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[PMID]:29411910
[Au] Autor:Palicelli A; Neri P; Marchioro G; De Angelis P; Bondonno G; Ramponi A
[Ad] Endereço:Department of Health Science, School of Medicine, University of Eastern Piedmont 'Amedeo Avogadro', Novara, Italy.
[Ti] Título:Paratesticular seminoma: echographic features and histological diagnosis with review of the literature.
[So] Source:APMIS;126(3):267-272, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Primary extratesticular seminomas exceptionally occur in the epididymis or in the paratesticular region/spermatic cord. Some old papers included poor histological description or insufficient photographic documentation, reducing the number of faithful cases: an up-to-date systematic review is lacking. We report the 4th primary seminoma of the paratesticular region/spermatic cord in a 35-year-old man, including the first echographic description. We provide review of the literature and etiopathogenetic discussion. Ultrasound examination showed a right paratesticular, solid, heterogeneous mass (iso-hypoechoic with hyperechoic striae; peri- and intra-lesional vascular signals) with no testicular involvement: the paratesticular origin was confirmed by pathological examination. Despite careful gross examination and extensive sampling, the 6.5-cm extratesticular tumor revealed only one microscopic focus with minimal invasion (<2 mm) of the atrophic testicular parenchyma. Intratubular germ cell neoplasia or morphologic features of a regressed testicular tumor (fibrosis/scar, necrosis, hyalinization, calcification, inflammation) were not found. Primary seminomas of the paratesticular region/spermatic cord occurred at an older mean age and presented as bigger lesions if compared to the 9 primary epididymal seminomas reported in literature. Clinical-pathological correlation and accurate sampling are mandatory for a correct diagnosis.
[Mh] Termos MeSH primário: Epididimo/patologia
Seminoma/patologia
Cordão Espermático/patologia
Neoplasias Testiculares/patologia
[Mh] Termos MeSH secundário: Adulto
Epididimo/diagnóstico por imagem
Seres Humanos
Masculino
Seminoma/diagnóstico por imagem
Cordão Espermático/diagnóstico por imagem
Neoplasias Testiculares/diagnóstico por imagem
Ultrassonografia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[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:180208
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12806


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[PMID]:28448657
[Au] Autor:Drögemöller BI; Monzon JG; Bhavsar AP; Borrie AE; Brooks B; Wright GEB; Liu G; Renouf DJ; Kollmannsberger CK; Bedard PL; Aminkeng F; Amstutz U; Hildebrand CA; Gunaretnam EP; Critchley C; Chen Z; Brunham LR; Hayden MR; Ross CJD; Gelmon KA; Carleton BC
[Ad] Endereço:Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
[Ti] Título:Association Between SLC16A5 Genetic Variation and Cisplatin-Induced Ototoxic Effects in Adult Patients With Testicular Cancer.
[So] Source:JAMA Oncol;3(11):1558-1562, 2017 Nov 01.
