Database : MEDLINE
Search on : Sertoli and Cell and Tumor [Words]
References found : 2453 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 246 go to page                         

  1 / 2453 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 29222199
[Au] Autor:Albany C; Einhorn L; Garbo L; Boyd T; Josephson N; Feldman DR
[Ad] Address:Indiana University Division of Hematology and Oncology, Indianapolis, Indiana, USA calbany@iu.edu.
[Ti] Title:Treatment of CD30-Expressing Germ Cell Tumors and Sex Cord Stromal Tumors with Brentuximab Vedotin: Identification and Report of Seven Cases.
[So] Source:Oncologist;23(3):316-323, 2018 Mar.
[Is] ISSN:1549-490X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Cytotoxic therapy for relapsed and refractory germ cell tumors or metastatic sex cord stromal tumors is rarely effective and is often accompanied by high adverse event rates. Expression of CD30 has been observed in testicular cancers, and patients with CD30-expressing embryonal carcinomas have worse progression-free survival and overall survival than those with CD30-negative tumors. The objective of this study (NCT01461538) was to characterize the antitumor activity of brentuximab vedotin in patients with CD30-expressing nonlymphomatous malignancies. Enrolled patients included seven patients with relapsed or refractory germ cell tumors or metastatic sex cord stromal tumors described in this case series. MATERIALS AND METHODS: Forty patients with relapsed or refractory germ cell tumors, metastatic sex cord stromal tumors, or testicular tumors were screened for CD30 expression; 14 patients had tumors that expressed CD30. Seven patients with CD30-expressing testicular cancer were enrolled in the treatment study: five patients with germ cell tumors, one patient with a Leydig cell tumor, and one patient with a Sertoli cell tumor. Patients were treated with brentuximab vedotin at initial doses of 1.8 or 2.4 mg/kg every 3 weeks. Response assessments were performed at cycles 2 and 4 and every 4 cycles thereafter while the patient was receiving treatment. RESULTS: Two of seven patients achieved an objective response, including one durable complete response and one partial response at a single time point. Both responding patients had germ cell tumors. Treatment with brentuximab vedotin was generally well tolerated. CONCLUSION: Treatment of relapsed or refractory germ cell tumors with brentuximab vedotin can induce durable responses with a manageable toxicity profile. IMPLICATIONS FOR PRACTICE: This case series of seven patients with relapsed or refractory CD30-expressing germ cell tumors (GCTs) or sex cord stromal tumors demonstrates that brentuximab vedotin has activity against GCTs and is well tolerated in heavily pretreated patients with these aggressive tumor types. One patient achieved a complete response that has been durable for almost 4 years since the discontinuation of treatment with brentuximab vedotin. Therefore, brentuximab vedotin may be a valuable option for physicians who care for this difficult-to-treat patient population.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1634/theoncologist.2017-0544

