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[PMID]:28456808
[Au] Autor:Batista RL; Rodrigues AS; Nishi MY; Feitosa ACR; Gomes NLRA; Junior JAF; Domenice S; Costa EMF; de Mendonça BB
[Ad] Endereço:Unidade de Endocrinologia do Desenvolvimento, Disciplina de Endocrinologia e Metabologia do Hospital das Clínicas, Laboratório de Hormônios e Genética Molecular (LIM/42), Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
[Ti] Título:Heterozygous Nonsense Mutation in the Androgen Receptor Gene Associated with Partial Androgen Insensitivity Syndrome in an Individual with 47,XXY Karyotype.
[So] Source:Sex Dev;11(2):78-81, 2017.
[Is] ISSN:1661-5433
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:There are only 2 patients with 47,XXY karyotype and androgen receptor (AR) gene mutation reported in the literature, and both are diagnosed as complete androgen insensitivity syndrome (CAIS). We report a 22-year-old female with 47,XXY karyotype and atypical external genitalia. Sequencing of AR revealed the heterozygous p.Asn849Lys*32 mutation, and extensive X chromosome microsatellite analysis showed homozygosity for Xp and heterozygosity for Xq, suggesting partial X maternal isodisomy. Partial androgen insensitivity syndrome (PAIS) developed in this case, probably because of the presence of the heterozygous AR mutation and random X- inactivation of the healthy allele. This is the first report of a female patient with 47,XXY karyotype and PAIS phenotype.
[Mh] Termos MeSH primário: Síndrome de Resistência a Andrógenos/genética
Códon sem Sentido/genética
Predisposição Genética para Doença
Cariótipo
Mutação/genética
Receptores Androgênicos/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Éxons/genética
Feminino
Heterozigoto
Homozigoto
Seres Humanos
Masculino
Repetições de Microssatélites/genética
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AR protein, human); 0 (Codon, Nonsense); 0 (Receptors, Androgen)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE
[do] DOI:10.1159/000468957


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[PMID]:29206995
[Au] Autor:Wyatt AW; Annala M; Aggarwal R; Beja K; Feng F; Youngren J; Foye A; Lloyd P; Nykter M; Beer TM; Alumkal JJ; Thomas GV; Reiter RE; Rettig MB; Evans CP; Gao AC; Chi KN; Small EJ; Gleave ME
[Ad] Endereço:Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, Canada; Institute of Biosciences and Medical Technology, University of Tampere, Tampere, Finland; Department of Medicine and Department of Radiation Oncology, UCSF Helen Diller Family Comprehensive
[Ti] Título:Concordance of Circulating Tumor DNA and Matched Metastatic Tissue Biopsy in Prostate Cancer.
[So] Source:J Natl Cancer Inst;109(12), 2017 Dec 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Real-time knowledge of the somatic genome can influence management of patients with metastatic castration-resistant prostate cancer (mCRPC). While routine metastatic tissue biopsy is challenging in mCRPC, plasma circulating tumor DNA (ctDNA) has emerged as a minimally invasive tool to sample the tumor genome. However, no systematic comparisons of matched "liquid" and "solid" biopsies have been performed that would enable ctDNA profiling to replace the need for direct tissue sampling. Methods: We performed targeted sequencing across 72 clinically relevant genes in 45 plasma cell-free DNA (cfDNA) samples collected at time of metastatic tissue biopsy. We compared ctDNA alterations with exome sequencing data generated from matched tissue and quantified the concordance of mutations and copy number alterations using the Fisher exact test and Pearson correlations. Results: Seventy-five point six percent of cfDNA samples had a ctDNA proportion greater than 2% of total cfDNA. In these patients, all somatic mutations identified in matched metastatic tissue biopsies were concurrently present in ctDNA. Furthermore, the hierarchy of variant allele fractions for shared mutations was remarkably similar between ctDNA and tissue. Copy number profiles between matched liquid and solid biopsy were highly correlated, and individual copy number calls in clinically actionable genes were 88.9% concordant. Detected alterations included AR amplifications in 22 (64.7%) samples, SPOP mutations in three (8.8%) samples, and inactivating alterations in tumor suppressors TP53 , PTEN , RB1 , APC , CDKN1B , BRCA2 , and PIK3R1 . In several patients, ctDNA sequencing revealed robust changes not present in paired solid biopsy, including clinically relevant alterations in the AR, WNT, and PI3K pathways. Conclusions: Our study shows that, in the majority of patients, a ctDNA assay is sufficient to identify all driver DNA alterations present in matched metastatic tissue and supports development of DNA biomarkers to guide mCRPC patient management based on ctDNA alone.