[Is] ISSN:2374-2445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Cisplatin-induced ototoxic effects are an important complication that affects testicular cancer survivors as a consequence of treatment. The identification of genetic variants associated with this adverse drug reaction will further our mechanistic understanding of its development and potentially lead to strategies to prevent ototoxic effects. Objective: To identify the genetic variants associated with cisplatin-induced ototoxic effects in adult testicular cancer patients. Design, Setting, and Participants: This retrospective study was performed by the Canadian Pharmacogenomics Network for Drug Safety using patients recruited from 5 adult oncology treatment centers across Canada. Male patients who were 17 years or older, diagnosed with germ cell testicular cancer, and previously treated with cisplatin-based chemotherapy were recruited from July 2009 to April 2013 using active surveillance methodology. Cisplatin-induced ototoxic effects were independently diagnosed by 2 audiologists. Patients were genotyped for 7907 variants using a custom pharmacogenomic array. Logistic regression was used to identify genetic variants that were significantly associated with ototoxic effects. The validity of these findings was confirmed through independent replication and cell-based functional assays. Exposures: Cisplatin-based chemotherapy. Main Outcomes and Measures: Cisplatin-induced ototoxic effects. Results: After exclusions, 188 patients (median [interquartile range] age, 31 [24-39] years) were enrolled in this study to form the discovery and replication cohorts. Association and fine-mapping analyses identified a protein-coding variant, rs4788863 in SLC16A5, that was associated with protection against cisplatin-induced ototoxic effects in 2 independent cohorts (combined cohort: odds ratio, 0.06; 95% CI, 0.02-0.22; P = 2.17 × 10-7). Functional validation of this transporter gene revealed that in vitro SLC16A5-silencing altered cellular responses to cisplatin treatment, supporting a role for SLC16A5 in the development of cisplatin-induced ototoxic effects. These results were further supported by the literature, which provided confirmatory evidence for the role that SLC16A5 plays in hearing. Conclusions and Relevance: This study has identified a novel association between protein-coding variation in SLC16A5 and cisplatin-induced ototoxic effects. These findings have provided insight into the molecular mechanisms of this adverse drug reaction in adult patients with germ cell testicular cancer. Given that previous studies have shown that cimetidine, an SLC16A5-inhibitor, prevents murine cisplatin-induced ototoxic effects, the findings from this study have important implications for otoprotectant strategies in humans.
[Mh] Termos MeSH primário: Antineoplásicos/efeitos adversos
Cisplatino/efeitos adversos
Perda Auditiva/induzido quimicamente
Perda Auditiva/genética
Transportadores de Ácidos Monocarboxílicos/genética
Variantes Farmacogenômicos
Neoplasias Testiculares/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Canadá
Relação Dose-Resposta a Droga
Predisposição Genética para Doença
Células HeLa
Perda Auditiva/diagnóstico
Perda Auditiva/metabolismo
Seres Humanos
Modelos Logísticos
Masculino
Transportadores de Ácidos Monocarboxílicos/efeitos dos fármacos
Transportadores de Ácidos Monocarboxílicos/metabolismo
Farmacogenética
Testes Farmacogenômicos
Fenótipo
Interferência de RNA
Estudos Retrospectivos
Fatores de Risco
Transfecção
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Monocarboxylic Acid Transporters); 0 (SLC16A5 protein, human); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1001/jamaoncol.2017.0502


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[PMID]:29330226
[Au] Autor:Chortis V; Johal NJ; Bancos I; Evans M; Skordilis K; Guest P; Cullen MH; Porfiri E; Arlt W
[Ad] Endereço:Institute of Metabolism and Systems ResearchUniversity of Birmingham, Birmingham, UK.
[Ti] Título:Mitotane treatment in patients with metastatic testicular Leydig cell tumor associated with severe androgen excess.
[So] Source:Eur J Endocrinol;178(3):K21-K27, 2018 Mar.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitotane (o,p'DDD) is established in the adjuvant and advanced-stage treatment of adrenocortical carcinoma and counteracts both tumor growth and tumor-related steroid production. Both the adrenal glands and the gonads are steroidogenically active organs and share a common embryogenic origin. Here, we describe the effects of mitotane in two patients with metastatic Leydig cell tumor (LCT) of the testes and associated severe androgen excess (serum testosterone 93 and 88 nmol/L, respectively; male reference range 7-27 nmol/L). Both men suffered from severe restlessness, insomnia and irritability, which they described as intolerable and disrupting normal life activities. Urinary steroid profiling by gas chromatography-mass spectrometry (GC-MS) confirmed excess androgen production and revealed concurrent overproduction of glucocorticoids and glucocorticoid precursors, which under physiological conditions are produced only by the adrenal glands but not by the gonads. In a palliative approach, they were commenced on mitotane, which achieved swift control of the hormone excess and the debilitating clinical symptoms, restoring normal quality of life. GC-MS demonstrated normalization of steroid production and decreased 5α-reductase activity, resulting in decreased androgen activation, and imaging demonstrated disease stabilization for 4-10 months. In conclusion, mitotane can be highly effective in controlling steroid excess in metastatic LCTs, with anti-tumor activity in some cases.
