Database : MEDLINE
Search on : medulloblastoma [Words]
References found : 8145 [refine]
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[PMID]: 29515120
[Au] Autor:Infante P; Faedda R; Bernardi F; Bufalieri F; Lospinoso Severini L; Alfonsi R; Mazzà D; Siler M; Coni S; Po A; Petroni M; Ferretti E; Mori M; De Smaele E; Canettieri G; Capalbo C; Maroder M; Screpanti I; Kool M; Pfister SM; Guardavaccaro D; Gulino A; Di Marcotullio L
[Ad] Address:Center for Life NanoScience@Sapienza, Istituto Italiano di Tecnologia, 00161, Rome, Italy.
[Ti] Title:Itch/ß-arrestin2-dependent non-proteolytic ubiquitylation of SuFu controls Hedgehog signalling and medulloblastoma tumorigenesis.
[So] Source:Nat Commun;9(1):976, 2018 Mar 07.
[Is] ISSN:2041-1723
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Suppressor of Fused (SuFu), a tumour suppressor mutated in medulloblastoma, is a central player of Hh signalling, a pathway crucial for development and deregulated in cancer. Although the control of Gli transcription factors by SuFu is critical in Hh signalling, our understanding of the mechanism regulating this key event remains limited. Here, we show that the Itch/ß-arrestin2 complex binds SuFu and induces its Lys63-linked polyubiquitylation without affecting its stability. This process increases the association of SuFu with Gli3, promoting the conversion of Gli3 into a repressor, which keeps Hh signalling off. Activation of Hh signalling antagonises the Itch-dependent polyubiquitylation of SuFu. Notably, different SuFu mutations occurring in medulloblastoma patients are insensitive to Itch activity, thus leading to deregulated Hh signalling and enhancing medulloblastoma cell growth. Our findings uncover mechanisms controlling the tumour suppressive functions of SuFu and reveal that their alterations are implicated in medulloblastoma tumorigenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41467-018-03339-0

  2 / 8145 MEDLINE  
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[PMID]: 29517209
[Au] Autor:Fudyma IA; Wadhwani NR
[Ti] Title:Medulloblastoma with extensive nodularity (SHH medulloblastoma).
[So] Source:Pol J Pathol;68(4):364-366, 2017.
[Is] ISSN:1233-9687
[Cp] Country of publication:Poland
[La] Language:eng
[Ab] Abstract:Medulloblastoma is the most common CNS embryonal tumor and the most common malignant tumor of childhood. Its overall incidence is 1.8 cases per 1 million people, with a childhood incidence of 6 cases per 1 million. 77 percent of patients are less than 19 years old. Medulloblastoma occurs in the 4th ventricle and usually presents with symptoms of increased intracranial pressure (headaches, nausea, vomiting) and signs of obstructive hydrocephalus. Medulloblastoma is both histologically and genetically defined with prognosis that depends on classification.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review

  3 / 8145 MEDLINE  
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[PMID]: 29309676
[Au] Autor:Chin AL; Moding EJ; Donaldson SS; Gibbs IC; Soltys SG; Hiniker SM; Pollom EL
[Ad] Address:Department of Radiation Oncology, Stanford University Medical Center, Stanford, California.
[Ti] Title:Survival Impact of Postoperative Radiotherapy Timing in Pediatric and Adolescent Medulloblastoma.
[So] Source:Neuro Oncol;, 2018 Jan 04.
[Is] ISSN:1523-5866
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: Radiation therapy (RT) remains a critical component of multimodality treatment for medulloblastoma. Traditionally, clinicians strive to start RT within 4-5 weeks of surgery, but the optimal timing after surgery remains unclear. Methods: Using the National Cancer Database, we identified pediatric and adolescent patients with medulloblastoma treated with curative-intent surgery, RT, and chemotherapy. Factors associated with early or delayed RT were identified using Pearson chi-squared tests. Overall survival (OS) differences based on RT timing were compared using the Kaplan-Meier estimator with log-rank tests. Patient, tumor, and treatment characteristics associated with OS were analyzed with univariate and multivariate Cox proportional hazard models. Results: Among the 1338 patients analyzed, early RT (defined as initiation ≤3 weeks after surgery) was associated with younger age, M1-3 disease, and subtotal resection. Patients who initiated RT early had decreased five-year OS compared with patients who initiated RT 3.1-4, 4.1-5, or >5 weeks after surgery (72.5%, 80.5%, 79.4%, and 77.8%, respectively; p=0.019), but there was no significant difference in OS among the latter three groups (p=0.788). On multivariate analysis, early RT versus the 3.1-4-week interval was significantly associated with poorer OS (adjusted HR 1.72; 95% CI 1.19-2.48; p=0.004), while time to RT of >5 weeks but within 90 days of surgery did not adversely impact OS (p=0.563). Conclusions: In this large national database analysis, delaying RT within 90 days of surgery was not associated with inferior outcomes. Although clinical judgment remains paramount, postoperative RT timing should allow for healing and the development of an optimal treatment plan.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/neuonc/noy001

