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[PMID]: 29411910
[Au] Autor:Palicelli A; Neri P; Marchioro G; De Angelis P; Bondonno G; Ramponi A
[Ad] Address:Department of Health Science, School of Medicine, University of Eastern Piedmont 'Amedeo Avogadro', Novara, Italy.
[Ti] Title: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] Country of publication:Denmark
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Epididymis/pathology
Seminoma/pathology
Spermatic Cord/pathology
Testicular Neoplasms/pathology
[Mh] MeSH terms secundary: Adult
Epididymis/diagnostic imaging
Humans
Male
Seminoma/diagnostic imaging
Spermatic Cord/diagnostic imaging
Testicular Neoplasms/diagnostic imaging
Ultrasonography
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180208
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12806

  2 / 25513 MEDLINE  
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[PMID]: 29519910
[Au] Autor:Rockwood N; Nwokolo N
[Ad] Address:Chelsea and Westminster Hospital NHS Foundation Trust, London, UK.
[Ti] Title:Syphilis the great pretender: when is cancer not cancer?
[So] Source:Sex Transm Infect;, 2018 Mar 08.
[Is] ISSN:1472-3263
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The number of cases of syphilis continues to rise in the UK, USA and elsewhere and may present to a variety of clinical specialties. We report a complex case of early acquired disseminated syphilis causing an ulceronodular rash (lues maligna), orchitis, osteitis and lung nodules in an immunocompetent man who has sex with men who presented to the genitourinary medicine clinic. Syphilis should be considered in the differential diagnoses of multiple clinical presentations and optimal management should involve multidisciplinary care.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  3 / 25513 MEDLINE  
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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] Address:Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
[Ti] Title: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] Country of publication:United States
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Antineoplastic Agents/adverse effects
Cisplatin/adverse effects
Hearing Loss/chemically induced
Hearing Loss/genetics
Monocarboxylic Acid Transporters/genetics
Pharmacogenomic Variants
Testicular Neoplasms/drug therapy
[Mh] MeSH terms secundary: Adolescent
Adult
Canada
Dose-Response Relationship, Drug
Genetic Predisposition to Disease
HeLa Cells
Hearing Loss/diagnosis
Hearing Loss/metabolism
Humans
Logistic Models
Male
Monocarboxylic Acid Transporters/drug effects
Monocarboxylic Acid Transporters/metabolism
Pharmacogenetics
Pharmacogenomic Testing
Phenotype
RNA Interference
Retrospective Studies
Risk Factors
Transfection
Young Adult
[Pt] Publication type:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Monocarboxylic Acid Transporters); 0 (SLC16A5 protein, human); Q20Q21Q62J (Cisplatin)
[Em] Entry month:1711
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Js] Journal subset:IM
[Da] Date of entry for processing:170428
[St] Status:MEDLINE
[do] DOI:10.1001/jamaoncol.2017.0502

  4 / 25513 MEDLINE  
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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] Address:Institute of Metabolism and Systems ResearchUniversity of Birmingham, Birmingham, UK.
[Ti] Title: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] Country of publication:England
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Antineoplastic Agents, Hormonal/therapeutic use
Hyperandrogenism/drug therapy
Leydig Cell Tumor/drug therapy
Mitotane/therapeutic use
Testicular Neoplasms/drug therapy
[Mh] MeSH terms secundary: 3-Oxo-5-alpha-Steroid 4-Dehydrogenase/metabolism
Androgens/biosynthesis
Gas Chromatography-Mass Spectrometry
Humans
Hyperandrogenism/etiology
Leydig Cell Tumor/complications
Leydig Cell Tumor/secondary
Male
Middle Aged
Neoplasm Metastasis
Quality of Life
Testicular Neoplasms/complications
Testicular Neoplasms/pathology
Treatment Outcome
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Androgens); 0 (Antineoplastic Agents, Hormonal); 78E4J5IB5J (Mitotane); EC 1.3.99.5 (3-Oxo-5-alpha-Steroid 4-Dehydrogenase)
[Em] Entry month:1802
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[Js] Journal subset:IM
[Da] Date of entry for processing:180114
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0542

  5 / 25513 MEDLINE  
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[PMID]: 29300865
[Au] Autor:Fan J; Wang K; Zirkin B; Papadopoulos V
[Ad] Address:Research Institute of the McGill University Health Centre and Department of Medicine, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.
[Ti] Title: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] Country of publication:United States
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: CRISPR-Cas Systems/genetics
Gonadal Steroid Hormones/biosynthesis
Leydig Cells/metabolism
Membrane Potential, Mitochondrial/genetics
Mutagenesis, Site-Directed
Mutation
Receptors, GABA/genetics
[Mh] MeSH terms secundary: Animals
Cell Line, Tumor
Leydig Cell Tumor/genetics
Leydig Cell Tumor/metabolism
Leydig Cell Tumor/pathology
Male
Mice
Mutagenesis, Site-Directed/methods
Phosphoproteins/genetics
Phosphoproteins/metabolism
Steroids/biosynthesis
Testicular Neoplasms/genetics
Testicular Neoplasms/metabolism
Testicular Neoplasms/pathology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Bzrp protein, mouse); 0 (Gonadal Steroid Hormones); 0 (Phosphoproteins); 0 (Receptors, GABA); 0 (Steroids); 0 (steroidogenic acute regulatory protein)
[Em] Entry month:1802
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180105
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03065