[Mh] Termos MeSH primário: Antineoplásicos Hormonais/uso terapêutico
Hiperandrogenismo/tratamento farmacológico
Tumor de Células de Leydig/tratamento farmacológico
Mitotano/uso terapêutico
Neoplasias Testiculares/tratamento farmacológico
[Mh] Termos MeSH secundário: 3-Oxo-5-alfa-Esteroide 4-Desidrogenase/metabolismo
Androgênios/biossíntese
Cromatografia Gasosa-Espectrometria de Massas
Seres Humanos
Hiperandrogenismo/etiologia
Tumor de Células de Leydig/complicações
Tumor de Células de Leydig/secundário
Masculino
Meia-Idade
Metástase Neoplásica
Qualidade de Vida
Neoplasias Testiculares/complicações
Neoplasias Testiculares/patologia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androgens); 0 (Antineoplastic Agents, Hormonal); 78E4J5IB5J (Mitotane); EC 1.3.99.5 (3-Oxo-5-alpha-Steroid 4-Dehydrogenase)
[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:180114
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0542


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[PMID]:29300865
[Au] Autor:Fan J; Wang K; Zirkin B; Papadopoulos V
[Ad] Endereço:Research Institute of the McGill University Health Centre and Department of Medicine, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.
[Ti] Título:CRISPR/Cas9‒Mediated Tspo Gene Mutations Lead to Reduced Mitochondrial Membrane Potential and Steroid Formation in MA-10 Mouse Tumor Leydig Cells.
[So] Source:Endocrinology;159(2):1130-1146, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The outer mitochondrial membrane translocator protein (TSPO) binds cholesterol with high affinity and is involved in mediating its delivery into mitochondria, the rate-limiting step in hormone-induced steroidogenesis. Specific ligand binding to TSPO has been shown to initiate steroid formation. However, recent studies of the genetic deletion of Tspo have provided conflicting results. Here, we address and extend previous studies by examining the effects of Tspo-specific mutations on steroid formation in hormone- and cyclic adenosine monophosphate (cAMP)-responsive MA-10 cells, using the CRISPR/Cas9 system. Two mutant subcell lines, nG1 and G2G, each carrying a Tspo exon2-specific genome modification, and two control subcell lines, G1 and HH, each carrying a wild-type Tspo, were produced. In response to dibutyryl cAMP, the nG1 and G2G cells produced progesterone at levels significantly lower than those produced by the corresponding control cells G1 and HH. Neutral lipid homeostasis, which provides free cholesterol for steroid biosynthesis, was altered significantly in the Tspo mutant cells. Interestingly, the mitochondrial membrane potential (ΔΨm) of the Tspo mutant cells was significantly reduced compared with that of the control cells, likely because of TSPO interactions with the voltage-dependent anion channel and tubulin at the outer mitochondrial membrane. Steroidogenic acute regulatory protein (STAR) expression was induced in nG1 cells, suggesting that reduced TSPO affected STAR synthesis and/or processing. Taken together, these results provide further evidence for the critical role of TSPO in steroid biosynthesis and suggest that it may function at least in part via its regulation of ΔΨm and effects on STAR.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas/genética
Hormônios Esteroides Gonadais/biossíntese
Células Intersticiais do Testículo/metabolismo
Potencial da Membrana Mitocondrial/genética
Mutagênese Sítio-Dirigida
Mutação
Receptores de GABA/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Tumor de Células de Leydig/genética
Tumor de Células de Leydig/metabolismo
Tumor de Células de Leydig/patologia
Masculino
Camundongos
Mutagênese Sítio-Dirigida/métodos
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Esteroides/biossíntese
Neoplasias Testiculares/genética
Neoplasias Testiculares/metabolismo
Neoplasias Testiculares/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bzrp protein, mouse); 0 (Gonadal Steroid Hormones); 0 (Phosphoproteins); 0 (Receptors, GABA); 0 (Steroids); 0 (steroidogenic acute regulatory protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180105
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03065


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[PMID]:29339528
[Au] Autor:Engels M; Gehrmann K; Falhammar H; Webb EA; Nordenström A; Sweep FC; Span PN; van Herwaarden AE; Rohayem J; Richter-Unruh A; Bouvattier C; Köhler B; Kortmann BB; Arlt W; Roeleveld N; Reisch N; Stikkelbroeck NMML; Claahsen-van der Grinten HL; dsd-LIFE group
[Ad] Endereço:Department of PediatricsAmalia Children's Hospital, Radboud University Medical Center, Nijmegen, the Netherlands.