[Mh] Termos MeSH primário: DNA Tumoral Circulante/sangue
Neoplasias de Próstata Resistentes à Castração/genética
Neoplasias de Próstata Resistentes à Castração/patologia
[Mh] Termos MeSH secundário: Proteína da Polipose Adenomatosa do Colo/genética
Proteína BRCA2/genética
Biomarcadores Tumorais/sangue
Biomarcadores Tumorais/genética
Inibidor de Quinase Dependente de Ciclina p27/genética
Variações do Número de Cópias de DNA
Seres Humanos
Biópsia Líquida
Masculino
Mutação
Metástase Neoplásica
Proteínas Nucleares/genética
PTEN Fosfo-Hidrolase/genética
Fosfatidilinositol 3-Quinases/genética
Receptores Androgênicos/genética
Proteínas Repressoras/genética
Proteínas de Ligação a Retinoblastoma/genética
Proteína Supressora de Tumor p53/genética
Ubiquitina-Proteína Ligases/genética
Via de Sinalização Wnt/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APC protein, human); 0 (Adenomatous Polyposis Coli Protein); 0 (BRCA2 Protein); 0 (BRCA2 protein, human); 0 (Biomarkers, Tumor); 0 (CDKN1B protein, human); 0 (Circulating Tumor DNA); 0 (Nuclear Proteins); 0 (RB1 protein, human); 0 (Receptors, Androgen); 0 (Repressor Proteins); 0 (Retinoblastoma Binding Proteins); 0 (SPOP protein, human); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.1.- (PIK3R1 protein, human); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx118


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[PMID]:29183075
[Au] Autor:Van Wagoner RM; Eichner A; Bhasin S; Deuster PA; Eichner D
[Ad] Endereço:Sports Medicine Research and Testing Laboratory, Salt Lake City, Utah.
[Ti] Título:Chemical Composition and Labeling of Substances Marketed as Selective Androgen Receptor Modulators and Sold via the Internet.
[So] Source:JAMA;318(20):2004-2010, 2017 11 28.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Recent reports have described the increasing use of nonsteroidal selective androgen receptor modulators, which have not been approved by the US Food and Drug Administration (FDA), to enhance appearance and performance. The composition and purity of such products is not known. Objective: To determine the chemical identity and the amounts of ingredients in dietary supplements and products marketed and sold through the internet as selective androgen receptor modulators and compare the analyzed contents with product labels. Design and Setting: Web-based searches were performed from February 18, 2016, to March 25, 2016, using the Google search engine on the Chrome and Internet Explorer web browsers to identify suppliers selling selective androgen receptor modulators. The products were purchased and the identities of the compounds and their amounts were determined from April to August 2016 using chain-of-custody and World Anti-Doping Association-approved analytical procedures. Analytical findings were compared against the label information. Exposures: Products marketed and sold as selective androgen receptor modulators. Main Outcomes and Measures: Chemical identities and the amount of ingredients in each product marketed and sold as selective androgen receptor modulators. Results: Among 44 products marketed and sold as selective androgen receptor modulators, only 23 (52%) contained 1 or more selective androgen receptor modulators (Ostarine, LGD-4033, or Andarine). An additional 17 products (39%) contained another unapproved drug, including the growth hormone secretagogue ibutamoren, the peroxisome proliferator-activated receptor-δ agonist GW501516, and the Rev-ErbA agonist SR9009. Of the 44 tested products, no active compound was detected in 4 (9%) and substances not listed on the label were contained in 11 (25%). In only 18 of the 44 products (41%), the amount of active compound in the product matched that listed on the label. The amount of the compounds listed on the label differed substantially from that found by analysis in 26 of 44 products (59%). Conclusions and Relevance: In this limited investigation involving chemical analyses of 44 products marketed as selective androgen receptor modulators and sold via the internet, most products contained unapproved drugs and substances. Only 52% contained selective androgen receptor modulators and many were inaccurately labeled.