  2 / 2453 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29299971
[Au] Autor:Wang M; Su P
[Ad] Address:a Family Planning Research Institute of Tongji Medical College , Huazhong University of Science and Technology , Hubei , P.R. China.
[Ti] Title:The role of the Fas/FasL signaling pathway in environmental toxicant-induced testicular cell apoptosis: An update.
[So] Source:Syst Biol Reprod Med;64(2):93-102, 2018 Apr.
[Is] ISSN:1939-6376
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The Fas/FasL signaling pathway is one of the major pathways that regulate apoptosis. Increasing studies have shown that the activation of the Fas/FasL signaling pathway is closely associated with testicular cell apoptosis. However, the mechanism involved is still unclear. We discuss recent findings regarding the molecular mechanisms by which environmental toxicants induce testicular pathology via Fas/FasL signaling. These findings suggest that Fas/FasL signaling is employed to impact the sensitivity (a response to external factors) of germ cells, disrupt steroidogenic hormone and cytokine metabolism mediated by Sertoli cells, and elicit the activation of NFAT (nuclear factor of activated T-cells) in Leydig cell apoptosis. Consequently, degeneration of testicular somatic (Sertoli and Leydig) and spermatogenic cells, leads to decreased numbers of mature sperm and subsequently translates into infertility issues. Collectively, these findings illustrate that it is beneficial to develop potential targets for a new generation of new pharmaceutical therapies that would alleviate testicular dysfunctions. ABBREVIATIONS: BTB: blood-testis barrier; DD: death domains; DR3: death receptor 3; DR4: death receptor 4; DR5: death receptor 5; DED: death effector domain; DISC: death-inducing signaling complex; ERα: estrogen receptor alpha; FADD: Fas-associated death domain; FSH: follicle- stimulating hormone; IL-1ß: interleukin 1 beta; LH: luteinizing hormone; LPS: lipopolysaccharide; mFas: membrane Fas; MMP2: matrix metalloproteinase-2; MTA1: metastasis-associated protein 1; NAC: N-acetylcysteine; NCCD: the Nomenclature Committee on Cell Death; NFAT: nuclear factor of activated T-cells; NF-kB: nuclear transcription factor-kappaB; NO: nitric oxide; NP: 4-nonylphenol; PCD: programmed cell death; PP1/PP2A: protein phosphatase 1 and 2A; ROS: reactive oxygen species; sFas: soluble Fas; T: testosterone; TGF-ß: transforming growth factor-beta; THD: TNF homology domain; TIMP-2: tissue inhibitor of metalloproteinase-2; TNF: tumor necrosis factor; TNF-α: tumor necrosis factor-alpha; TNF-R1: Tumor necrosis factor receptor 1; TNFRSF1A: TNF receptor superfamily member 1A.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:In-Process
[do] DOI:10.1080/19396368.2017.1422046

  3 / 2453 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29502380
[Au] Autor:Ren M; Cong XF; Zhao SS; Zhang Y; Yang L
[Ad] Address:Department of Oncology, the First Hospital of Jilin University, Changchun 130021, China.
[Ti] Title:[DICER1 mutaiton identified in sisters with Ovarian Sertoli-Leydig cell tumor].
[So] Source:Zhonghua Zhong Liu Za Zhi;40(2):159-160, 2018 Feb 23.
[Is] ISSN:0253-3766
[Cp] Country of publication:China
[La] Language:chi
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:In-Data-Review
[do] DOI:10.3760/cma.j.issn.0253-3766.2018.02.016

  4 / 2453 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29469200
[Au] Autor:Verrier F; Dubois d'Enghien C; Gauthier-Villars M; Bonadona V; Faure-Conter C; Dijoud F; Stoppa-Lyonnet D; Houdayer C; Golmard L
[Ad] Address:Service de Génétique, Institut Curie, Paris, France.
[Ti] Title:Mutiple DICER1-related lesions associated with a germline deep intronic mutation.
[So] Source:Pediatr Blood Cancer;, 2018 Feb 22.
[Is] ISSN:1545-5017
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Germline DICER1 pathogenic variants predispose to numerous benign and malignant tumors. In this report, we describe DICER1 gene analysis in an adolescent diagnosed with multinodular goiter, ovarian Sertoli-Leydig cell tumor, and lung cyst. DICER1 mutational screening at the DNA level failed to detect any pathogenic variant. Subsequent messenger RNA (mRNA) analysis revealed a 132 nucleotide intronic sequence exonization. This truncating event was caused by a deep intronic mutation generating a de novo acceptor splice site. This study demonstrates that some undetected DICER1 mutations should be investigated at the mRNA level.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[St] Status:Publisher
[do] DOI:10.1002/pbc.27005