  6 / 25513 MEDLINE  
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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] Address:Department of PediatricsAmalia Children's Hospital, Radboud University Medical Center, Nijmegen, the Netherlands.
[Ti] Title: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] Country of publication:England
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Adrenal Hyperplasia, Congenital/blood
Androstenedione/blood
Gonadotropins/blood
Hypogonadism/blood
Testosterone/blood
[Mh] MeSH terms secundary: Adolescent
Adrenal Hyperplasia, Congenital/complications
Adrenal Hyperplasia, Congenital/epidemiology
Adrenal Rest Tumor/blood
Adrenal Rest Tumor/epidemiology
Adult
Aged
Cross-Sectional Studies
Europe/epidemiology
Humans
Hydroxyprogesterones/blood
Hypogonadism/complications
Male
Middle Aged
Odds Ratio
Oligospermia/complications
Prevalence
Semen Analysis
Sperm Count
Sperm Motility
Testicular Neoplasms/blood
Testicular Neoplasms/epidemiology
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Gonadotropins); 0 (Hydroxyprogesterones); 3XMK78S47O (Testosterone); 409J2J96VR (Androstenedione)
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[Js] Journal subset:IM
[Da] Date of entry for processing:180118
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0862

  7 / 25513 MEDLINE  
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[PMID]: 28462701
[Au] Autor:Faa A; Gerosa C; Fanni D; Floris G; Eyken PV; Lachowicz JI; Nurchi VM
[Ad] Address:Istituto di Anatomia Patologica, Dipartimento di Scienze Chirurgiche, University of Cagliari; AOU Cagliari, Cagliari. Italy.
[Ti] Title:Depleted Uranium and Human Health.
[So] Source:Curr Med Chem;25(1):49-64, 2018.
[Is] ISSN:1875-533X
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Depleted uranium (DU) is generally considered an emerging pollutant, first extensively introduced into environment in the early nineties in Iraq, during the military operation called "Desert Storm". DU has been hypothesized to represent a hazardous element both for soldiers exposed as well as for the inhabitants of the polluted areas in the war zones. In this review, the possible consequences on human health of DU released in the environment are critically analyzed. In the first part, the chemical properties of DU and the principal civil and military uses are summarized. A concise analysis of the mechanisms underlying absorption, blood transport, tissue distribution and excretion of DU in the human body is the subject of the second part of this article. The following sections deal with pathological condition putatively associated with overexposure to DU. Developmental and birth defects, the Persian Gulf syndrome, and kidney diseases that have been associated to DU are the arguments treated in the third section. Finally, data regarding DU exposure and cancer insurgence will be critically analyzed, including leukemia/lymphoma, lung cancer, uterine cervix cancer, breast cancer, bladder cancer and testicular cancer. The aim of the authors is to give a contribution to the debate on DU and its effects on human health and disease.
[Mh] MeSH terms primary: Neoplasms/chemically induced
Uranium
[Mh] MeSH terms secundary: Humans
Uranium/adverse effects
Uranium/metabolism
Uranium/pharmacokinetics
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:4OC371KSTK (Uranium)
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[Js] Journal subset:IM
[Da] Date of entry for processing:170503
[St] Status:MEDLINE
[do] DOI:10.2174/0929867324666170426102343