[Mh] Termos MeSH primário: Anabolizantes/química
Comércio
Rotulagem de Medicamentos
Internet
Substâncias para Melhoria do Desempenho/química
Receptores Androgênicos
[Mh] Termos MeSH secundário: Acetamidas/análise
Aminofenóis/análise
Anilidas/análise
Aprovação de Drogas
Tráfico de Drogas
Nitrilos/análise
Pirrolidinas/análise
Estados Unidos
United States Food and Drug Administration
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (4-(2-(2,2,2-trifluoro-1-hydroxyethyl)pyrrolidin-1-yl)-2-(trifluoromethyl)benzonitrile); 0 (Acetamides); 0 (Aminophenols); 0 (Anabolic Agents); 0 (Anilides); 0 (Nitriles); 0 (Performance-Enhancing Substances); 0 (Pyrrolidines); 0 (Receptors, Androgen); 7UT2HAH49H (andarine); O3571H3R8N (ostarine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.17069


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[PMID]:27771279
[Au] Autor:Miyamoto DT; Lee RJ
[Ad] Endereço:Massachusetts General Hospital Cancer Center, Boston, MA; Department of Radiation Oncology, Massachusetts General Hospital, Boston, MA; Harvard Medical School, Boston, MA. Electronic address: dmiyamoto@mgh.harvard.edu.
[Ti] Título:Cell-free and circulating tumor cell-based biomarkers in men with metastatic prostate cancer: Tools for real-time precision medicine?
[So] Source:Urol Oncol;34(11):490-501, 2016 11.
[Is] ISSN:1873-2496
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The recent expansion of therapeutic options for the treatment of metastatic prostate cancer highlights the need for precision medicine approaches to enable the rational selection of appropriate therapies for individual patients. In this context, circulating biomarkers in the peripheral blood are attractive as readily accessible tools for predicting and monitoring therapeutic response. In the case of circulating tumor cells and circulating tumor DNA, they may also serve as a noninvasive means of assessing molecular aberrations in tumors at multiple time points before and during therapy. These so-called "liquid biopsies" can provide a snapshot view of tumor molecular architecture and may enable clinicians to monitor the molecular status of tumors as they evolve during treatment, thus allowing for individualized precision therapeutic decisions for patients over time. In this review, we outline recent progress in the field of circulating biomarkers in metastatic prostate cancer and evaluate their potential for enabling this vision of real-time precision medicine.
[Mh] Termos MeSH primário: Adenocarcinoma/secundário
Biomarcadores Tumorais/sangue
DNA de Neoplasias/sangue
Células Neoplásicas Circulantes/química
Medicina de Precisão/métodos
Neoplasias da Próstata/sangue
[Mh] Termos MeSH secundário: Adenocarcinoma/sangue
Adenocarcinoma/tratamento farmacológico
Adenocarcinoma/genética
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Ensaios Clínicos como Assunto
Sistemas de Computação
Dosagem de Genes
Seres Humanos
Masculino
Estudos Multicêntricos como Assunto
Mutação
Proteínas de Neoplasias/sangue
Proteínas de Neoplasias/genética
Medicina de Precisão/tendências
Prognóstico
Neoplasias da Próstata/tratamento farmacológico
Neoplasias da Próstata/genética
Receptores Androgênicos/sangue
Receptores Androgênicos/genética
Análise de Célula Única
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (AR protein, human); 0 (Biomarkers, Tumor); 0 (DNA, Neoplasm); 0 (Neoplasm Proteins); 0 (Receptors, Androgen)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


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[PMID]:29307525
[Au] Autor:Candenas L; Pinto FM; Cejudo-Román A; González-Ravina C; Fernández-Sánchez M; Pérez-Hernández N; Irazusta J; Subirán N
[Ad] Endereço:Instituto de Investigaciones Químicas (L.C., F.M.P., A.C.-R., N.P.), CSIC, Seville, Spain. Electronic address: luzcandenas@iiq.csic.es.