[Ti] Título:Gonadal function in adult male patients with congenital adrenal hyperplasia.
[So] Source:Eur J Endocrinol;178(3):285-294, 2018 Mar.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CONTEXT: Current knowledge on gonadal function in congenital adrenal hyperplasia (CAH) is mostly limited to single-center/country studies enrolling small patient numbers. Overall data indicate that gonadal function can be compromised in men with CAH. OBJECTIVE: To determine gonadal function in men with CAH within the European 'dsd-LIFE' cohort. DESIGN: Cross-sectional clinical outcome study, including retrospective data from medical records. METHODS: Fourteen academic hospitals included 121 men with CAH aged 16-68 years. Main outcome measures were serum hormone concentrations, semen parameters and imaging data of the testes. RESULTS: At the time of assessment, 14/69 patients had a serum testosterone concentration below the reference range; 7 of those were hypogonadotropic, 6 normogonadotropic and 1 hypergonadotropic. In contrast, among the patients with normal serum testosterone (55/69), 4 were hypogonadotropic, 44 normogonadotropic and 7 hypergonadotropic. The association of decreased testosterone with reduced gonadotropin concentrations (odds ratio (OR) = 12.8 (2.9-57.3)) was weaker than the association between serum androstenedione/testosterone ratio ≥1 and reduced gonadotropin concentrations (OR = 39.3 (2.1-732.4)). Evaluation of sperm quality revealed decreased sperm concentrations (15/39), motility (13/37) and abnormal morphology (4/28). Testicular adrenal rest tumor (TART)s were present in 39/80 patients, with a higher prevalence in patients with the most severe genotype (14/18) and in patients with increased current 17-hydroxyprogesterone 20/35) or androstenedione (12/18) serum concentrations. Forty-three children were fathered by 26/113 patients. CONCLUSIONS: Men with CAH have a high risk of developing hypothalamic-pituitary-gonadal disturbances and spermatogenic abnormalities. Regular assessment of endocrine gonadal function and imaging for TART development are recommended, in addition to measures for fertility protection.
[Mh] Termos MeSH primário: Hiperplasia Suprarrenal Congênita/sangue
Androstenodiona/sangue
Gonadotropinas/sangue
Hipogonadismo/sangue
Testosterona/sangue
[Mh] Termos MeSH secundário: Adolescente
Hiperplasia Suprarrenal Congênita/complicações
Hiperplasia Suprarrenal Congênita/epidemiologia
Tumor de Resto Suprarrenal/sangue
Tumor de Resto Suprarrenal/epidemiologia
Adulto
Idoso
Estudos Transversais
Europa (Continente)/epidemiologia
Seres Humanos
Hidroxiprogesteronas/sangue
Hipogonadismo/complicações
Masculino
Meia-Idade
Razão de Chances
Oligospermia/complicações
Prevalência
Análise do Sêmen
Contagem de Espermatozoides
Motilidade Espermática
Neoplasias Testiculares/sangue
Neoplasias Testiculares/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gonadotropins); 0 (Hydroxyprogesterones); 3XMK78S47O (Testosterone); 409J2J96VR (Androstenedione)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0862


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[PMID]:29197138
[Au] Autor:Chen Y; Lu J; Xia L; Xue D; Yu X; Shen D; Xu L; Li G
[Ad] Endereço:Department of Urology and Chawnshang Chang Liver Cancer Center, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
[Ti] Título:Testicular orphan receptor 4 promotes tumor progression and implies poor survival through AKT3 regulation in seminoma.