  5 / 2453 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29324788
[Au] Autor:Saeidi S; Shapouri F; de Iongh RU; Casagranda F; Sutherland JM; Western PS; McLaughlin EA; Familari M; Hime GR
[Ad] Address:Department of Anatomy and Neuroscience, University of Melbourne, Parkville, Australia.
[Ti] Title:Esrp1 is a marker of mouse fetal germ cells and differentially expressed during spermatogenesis.
[So] Source:PLoS One;13(1):e0190925, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:ESRP1 regulates alternative splicing, producing multiple transcripts from its target genes in epithelial tissues. It is upregulated during mesenchymal to epithelial transition associated with reprogramming of fibroblasts to iPS cells and has been linked to pluripotency. Mouse fetal germ cells are the founders of the adult gonadal lineages and we found that Esrp1 mRNA was expressed in both male and female germ cells but not in gonadal somatic cells at various stages of gonadal development (E12.5-E15.5). In the postnatal testis, Esrp1 mRNA was highly expressed in isolated cell preparations enriched for spermatogonia but expressed at lower levels in those enriched for pachytene spermatocytes and round spermatids. Co-labelling experiments with PLZF and c-KIT showed that ESRP1 was localized to nuclei of both Type A and B spermatogonia in a speckled pattern, but was not detected in SOX9+ somatic Sertoli cells. No co-localization with the nuclear speckle marker, SC35, which has been associated with post-transcriptional splicing, was observed, suggesting that ESRP1 may be associated with co-transcriptional splicing or have other functions. RNA interference mediated knockdown of Esrp1 expression in the seminoma-derived Tcam-2 cell line demonstrated that ESRP1 regulates alternative splicing of mRNAs in a non-epithelial cell germ cell tumour cell line.
[Mh] MeSH terms primary: Germ Cells/metabolism
RNA-Binding Proteins/metabolism
Spermatogenesis/physiology
Testis/growth & development
Testis/metabolism
[Mh] MeSH terms secundary: Alternative Splicing
Animals
Cell Line, Tumor
Cells, Cultured
Female
Gene Expression
Germ Cells/cytology
Male
Mice, Inbred C57BL
RNA, Messenger/metabolism
Testis/cytology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (ESRP1 protein, mouse); 0 (RNA, Messenger); 0 (RNA-Binding Proteins)
[Em] Entry month:1802
[Cu] Class update date: 180206
[Lr] Last revision date:180206
[Js] Journal subset:IM
[Da] Date of entry for processing:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190925

  6 / 2453 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29343557
[Au] Autor:Schultz KAP; Williams GM; Kamihara J; Stewart DR; Harris AK; Bauer AJ; Turner J; Shah R; Schneider K; Schneider KW; Carr AG; Harney LA; Baldinger S; Frazier AL; Orbach D; Schneider DT; Malkin D; Dehner LP; Messinger YH; Hill A
[Ad] Address:Cancer and Blood Disorders, International Pleuropulmonary Blastoma Registry and Children's Hospitals and Clinics of Minnesota krisann.schultz@childrensmn.org.
[Ti] Title:DICER1 and associated conditions: Identification of at-risk individuals and recommended surveillance strategies.
[So] Source:Clin Cancer Res;, 2018 Jan 17.
[Is] ISSN:1078-0432
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pathogenic germline DICER1 variants cause a hereditary cancer predisposition syndrome with a variety of manifestations. In addition to conferring increased cancer risks for pleuropulmonary blastoma (PPB) and ovarian sex cord-stromal tumors, particularly Sertoli-Leydig cell tumor, individuals with pathogenic germline DICER1 variants may also develop lung cysts, cystic nephroma, renal sarcoma and Wilms tumor, nodular hyperplasia of the thyroid, nasal chondromesenchymal hamartoma, ciliary body medulloepithelioma, genitourinary embryonal rhabdomyosarcoma and brain tumors including pineoblastoma and pituitary blastoma. In May 2016, the International PPB Registry convened the inaugural International DICER1 Symposium to develop consensus testing, surveillance and treatment recommendations. Attendees from North America, Europe and Russia provided expert representation from the disciplines of pediatric oncology, endocrinology, genetics, genetic counseling, radiology, pediatric surgery, pathology and clinical research. Recommendations are provided for genetic testing, prenatal management, and surveillance for DICER1-associated pulmonary, renal, gynecologic, thyroid, ophthalmologic, otolaryngologic, central nervous system tumors and gastrointestinal polyps. Risk for most DICER1-associated neoplasms is highest in early childhood and decreases in adulthood. Individual and caregiver education and judicious imaging-based surveillance are the primary recommended approaches. These testing and surveillance recommendations reflect a consensus of expert opinion and current literature. As DICER1 research expands, guidelines for screening and treatment will continue to be updated.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180118
[Lr] Last revision date:180118
[St] Status:Publisher