[Ti] Título:Veratridine-sensitive Na channels regulate human sperm fertilization capacity.
[So] Source:Life Sci;196:48-55, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The sperm plasma membrane contains specific ion channels and transporters that initiate changes in Ca , Na , K and H ions in the sperm cytoplasm. Ion channels are key regulators of the sperm membrane potential, cytoplasmic Ca and intracellular pH (pH ), which leads to regulate motility, capacitation, acrosome reaction and other physiological processes crucial for successful fertilization. Expression of epithelial sodium channels (ENaC) and voltage-gated sodium channels (Na ) in human spermatozoa has been reported, but the role of Na fluxes sodium channels in the regulation of sperm cell function remains poorly understood. In this context, we aimed to analyze the physiological role of Na channels in human sperm. MAIN METHODS: Motility and hyperactivation analysis was conducted by CASA analysis. Flow cytometry and spectrophotometry approaches were carried out to measure Capacitation, Acrosome reaction, immunohistochemistry for Tyr-residues phosporylation, [Ca ] levels and membrane potential. KEY FINDINGS: Functional studies showed that veratridine, a voltage-gated sodium channel activator, increased sperm progressive motility without producing hyperactivation while the Na antagonist lidocaine did induce hyperactivated motility. Veratridine increased protein tyrosine phosphorylation, an event occurring during capacitation, and its effects were inhibited in the presence of lidocaine and tetrodotoxin. Veratridine had no effect on the acrosome reaction by itself, but was able to block the progesterone-induced acrosome reaction. Moreover, veratridine caused a membrane depolarization and modified the effect of progesterone on [Ca ] and sperm membrane potential. SIGNIFICANCE: Our results suggest that veratridine-sensitive Na channels are involved on human sperm fertility acquisition regulating motility, capacitation and the progesterone-induced acrosome reaction in human sperm.
[Mh] Termos MeSH primário: Fertilização/efeitos dos fármacos
Agonistas de Canais de Sódio/farmacologia
Canais de Sódio/efeitos dos fármacos
Espermatozoides/efeitos dos fármacos
Veratridina/farmacologia
[Mh] Termos MeSH secundário: Reação Acrossômica/efeitos dos fármacos
Adolescente
Adulto
Feminino
Seres Humanos
Imuno-Histoquímica
Técnicas In Vitro
Lidocaína/farmacologia
Masculino
Potenciais da Membrana/efeitos dos fármacos
Progesterona/antagonistas & inibidores
Progesterona/farmacologia
Receptores Androgênicos/efeitos dos fármacos
Sêmen/efeitos dos fármacos
Sódio/metabolismo
Bloqueadores dos Canais de Sódio/farmacologia
Capacitação Espermática/efeitos dos fármacos
Motilidade Espermática/efeitos dos fármacos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Androgen); 0 (Sodium Channel Agonists); 0 (Sodium Channel Blockers); 0 (Sodium Channels); 4G7DS2Q64Y (Progesterone); 71-62-5 (Veratridine); 98PI200987 (Lidocaine); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


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[PMID]:29228299
[Au] Autor:Goicochea NL; Garnovskaya M; Blanton MG; Chan G; Weisbart R; Lilly MB
[Ad] Endereço:Department of Medicine, Division of Hematology/Oncology, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas St., Charleston, SC 29425, USA.
[Ti] Título:Development of cell-penetrating bispecific antibodies targeting the N-terminal domain of androgen receptor for prostate cancer therapy.
[So] Source:Protein Eng Des Sel;30(12):785-793, 2017 12 01.