[So] Source:Cancer Sci;109(2):384-394, 2018 Feb.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Seminoma is the most common testicular germ cell tumor worldwide and mainly occurs in 15-35-year-old young men. Early studies have indicated that testicular nuclear receptor 4 (TR4) first cloned from testis is involved in the invasion and metastasis of several human tumors; however, little attention is paid to the function of TR4 in seminoma. Our immunohistochemical (IHC) staining results showed that patients with advanced stage tumors tended to have higher expression of TR4. Importantly, there was a significant association between elevated TR4 expression and reduced overall survival in seminoma patients. In vitro MTS, western blot and transwell assays, after manipulating TR4 expression in Tcam-2 cells, revealed that TR4 induced epithelial-to-mesenchymal transition (EMT) and promoted Tcam-2 cell proliferation and invasion. Mechanism dissection demonstrated that AKT3, a critical component in the signaling pathway, played a crucial role in mediating TR4-promoted Tcam-2 cell proliferation and invasion. We further revealed that TR4 modulated AKT3 at the transcriptional level via chromatin immunoprecipitation and luciferase assays. Meanwhile, addition of the AKT3 siRNA blocked the function of TR4. Overall, these findings first elucidate that TR4 is a novel prognostic marker and plays a critical role in the metastatic capacity of Tcam-2 cells by EMT regulation and, consequently, targeting TR4-AKT3 pathway may serve as a potential therapeutic approach for seminoma.
[Mh] Termos MeSH primário: Proteínas Proto-Oncogênicas c-akt/genética
Receptores de Esteroides/metabolismo
Receptores dos Hormônios Tireóideos/metabolismo
Seminoma/patologia
Neoplasias Testiculares/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Células COS
Linhagem Celular Tumoral
Proliferação Celular
Cercopithecus aethiops
Progressão da Doença
Transição Epitelial-Mesenquimal
Regulação Neoplásica da Expressão Gênica
Células HEK293
Seres Humanos
Masculino
Meia-Idade
Invasividade Neoplásica
Estadiamento de Neoplasias
Prognóstico
Proteínas Proto-Oncogênicas c-akt/metabolismo
Seminoma/genética
Seminoma/metabolismo
Transdução de Sinais
Neoplasias Testiculares/genética
Neoplasias Testiculares/metabolismo
Regulação para Cima
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NR2C2 protein, human); 0 (Receptors, Steroid); 0 (Receptors, Thyroid Hormone); EC 2.7.11.1 (AKT3 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171203
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13461


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[PMID]:29314802
[Au] Autor:Prelevic R; Milev B; Milovic N; Ignjatovic M; Spasic A; Petrovic N
[Ti] Título:Gigantic spermatocytic seminoma: A rare tumor of germ cell origin.
[So] Source:Vojnosanit Pregl;73(7):679-81, 2016 Jul.
[Is] ISSN:0042-8450
[Cp] País de publicação:Serbia
[La] Idioma:eng
[Ab] Resumo:Introduction: Spermatocytic seminoma represents a rare hystologic type of malignant testicular germ cell tumor with slow course and low malignant potential. Case report: We presented a 69-year-old patient with atypical clinical presentation of spermatocytic seminoma initially diagnosed as gigantic hydrocoellae which compromised walking. After long term evolution clincal picture presented with signs and symptoms of acute scrotum. Preoperative echosonography was performed and the diagnosis of testicular infiltrative tumor was established. After that left scrotal orchiectomy was performed. Patohistological examination revealed spermatocytic seminoma Conclusion: Inspite good prognosis there is a low probability of development of high grade malignancy sinchronous sarcoma within the testis with a high potential for lymphogenic and hematogenic dissemination. Individual approach is necessary in accordance with the pathohistological diagnosis.