  7 / 2453 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29251108
[Au] Autor:Das M; Howell M; Foran EA; Iyre R; Mohapatra SS; Mohapatra S
[Ad] Address:1 Center for Research and Education in Nanobioengineering, University of South Florida College of Medicine, Tampa, FL, USA.
[Ti] Title:Sertoli Cells Loaded with Doxorubicin in Lipid Micelles Reduced Tumor Burden and Dox-Induced Toxicity.
[So] Source:Cell Transplant;26(10):1694-1702, 2017 Oct.
[Is] ISSN:1555-3892
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The toxic side effects of doxorubicin (Dox) limit its long-term use as a lung cancer chemotherapeutic. Additionally, drug delivery to the deep lung is challenging. To address these challenges, isolated rat Sertoli cells (SCs) were preloaded with Dox conjugated to lipid micelle nanoparticles (SC-DLMNs) and delivered to mouse lungs. These immunocompetent cells, when injected intravenously, travel to the lung, deliver the payload, and get cleared by the system quickly without causing any adverse reaction. We observed that SC-DLMNs effectively treated Lewis lung carcinoma 1-induced lung tumors in mice and the drug efficacy was comparable to SC-Dox treatment. Mice treated with SC-DLMNs also showed significantly less toxicity compared to those treated with SC-Dox. The encapsulation of Dox in lipid micelle nanoparticles reduced the toxicity of Dox and the SC-based delivery method ensured drug delivery to the deep lung without evoking any immune response. Taken together, these results provide a novel SC-based nanoparticle drug delivery method for improved therapeutic outcome of cardiotoxic antilung cancer drugs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180111
[Lr] Last revision date:180111
[St] Status:In-Process
[do] DOI:10.1177/0963689717721223

  8 / 2453 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29187512
[Au] Autor:Apellaniz-Ruiz M; de Kock L; Sabbaghian N; Guaraldi F; Ghizzoni L; Beccuti G; Foulkes WD
[Ad] Address:Lady Davis InstituteSegal Cancer Centre, Jewish General Hospital, Montréal, Québec, Canada.
[Ti] Title:Familial multinodular goiter and Sertoli-Leydig cell tumors associated with a large intragenic in-frame deletion.
[So] Source:Eur J Endocrinol;178(2):K11-K19, 2018 Feb.
[Is] ISSN:1479-683X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Familial multinodular goiter (MNG), with or without ovarian Sertoli-Leydig cell tumor (SLCT), has been linked to DICER1 syndrome. We aimed to search for the presence of a germline mutation in a large family with a remarkable history of MNG and SLCT, and to further explore the relevance of the identified mutation. DESIGN AND METHODS: Sanger sequencing, Fluidigm Access Array and multiplex ligation-dependent probe amplification (MLPA) techniques were used to screen for mutations in germline DNA from 16 family members. Where available, tumor DNA was also studied. mRNA and protein extracted from carriers' lymphocytes were used to characterize the expression of the mutant DICER1. RESULTS: Nine of 16 tested individuals carried a germline, in-frame deletion (c.4207-41_5364+1034del), which resulted in the loss of exons 23 and 24 from the cDNA. The mutant transcript does not undergo nonsense-mediated decay and the protein is devoid of specific metal ion-binding amino acids (p.E1705 and p.D1709) in the RNase IIIb domain. In addition, characteristic somatic 'second hit' mutations in this region were found on the other allele in tumors. CONCLUSIONS: Patients with DICER1 syndrome usually present a combination of a typically truncating germline mutation and a tumor-specific hotspot missense mutation within the sequence encoding the RNase IIIb domain. The in-frame deletion found in this family suggests that the germline absence of p.E1705 and p.D1709, which are crucial for RNase IIIb activity, may be enough to permit DICER1 syndrome to occur.
[Mh] MeSH terms primary: DEAD-box RNA Helicases/genetics
Goiter, Nodular/genetics
Ribonuclease III/genetics
Sertoli-Leydig Cell Tumor/genetics
[Mh] MeSH terms secundary: Adolescent
Adult
Aged
Breast Neoplasms/genetics
DNA/analysis
DNA/blood
Female
Fibroadenoma/genetics
Genetic Predisposition to Disease
Germ-Line Mutation/genetics
Goiter, Nodular/surgery
Humans
Lymphocytes/chemistry
Male
Ovarian Neoplasms/genetics
Ovarian Neoplasms/surgery
Pedigree
RNA, Messenger, Stored/blood
Sequence Analysis, DNA
Sequence Deletion
Sertoli-Leydig Cell Tumor/surgery
Syndrome
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (RNA, Messenger, Stored); 9007-49-2 (DNA); EC 3.1.26.3 (DICER1 protein, human); EC 3.1.26.3 (Ribonuclease III); EC 3.6.4.13 (DEAD-box RNA Helicases)
[Em] Entry month:1801
[Cu] Class update date: 180110
[Lr] Last revision date:180110
[Js] Journal subset:IM
[Da] Date of entry for processing:171201
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0904