[Is] ISSN:1741-0134
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Castration-resistant prostate cancer cells exhibit continued androgen receptor signaling in spite of low levels of ligand. Current therapies to block androgen receptor signaling act by inhibiting ligand production or binding. We developed bispecific antibodies capable of penetrating cells and binding androgen receptor outside of the ligand-binding domain. Half of the bispecific antibody molecule consists of a single-chain variable fragment of 3E10, an anti-DNA antibody that enters cells. The other half is a single-chain variable fragment version of AR441, an anti-AR antibody. The resulting 3E10-AR441 bispecific antibody enters human LNCaP prostate cells and accumulates in the nucleus. The antibody binds to wild-type, mutant and splice variant androgen receptor. Binding affinity of 3E10-AR441 to androgen receptor (284 nM) was lower than that of the parental AR441 mAb (4.6 nM), but could be improved (45 nM) through alternative placement of the affinity tags, and ordering of the VH and VK domains. The 3E10-AR441 bispecific antibody blocked genomic signaling by wild-type or splice variant androgen receptor in LNCaP cells. It also blocked non-genomic signaling by the wild-type receptor. Furthermore, bispecific antibody inhibited the growth of C4-2 prostate cancer cells under androgen-stimulated conditions. The 3E10-AR441 biAb can enter prostate cancer cells and inhibits androgen receptor function in a ligand-independent manner. It may be an attractive prototype agent for prostate cancer therapy.
[Mh] Termos MeSH primário: Anticorpos Biespecíficos/metabolismo
Neoplasias da Próstata/metabolismo
Receptores Androgênicos/metabolismo
[Mh] Termos MeSH secundário: Anticorpos Biespecíficos/análise
Anticorpos Biespecíficos/farmacocinética
Anticorpos Biespecíficos/farmacologia
Linhagem Celular Tumoral
Núcleo Celular/química
Núcleo Celular/metabolismo
Seres Humanos
Masculino
Ligação Proteica
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AR protein, human); 0 (Antibodies, Bispecific); 0 (Receptors, Androgen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.1093/protein/gzx058


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[PMID]:28454723
[Au] Autor:Ma Y; Fu S; Lu L; Wang X
[Ad] Endereço:School of Kinesiology, Shanghai University of Sport, Shanghai 200438, China.
[Ti] Título:Role of androgen receptor on cyclic mechanical stretch-regulated proliferation of C2C12 myoblasts and its upstream signals: IGF-1-mediated PI3K/Akt and MAPKs pathways.
[So] Source:Mol Cell Endocrinol;450:83-93, 2017 Jul 15.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:OBJECTS: To detect the effects of androgen receptor (AR) on cyclic mechanical stretch-modulated proliferation of C2C12 myoblasts and its pathways: roles of IGF-1, PI3K and MAPK. METHODS: C2C12 were randomly divided into five groups: un-stretched control, six or 8 h of fifteen percent stretch, and six or 8 h of twenty percent stretch. Cyclic mechanical stretch of C2C12 were completed using a computer-controlled FlexCell Strain Unit. Cell proliferation and IGF-1 concentration in medium were detected by CCK8 and ELISA, respectively. Expressions of AR and IGF-1R, and expressions and activities of PI3K, p38 and ERK1/2 in stretched C2C12 cells were determined by Western blot. RESULTS: â‘ The proliferation of C2C12 cells, IGF-1 concentration in medium, expressions of AR and IGF-1R, and activities of PI3K, p38 and ERK1/2 were increased by 6 h of fifteen percent stretch, while decreased by twenty percent stretch for six or 8 h â‘¡The fifteen percent stretch-increased proliferation of C2C12 cells was reversed by AR inhibitor, Flutamide. â‘¢The increases of AR expression, activities of PI3K, p38 and ERK1/2 resulted from fifteen percent stretch were attenuated by IGF-1 neutralizing antibody, while twenty percent stretch-induced decreases of the above indicators were enhanced by recombinant IGF-1. â‘£Specific inhibitors of p38, ERK1/2 and PI3K all decreased the expression of AR in fifteen percent and twenty percent of stretched C2C12 cells. CONCLUSIONS: Cyclic mechanical stretch modulated the proliferation of C2C12 cells, which may be attributed to the alterations of AR via IGF-1-PI3K/Akt and IGF-1-MAPK (p38, ERK1/2) pathways in C2C12 cells.