[Mh] Termos MeSH primário: Seminoma/patologia
Neoplasias Testiculares/patologia
[Mh] Termos MeSH secundário: Diagnóstico Diferencial
Seres Humanos
Masculino
Orquiectomia/métodos
Seminoma/cirurgia
Hidrocele Testicular/diagnóstico
Neoplasias Testiculares/cirurgia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.2298/VSP150527081P


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[PMID]:29183799
[Au] Autor:Xing JS; Bai ZM
[Ad] Endereço:Department of Urinary Surgery, Central South University Xiangya School of Medicine Affiliated Haikou Hospital(Haikou People's Hospital), Haikou 570208, PR China.
[Ti] Título:Is testicular dysgenesis syndrome a genetic, endocrine, or environmental disease, or an unexplained reproductive disorder?
[So] Source:Life Sci;194:120-129, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Progressive increases in the incidence of male reproductive disorders inclusive of hypospadias, cryptorchidism, poor semen quality, and testicular germ cell cancer (TGCC) have been observed in recent times. The central hypothesis of this study asserted that these disorders may all collectively signify testicular dysgenesis syndrome (TDS). This review aimed to provide evidence verifying the reality of TDS based on four key aspects: environmental endocrine-disrupting chemicals (EDCs), genetic factors, intrauterine growth disorders and lifestyle factors. Although TDS might result from genetic polymorphisms or aberration, recent evidence has highlighted links indicating the conditions associations to both environmental and lifestyle factors due to the rapid temporal changes in the clinical symptoms observed over recent decades. Based on our review of genetic and environmental factors, a key observation of our study suggested that there is an urgent need to prioritize research in reproductive physiology and pathophysiology, particularly in highly industrialized countries facing decreasing populations. At present, current research has yet to elucidate the mechanisms of TDS, in addition to the lack of genuine consideration of a variety of potentially key factors and TDS mechanisms. In conclusion, our study revealed that environmental exposures owing to modern lifestyles are primary factors involved in the associated trends of the syndrome, which are capable of affecting the adult endocrine system via direct means or through epigenetic mechanisms.
[Mh] Termos MeSH primário: Disgenesia Gonadal/etiologia
Infertilidade Masculina/etiologia
Doenças Testiculares/etiologia
Testículo/patologia
[Mh] Termos MeSH secundário: Animais
Disruptores Endócrinos/efeitos adversos
Retardo do Crescimento Fetal/genética
Retardo do Crescimento Fetal/patologia
Disgenesia Gonadal/genética
Disgenesia Gonadal/patologia
Seres Humanos
Infertilidade Masculina/genética
Infertilidade Masculina/patologia
Estilo de Vida
Masculino
Neoplasias Embrionárias de Células Germinativas/etiologia
Neoplasias Embrionárias de Células Germinativas/genética
Neoplasias Embrionárias de Células Germinativas/patologia
Polimorfismo Genético
Doenças Testiculares/genética
Doenças Testiculares/patologia
Neoplasias Testiculares/etiologia
Neoplasias Testiculares/genética
Neoplasias Testiculares/patologia
Testículo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Endocrine Disruptors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


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[PMID]:29406056
[Au] Autor:Smith ZL; Werntz RP; Eggener SE
[Ad] Endereço:Section of Urology, Department of Surgery, The University of Chicago Medicine, 5841 South Maryland Avenue, MC 6038, Chicago, IL 60637, USA. Electronic address: zachary.smith@uchospitals.edu.
[Ti] Título:Testicular Cancer: Epidemiology, Diagnosis, and Management.
[So] Source:Med Clin North Am;102(2):251-264, 2018 Mar.
