grade, hormone-dependent human prostate cancer xenograft PAC120. Tumor-bearing mice were treated by Luteinizing-Hormone Releasing Hormone (LHRH) antagonist alone, continuous or intermittent regimen, or combined with androgen receptor (AR) antagonists (bicalutamide or flutamide). Tumor growth was monitored. Biological changes were studied as for genomic alterations, AR mutations and protein expression in a large series of recurrent tumors according to hormone therapy modalities. Therapies targeting Her-2 or AKT were tested in combination with castration. All statistical tests were two-sided. Tumor growth was inhibited by continuous administration of the LH-RH antagonist degarelix (castration), but 40% of tumors recurred. Intermittent castration or complete blockade induced by degarelix and antiandrogens combination, inhibited tumor growth but increased the risk of recurrence (RR) as compared to continuous castration (RR(intermittent): 14.5, RR(complete blockade): 6.5 and 1.35). All recurrent tumors displayed new quantitative genetic alterations and AR mutations, whatever the treatment modalities. AR amplification was found after complete blockade. Increased expression of Her-2/neu with frequent ERK/AKT activation was detected in all variants. Combination of castration with a Her-2/neu inhibitor decreased recurrence risk (0.17) and combination with an mTOR inhibitor prevented it. Anti-hormone treatments influence risk of recurrence although tumor growth inhibition was initially similar. Recurrent tumors displayed genetic instability, AR mutations, and alterations of phosphorylation pathways. We postulated that Her-2/AKT pathways allowed salvage of tumor cells under castration and we demonstrated that their inhibition prevented tumor recurrence in our model.
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- 2012
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17. A splicing variant of the androgen receptor detected in a metastatic prostate cancer exhibits exclusively cytoplasmic actions.
- Author
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Jagla M, Fève M, Kessler P, Lapouge G, Erdmann E, Serra S, Bergerat JP, and Céraline J
- Subjects
- Animals, COS Cells, Cell Line, Tumor, Chlorocebus aethiops, DNA, Complementary genetics, Gene Amplification, Haplorhini, Humans, Male, Neoplasm Metastasis genetics, Restriction Mapping, Transfection, Alternative Splicing, Genetic Variation, Prostatic Neoplasms genetics, Prostatic Neoplasms pathology, Receptors, Androgen genetics
- Abstract
The androgen receptor (AR) is a ligand-activated transcription factor that displays genomic actions characterized by binding to androgen-response elements in the promoter of target genes as well as nongenomic actions that do not require nuclear translocation and DNA binding. In this study, we report exclusive cytoplasmic actions of a splicing variant of the AR detected in a metastatic prostate cancer. This AR variant, named AR23, results from an aberrant splicing of intron 2, wherein the last 69 nucleotides of the intronic sequence are retained, leading to the insertion of 23 amino acids between the two zinc fingers in the DNA-binding domain. We show that the nuclear entry of AR23 upon dihydrotestosterone (DHT) stimulation is impaired. Alternatively, DHT-activated AR23 forms cytoplasmic and perinuclear aggregates that partially colocalize with the endoplasmic reticulum and are devoid of genomic actions. However, in LNCaP cells, this cytoplasmic DHT-activated AR23 remains partially active as evidenced by the activation of transcription from androgen-responsive promoters, the stimulation of NF-kappaB transcriptional activity and by the decrease of AP-1 transcriptional activity. Our data reveal novel cytoplasmic actions for this splicing AR variant, suggesting a contribution in prostate cancer progression.
- Published
- 2007
- Full Text
- View/download PDF
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