[Mh] Termos MeSH primário: Fator de Crescimento Insulin-Like I/metabolismo
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Mioblastos/citologia
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores Androgênicos/metabolismo
Estresse Mecânico
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/farmacologia
Linhagem Celular
Proliferação Celular/efeitos dos fármacos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Camundongos
Mioblastos/efeitos dos fármacos
Mioblastos/enzimologia
Mioblastos/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Receptor IGF Tipo 1/metabolismo
Proteínas Recombinantes/farmacologia
Transdução de Sinais/efeitos dos fármacos
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Protein Kinase Inhibitors); 0 (Receptors, Androgen); 0 (Recombinant Proteins); 67763-96-6 (Insulin-Like Growth Factor I); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Receptor, IGF Type 1); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:29254307
[Au] Autor:Goren A; Shapiro J; Naccarato T; Situm M; Kovacevic M; Lonky N; Lotti T; McCoy J
[Ad] Endereço:Applied Biology, Inc., Irvine, CA, USA.
[Ti] Título:Social selection favours offspring prone to the development of androgenetic alopecia.
[So] Source:J Biol Regul Homeost Agents;31(4):1013-1016, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:In recent years, dermatologists have observed an increase in the incidence of male androgenetic alopecia (AGA). In a survey of 41 dermatologists, 88% reported an increase in incidence of AGA in men younger than 30 years. This phenomenon has no apparent explanation. However, due to the strong genetic inheritance component of AGA, a social or environmental factor which favours the inheritance of genes that increase the risk of developing AGA is suspected. To date, the strongest predictor of AGA in men has been the length of the CAG repeat located in the androgen receptor gene (AR gene) on the X chromosome. The same genetic variant in women is associated with ovulation at a later age, higher antral follicle count, and lower risk for premature ovarian failure. This led us to theorize that, due to social pressure to conceive later in life, women carriers of the short CAG repeat in the AR gene would have a selective advantage to conceive later in life and would thus favour male offspring exhibiting AGA.
[Mh] Termos MeSH primário: Alopecia/genética
Predisposição Genética para Doença
Herança Materna
Receptores Androgênicos/genética
[Mh] Termos MeSH secundário: Adulto
Fatores Etários
Alopecia/diagnóstico
Cromossomos Humanos X/química
Cromossomos Humanos X/metabolismo
Feminino
Fertilização/genética
Expressão Gênica
Seres Humanos
Masculino
Folículo Ovariano/citologia
Folículo Ovariano/fisiologia
Ovulação/genética
Receptores Androgênicos/química
Seleção Genética
Fatores Socioeconômicos
Repetições de Trinucleotídeos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Androgen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:28465296
[Au] Autor:Nyquist MD; Corella A; Burns J; Coleman I; Gao S; Tharakan R; Riggan L; Cai C; Corey E; Nelson PS; Mostaghel EA
[Ad] Endereço:Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington.
[Ti] Título:Exploiting AR-Regulated Drug Transport to Induce Sensitivity to the Survivin Inhibitor YM155.
[So] Source:Mol Cancer Res;15(5):521-531, 2017 05.
[Is] ISSN:1557-3125
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Androgen receptor (AR) signaling is fundamental to prostate cancer and is the dominant therapeutic target in metastatic disease. However, stringent androgen deprivation therapy regimens decrease quality of life and have been largely unsuccessful in curtailing mortality. Recent clinical and preclinical studies have taken advantage of the dichotomous ability of AR signaling to elicit growth-suppressive and differentiating effects by administering hyperphysiologic levels of testosterone. In this study, high-throughput drug screening identified a potent synergy between high-androgen therapy and YM155, a transcriptional inhibitor of survivin (BIRC5). This interaction was mediated by the direct transcriptional upregulation of the YM155 transporter SLC35F2 by the AR. Androgen-mediated YM155-induced cell death was completely blocked by the overexpression of multidrug resistance transporter ABCB1. SLC35F2 expression was significantly correlated with intratumor androgen levels in four distinct patient-derived xenograft models, and with AR activity score in a large gene expression dataset of castration-resistant metastases. A subset of tumors had significantly elevated SLC35F2 expression and, therefore, may identify patients who are highly responsive to YM155 treatment. IMPLICATIONS: The combination of androgen therapy with YM155 represents a novel drug synergy, and SLC35F2 may serve as a clinical biomarker of response to YM155.