  8 / 25513 MEDLINE  
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[PMID]: 29332416
[Au] Autor:Böröcz K; Hayden Z; Mészáros V; Csizmadia Z; Farkas K; Kellermayer Z; Balogh P; Nagy F; Berki T
[Ad] Address:Klinikai Központ, Immunológiai és Biotechnológiai Intézet, Pécsi Tudományegyetem, Általános Orvostudományi Kar Pécs, Szigeti út 12., 7624.
[Ti] Title:Az autoimmun encephalitisek laboratóriumi vizsgálati lehetoségei. [Autoimmune encephalitis: possibilities in the laboratory investigation].
[So] Source:Orv Hetil;159(3):107-112, 2018 Jan.
[Is] ISSN:0030-6002
[Cp] Country of publication:Hungary
[La] Language:hun
[Ab] Abstract:INTRODUCTION: The role of autoimmune responses against central nervous system (CNS) antigens in encephalitis presenting with non-classified neurologic or psychiatric symptoms has been appreciated in the past decade. Paraneoplastic limbic encephalitis has a poor prognosis and is most commonly associated with lung, ovarium, and testicular neoplasms, leading to immune reactions against intracellular antigens (anti-Hu/ANNA1, anti-Ri/ANNA2, anti-CV2/CRMP5 and anti-Ma2/Ta). In contrast, the recently described autoimmune encephalitis subtypes present with a broad spectrum of symptoms, respond to autoimmune therapies well and usually associate with autoantibodies against neuronal cell surface receptors (NMDAR, GABA R, AMPAR) or synaptic proteins (LGI1, CASPR2). AIM: Our aim is to bring to awareness the increasing number of autoimmune encephalitis patients requiring neurologic, psychiatric and intensive care and to emphasize the significance of detecting various autoantibodies in diagnosing patients. METHOD: In the past 6 years, our laboratory received 836 autoimmune encephalitis diagnostic test requests from a total of 717 patients. Serum and cerebrospinal fluid (CSF) samples were analysed with indirect immunofluorescence using a BIOCHIP consisting of cell lines transfected with 6 different receptor proteins. RESULTS: IgG autoantibodies against receptor proteins were present in 7.5% of patients. The frequency of positive samples was the following: NMDAR > LGI1 > GABA R > CASPR2. CONCLUSION: Detecting autoantibodies facilitates the diagnosis of autoimmune encephalitis in an early stage. Patients diagnosed early can be effectively treated with plasmapheresis and immunosuppressive drugs. The efficiency of therapies can be monitored by autoantibody detection. Therefore, the diagnostic immune laboratory plays an important role in proper diagnosis and in the prevention of rapidly progressing symptoms. Orv Hetil. 2018; 159(3): 107-112.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[St] Status:In-Process
[do] DOI:10.1556/650.2018.30951

  9 / 25513 MEDLINE  
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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] Address:Department of Urology and Chawnshang Chang Liver Cancer Center, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
[Ti] Title: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] Country of publication:England
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Proto-Oncogene Proteins c-akt/genetics
Receptors, Steroid/metabolism
Receptors, Thyroid Hormone/metabolism
Seminoma/pathology
Testicular Neoplasms/pathology
[Mh] MeSH terms secundary: Adult
Aged
Aged, 80 and over
Animals
COS Cells
Cell Line, Tumor
Cell Proliferation
Cercopithecus aethiops
Disease Progression
Epithelial-Mesenchymal Transition
Gene Expression Regulation, Neoplastic
HEK293 Cells
Humans
Male
Middle Aged
Neoplasm Invasiveness
Neoplasm Staging
Prognosis
Proto-Oncogene Proteins c-akt/metabolism
Seminoma/genetics
Seminoma/metabolism
Signal Transduction
Testicular Neoplasms/genetics
Testicular Neoplasms/metabolism
Up-Regulation
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance: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] Entry month:1802
[Cu] Class update date: 180216
[Lr] Last revision date:180216
[Js] Journal subset:IM
[Da] Date of entry for processing:171203
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13461

  10 / 25513 MEDLINE  
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[PMID]: 29245176
[Au] Autor:Isaksson S; Bogefors K; Ståhl O; Eberhard J; Giwercman YL; Leijonhufvud I; Link K; Øra I; Romerius P; Bobjer J; Giwercman A
[Ad] Address:Molecular Reproductive Medicine Unit, Department of Translational Medicine, Lund University, Malmö, Sweden.
[Ti] Title:High risk of hypogonadism in young male cancer survivors.
[So] Source:Clin Endocrinol (Oxf);88(3):432-441, 2018 Mar.
[Is] ISSN:1365-2265
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Cancer and its treatment in childhood and young adulthood can cause hypogonadism, leading to increased risk of long-term morbidity and mortality. The aim of this study was to evaluate the risk of presenting with biochemical signs of hypogonadism in testicular cancer survivors (TCS) and male childhood cancer survivors (CCS) in relation to the type of treatment given. DESIGN: Case-control study. PATIENTS: Ninety-two TCS, 125 CCS (mean age 40 and median age 34 years, respectively; mean follow-up time 9.2 and 24 years, respectively) and a corresponding number of age-matched controls. MEASUREMENTS: Fasting morning blood samples were analysed for total testosterone (TT), follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The odds ratios (OR) for hypogonadism, defined as primary, secondary, compensated or ongoing androgen replacement, were calculated for TCS and CCS and for subgroups defined by diagnosis and treatment. RESULTS: Hypogonadism was found in 26% of CCS and 36% of TCS, respectively (OR: 2.1, P = .025 and OR = 2.3, P = .021). Among CCS, the OR was further increased in those given testicular irradiation (OR = 28, P = .004). Radiotherapy other than cranial or testicular irradiation plus chemotherapy, or cranial irradiation without chemotherapy, associated also with increased ORs (OR = 3.7, P = .013, and OR = 4.4, P = .038, respectively). Among TCS, those receiving >4 cycles of cisplatin-based chemotherapy had OR = 17, P = .015. CONCLUSIONS: Biochemical signs of testosterone deficiency are recognized as markers of decreased life expectancy. Thus, the risk of hypogonadism in TCS and CCS should be recognized and emphasizes the need of long-term follow-up for these men.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180215
[Lr] Last revision date:180215
[St] Status:In-Data-Review
[do] DOI:10.1111/cen.13534


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