  4 / 8145 MEDLINE  
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[PMID]: 29186568
[Au] Autor:Guerrini-Rousseau L; Dufour C; Varlet P; Masliah-Planchon J; Bourdeaut F; Guillaud-Bataille M; Abbas R; Bertozzi AI; Fouyssac F; Huybrechts S; Puget S; Bressac-De Paillerets B; Caron O; Sevenet N; Dimaria M; Villebasse S; Delattre O; Valteau-Couanet D; Grill J; Brugières L
[Ad] Address:Département de Cancérologie de l'Enfant et de l'Adolescent, Gustave Roussy, Université Paris-Saclay, Villejuif, France.
[Ti] Title:Germline SUFU mutation carriers and medulloblastoma: clinical characteristics, cancer risk and prognosis.
[So] Source:Neuro Oncol;, 2017 Nov 24.
[Is] ISSN:1523-5866
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: Germline SUFU mutations predispose to SHH medulloblastoma. Germline SUFU mutations have been reported in nevoid basal cell carcinoma syndrome (NBCCS), but little is known about the cancer risk and clinical spectrum. Patients and methods: We performed a retrospective review of all patients with medulloblastoma and a germline SUFU mutation in France. Results: Twenty-two patients from 17 families were identified with a medulloblastoma and a germline SUFU mutation (median age at diagnosis: 16.5 months). Macrocrania was present in 20 patients, but only 5 met the diagnostic criteria for NBCCS. Despite treatment with surgery and chemotherapy, to avoid radiotherapy in all patients except one, the outcome was worse than expected for SHH medulloblastoma, due to the high incidence of local relapses (8/22 patients) and second malignancies (n=6 in 4/22 patients). The 5-year progression-free survival and overall survival rates were 42% and 66%. Mutations were inherited in 79% of patients, and 34 additional SUFU mutation carriers were identified within 14 families. Medulloblastoma penetrance was incomplete, but higher than in PTCH1 mutation carriers. Besides medulloblastoma, 19 other tumors were recorded among the 56 SUFU mutation carriers, including basal cell carcinoma (BCC) in two patients and meningioma in three patients. Conclusion: Germline SUFU mutations strongly predispose to medulloblastoma in the first years of life, with worse prognosis than usually observed for SHH medulloblastoma. The clinical spectrum differs between SUFU and PTCH1 mutation carriers and BCC incidence is much lower in SUFU mutation carriers. The optimal treatment of SUFU mutation-associated medulloblastoma has not been defined.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/neuonc/nox228

  5 / 8145 MEDLINE  
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[PMID]: 28453743
[Au] Autor:Kline CN; Joseph NM; Grenert JP; van Ziffle J; Talevich E; Onodera C; Aboian M; Cha S; Raleigh DR; Braunstein S; Torkildson J; Samuel D; Bloomer M; Campomanes AGA; Banerjee A; Butowski N; Raffel C; Tihan T; Bollen AW; Phillips JJ; Korn WM; Yeh I; Bastian BC; Gupta N; Mueller S; Perry A; Nicolaides T; Solomon DA
[Ad] Address:Division of Pediatric Hematology/Oncology, Department of Pediatrics, University of California San Francisco (UCSF), San Francisco, California, USA.
[Ti] Title:Targeted next-generation sequencing of pediatric neuro-oncology patients improves diagnosis, identifies pathogenic germline mutations, and directs targeted therapy.
[So] Source:Neuro Oncol;19(5):699-709, 2017 05 01.
[Is] ISSN:1523-5866
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: Molecular profiling is revolutionizing cancer diagnostics and leading to personalized therapeutic approaches. Herein we describe our clinical experience performing targeted sequencing for 31 pediatric neuro-oncology patients. Methods: We sequenced 510 cancer-associated genes from tumor and peripheral blood to identify germline and somatic mutations, structural variants, and copy number changes. Results: Genomic profiling was performed on 31 patients with tumors including 11 high-grade gliomas, 8 medulloblastomas, 6 low-grade gliomas, 1 embryonal tumor with multilayered rosettes, 1 pineoblastoma, 1 uveal ganglioneuroma, 1 choroid plexus carcinoma, 1 chordoma, and 1 high-grade neuroepithelial tumor. In 25 cases (81%), results impacted patient management by: (i) clarifying diagnosis, (ii) identifying pathogenic germline mutations, or (iii) detecting potentially targetable alterations. The pathologic diagnosis was amended after genomic profiling for 6 patients (19%), including a high-grade glioma to pilocytic astrocytoma, medulloblastoma to pineoblastoma, ependymoma to high-grade glioma, and medulloblastoma to CNS high-grade neuroepithelial tumor with BCOR alteration. Multiple patients had pathogenic germline mutations, many of which were previously unsuspected. Potentially targetable alterations were identified in 19 patients (61%). Additionally, novel likely pathogenic alterations were identified in 3 cases: an in-frame RAF1 fusion in a BRAF wild-type pleomorphic xanthoastrocytoma, an inactivating ASXL1 mutation in a histone H3 wild-type diffuse pontine glioma, and an in-frame deletion within exon 2 of MAP2K1 in a low-grade astrocytic neoplasm. Conclusions: Our experience demonstrates the significant impact of molecular profiling on diagnosis and treatment of pediatric brain tumors and confirms its feasibility for use at the time of diagnosis or recurrence.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1704
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process
[do] DOI:10.1093/neuonc/now254