[Is] ISSN:1557-9859
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There were an estimated 8720 new cases of testicular cancer (TC) in the United States in 2016. The cause of the disease is complex, with several environmental and genetic risk factors. Although rare, the incidence has been steadily increasing. Fortunately, substantial advances in treatment have occurred over the last few decades, making TC one of the most curable malignancies. However, because TC typically occurs in younger men, considerations of the treatment impact on fertility, quality of life, and long-term toxicity are paramount; an individualized approach must be taken with patients based on their clinical and pathologic findings.
[Mh] Termos MeSH primário: Neoplasias Testiculares/diagnóstico
Neoplasias Testiculares/terapia
[Mh] Termos MeSH secundário: Seres Humanos
Masculino
Neoplasias Testiculares/epidemiologia
Neoplasias Testiculares/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  10 / 21452 MEDLINE  
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[PMID]:28471449
[Au] Autor:Özata DM; Li X; Lee L; Liu J; Warsito D; Hajeri P; Hultman I; Fotouhi O; Marklund S; Ährlund-Richter L; Juhlin CC; Larsson C; Lui WO
[Ad] Endereço:Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
[Ti] Título:Loss of miR-514a-3p regulation of PEG3 activates the NF-kappa B pathway in human testicular germ cell tumors.
[So] Source:Cell Death Dis;8(5):e2759, 2017 May 04.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Deregulation of microRNAs (miRNAs) contributes to the development and progression of many cancer types; however, their functions in the pathogenesis of testicular germ cell tumor (TGCT) remain unclear. Here, we determined miRNA expression profiles of TGCTs and normal testes using small RNA sequencing, and identified several deregulated miRNAs in TGCTs, including the miR-506~514 cluster. In functional studies in vitro we demonstrated that miR-514a-3p induced apoptosis through direct regulation of the paternally expressed gene 3 (PEG3), and ectopically expressed PEG3 could rescue the apoptotic effect of miR-514a-3p overexpression. Silencing of PEG3 or miR-514a-3p overexpression reduced nuclear accumulation of p50 and NF-κB reporter activity. Furthermore, PEG3 was co-immunoprecipitated with tumor necrosis factor receptor-associated factor 2 (TRAF2) in TGCT cell lysates. We propose a model of PEG3-mediated activation of NF-κB in TGCT. Loss of miR-514a-3p expression in TGCT increases PEG3 expression that recruits TRAF2 and activates the NF-kappa B pathway, which protects germ cells from apoptosis. Importantly, we observed strong expression of PEG3 and nuclear p50 in the majority of TGCTs (83% and 78%, respectively). In conclusion, our study describes a novel function for miR-514a-3p in TGCT and highlights an unrecognized mechanism of PEG3 regulation and NF-κB activation in TGCT.
[Mh] Termos MeSH primário: Fatores de Transcrição Kruppel-Like/metabolismo
MicroRNAs/metabolismo
NF-kappa B/metabolismo
Neoplasias Embrionárias de Células Germinativas/patologia
Neoplasias Testiculares/patologia
[Mh] Termos MeSH secundário: Antagomirs/metabolismo
Apoptose
Sequência de Bases
Linhagem Celular Tumoral
Metilação de DNA
Seres Humanos
Imunoprecipitação
Fatores de Transcrição Kruppel-Like/antagonistas & inibidores
Fatores de Transcrição Kruppel-Like/genética
Masculino
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Subunidade p50 de NF-kappa B/metabolismo
Neoplasias Embrionárias de Células Germinativas/metabolismo
Poli(ADP-Ribose) Polimerases/metabolismo
Regiões Promotoras Genéticas
Interferência de RNA
Alinhamento de Sequência
Transdução de Sinais
Fator 2 Associado a Receptor de TNF/metabolismo
Neoplasias Testiculares/metabolismo
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antagomirs); 0 (Kruppel-Like Transcription Factors); 0 (MicroRNAs); 0 (NF-kappa B); 0 (NF-kappa B p50 Subunit); 0 (PEG3 protein, human); 0 (TNF Receptor-Associated Factor 2); EC 2.4.2.30 (Poly(ADP-ribose) Polymerases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2016.464



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