[Mh] Termos MeSH primário: Androgênios/administração & dosagem
Imidazóis/administração & dosagem
Proteínas de Membrana Transportadoras/genética
Naftoquinonas/administração & dosagem
Neoplasias da Próstata/tratamento farmacológico
Receptores Androgênicos/metabolismo
[Mh] Termos MeSH secundário: Androgênios/farmacologia
Animais
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Sinergismo Farmacológico
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Imidazóis/farmacologia
Masculino
Camundongos
Naftoquinonas/farmacologia
Neoplasias da Próstata/genética
Neoplasias da Próstata/metabolismo
Transdução de Sinais/efeitos dos fármacos
Testosterona/administração & dosagem
Testosterona/farmacologia
Resultado do Tratamento
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AR protein, human); 0 (Androgens); 0 (Imidazoles); 0 (Membrane Transport Proteins); 0 (Naphthoquinones); 0 (Receptors, Androgen); 0 (SLC35F2 protein, human); 0 (YM 155); 3XMK78S47O (Testosterone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1158/1541-7786.MCR-16-0315-T


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[PMID]:27779102
[Au] Autor:Al Fayi MS; Gou X; Forootan SS; Al-Jameel W; Bao Z; Rudland PR; Cornford PA; Hussain SA; Ke Y
[Ad] Endereço:Molecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, the Cancer Research Centre Building, Liverpool, United Kingdom.
[Ti] Título:The increased expression of fatty acid-binding protein 9 in prostate cancer and its prognostic significance.
[So] Source:Oncotarget;7(50):82783-82797, 2016 Dec 13.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In contrast to numerous studies conducted to investigate the crucial role of fatty acid binding protein 5 (FABP5) in prostate cancer, investigations on the possible involvement of other FABPs are rare. Here we first measured the mRNA levels of 10 FABPs in benign and malignant prostate cell lines and identified the differentially expressed FABP6 and FABP9 mRNAs whose levels in all malignant cell lines were higher than those in the benign cells. Thereafter we assessed the expression status of FABP6 and FABP9 in both prostate cell lines and in human tissues. FABP6 protein was overexpressed only in 1 of the 5 malignant cell lines and its immunostaining intensities were not significantly different between benign and malignant prostate tissues. In contrast, FABP9 protein was highly expressed in highly malignant cell lines PC-3 and PC3-M, but its level in the benign PNT-2 and other malignant cell lines was not detectable. When analysed in an archival set of human prostate tissues, immunohistochemical staining intensity for FABP9 was significantly higher in carcinomas than in benign cases and the increase in FABP9 was significantly correlated with reduced patient survival times. Moreover, the increased level of staining for FABP9 was significantly associated with the increased joint Gleason scores (GS) and androgen receptor index (AR). Suppression of FABP9 expression in highly malignant PC3-M cells inhibited their invasive potential. Our results suggest that FABP9 is a valuable prognostic marker to predict the outcomes of prostate cancer patients, perhaps by playing an important role in prostate cancer cell invasion.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Proteínas de Ligação a Ácido Graxo/metabolismo
Neoplasias da Próstata/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/genética
Linhagem Celular Tumoral
Movimento Celular
Proteínas de Ligação a Ácido Graxo/genética
Hormônios Gastrointestinais/genética
Hormônios Gastrointestinais/metabolismo
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Masculino
Gradação de Tumores
Invasividade Neoplásica
Valor Preditivo dos Testes
Neoplasias da Próstata/genética
Neoplasias da Próstata/patologia
Neoplasias da Próstata/terapia
Interferência de RNA
RNA Mensageiro/genética
Receptores Androgênicos/metabolismo
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AR protein, human); 0 (Biomarkers, Tumor); 0 (Fatty Acid-Binding Proteins); 0 (Gastrointestinal Hormones); 0 (RNA, Messenger); 0 (Receptors, Androgen); 117849-44-2 (fatty acid-binding protein 6)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.12635



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