  9 / 2453 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29319913
[Au] Autor:Moreau AM; Scruggs JL
[Ad] Address:Department of Defense Veterinary Pathology Residence Program (DODVPRP), Joint Pathology Center, Silver Spring, MD, USA.
[Ti] Title:What is your diagnosis? Inguinal mass in a dog.
[So] Source:Vet Clin Pathol;, 2018 Jan 10.
[Is] ISSN:1939-165X
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180110
[Lr] Last revision date:180110
[St] Status:Publisher
[do] DOI:10.1111/vcp.12548

  10 / 2453 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 28748527
[Au] Autor:Kim J; Field A; Schultz KAP; Hill DA; Stewart DR
[Ad] Address:Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD.
[Ti] Title:The prevalence of DICER1 pathogenic variation in population databases.
[So] Source:Int J Cancer;141(10):2030-2036, 2017 Nov 15.
[Is] ISSN:1097-0215
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The DICER1 syndrome is associated with a variety of rare benign and malignant tumors, including pleuropulmonary blastoma (PPB), cystic nephroma (CN) and Sertoli-Leydig cell tumor (SLCT). The prevalence and penetrance of pathogenic DICER1 variation in the general population is unknown. We examined three publicly-available germline whole exome sequence datasets: Exome Aggregation Consortium (ExAC), 1,000 Genomes (1,000 G) and the Exome Sequencing Project (ESP). To avoid over-estimation of pathogenic DICER1 variation from cancer-associated exomes, we excluded The Cancer Genome Atlas (TCGA) variants from ExAC. All datasets were annotated with snpEff and ANNOVAR and variants were classified into four categories: likely benign (LB), unknown significance (VUS), likely pathogenic (LP), or pathogenic (P). The prevalence of DICER1 P/LP variants was 1:870 to 1:2,529 in ExAC-nonTCGA (53,105 exomes) estimated by metaSVM and REVEL/CADD, respectively. A more stringent prevalence calculation considering only loss-of-function and previously-published pathogenic variants detected in ExAC-nonTCGA, yielded a prevalence of 1:10,600. Despite the rarity of most DICER1 syndrome tumors, pathogenic DICER1 variation is more common than expected. If confirmed, these findings may inform future sequencing-based newborn screening programs for PPB, CN and SLCT, in which early detection improves prognosis.
[Mh] MeSH terms primary: Biomarkers/metabolism
DEAD-box RNA Helicases/genetics
Kidney Diseases, Cystic/genetics
Ovarian Neoplasms/genetics
Pulmonary Blastoma/genetics
Ribonuclease III/genetics
Sertoli-Leydig Cell Tumor/genetics
[Mh] MeSH terms secundary: Early Detection of Cancer
Female
Genetic Predisposition to Disease
Germ-Line Mutation
Humans
Kidney Diseases, Cystic/epidemiology
Ovarian Neoplasms/epidemiology
Prevalence
Prognosis
Pulmonary Blastoma/epidemiology
Sertoli-Leydig Cell Tumor/epidemiology
United States/epidemiology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Biomarkers); EC 3.1.26.3 (DICER1 protein, human); EC 3.1.26.3 (Ribonuclease III); EC 3.6.4.13 (DEAD-box RNA Helicases)
[Em] Entry month:1710
[Cu] Class update date: 180104
[Lr] Last revision date:180104
[Js] Journal subset:IM
[Da] Date of entry for processing:170728
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30907


page 1 of 246 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information