  6 / 8145 MEDLINE  
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[PMID]: 29511348
[Au] Autor:Bolin S; Borgenvik A; Persson CU; Sundström A; Qi J; Bradner JE; Weiss WA; Cho YJ; Weishaupt H; Swartling FJ
[Ad] Address:Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
[Ti] Title:Combined BET bromodomain and CDK2 inhibition in MYC-driven medulloblastoma.
[So] Source:Oncogene;, 2018 Mar 07.
[Is] ISSN:1476-5594
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Medulloblastoma (MB) is the most common malignant brain tumor in children. MYC genes are frequently amplified and correlate with poor prognosis in MB. BET bromodomains recognize acetylated lysine residues and often promote and maintain MYC transcription. Certain cyclin-dependent kinases (CDKs) are further known to support MYC stabilization in tumor cells. In this report, MB cells were suppressed by combined targeting of MYC expression and MYC stabilization using BET bromodomain inhibition and CDK2 inhibition, respectively. Such combination treatment worked synergistically and caused cell cycle arrest as well as massive apoptosis. Immediate transcriptional changes from this combined MYC blockade were found using RNA-Seq profiling and showed remarkable similarities to changes in MYC target gene expression when MYCN was turned off with doxycycline in our MYCN-inducible animal model for Group 3 MB. In addition, the combination treatment significantly prolonged survival as compared to single-agent therapy in orthotopically transplanted human Group 3 MB with MYC amplifications. Our data suggest that dual inhibition of CDK2 and BET bromodomains can be a novel treatment approach for suppressing MYC-driven cancer.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1038/s41388-018-0135-1

  7 / 8145 MEDLINE  
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[PMID]: 29484388
[Au] Autor:Estekizadeh A; Landázur N; Bartek J; Beltoft Brøchner C; Davoudi B; Broholm H; Karimi M; Ekström TJ; Rahbar A
[Ad] Address:Department of Clinical Neuroscience and Center for Molecular Medicine, Karolinska Institutet, SE_17176 Stockholm, Sweden.
[Ti] Title:Increased cytomegalovirus replication by 5-Azacytidine and viral-induced cytoplasmic expression of DNMT­1 in medulloblastoma and endothelial cells.
[So] Source:Int J Oncol;52(4):1317-1327, 2018 Apr.
[Is] ISSN:1791-2423
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Among all brain tumors diagnosed in children, medulloblastomas (MBs) are associated with a poor prognosis. The etiology of MB is not fully understood, yet the impact of epigenetic alterations of oncogenes has previously been established. During the past decade, the human cytomegalovirus (HCMV) has been detected in several types of cancer, including MB. Since DNA methylation occurs in the cell nucleus and this is considered a host defence response, we studied the impact of HCMV infection on DNA methyltransferase (DNMT­1) in MB (D324) cells, human umbilical vein endothelial cells (HUVECs) as well as in MB tissue sections. We hypothesized that infection and DNMT­1 intracellular localization are linked. Uninfected and HCMV­infected D324 cells and HUVECs were analyzed for HCMV immediate early (HCMV­IE) protein, HCMV­glycoprotein B (HCMV­gB) and DNMT­1 using immunofluorescence staining and quantitative ELISA. DNMT­1 localized to the nucleus of uninfected and HCMV­IE- expressing D324 cells and HUVECs, but accumulated in the extra nuclear space in all HCMV­gB-positive cells. Inhibition of HCMV late protein expression by Cymevene® (ganciclovir) prevented the cytoplasmic localization of DNMT­1. Treatment of HCMV­ infected D324 cells and HUVECs with the methylation inhibitor 5-Azacytidine (5AZA), significantly increased HCMV­IE and HCMV­gB gene transcription and protein expression. Immunohistochemical staining of DNMT­1 and HCMV proteins in MB cancer tissue sections revealed both nuclear and cytoplasmic DNMT­1 localization. In conclusion, DNMT­1 resides in the cytoplasm of HCMV­gB-expressing HUVECs and D324 cells. Increased viral protein synthesis in 5AZA-treated cells suggests that HCMV replication may benefit from a DNA methyltransferase-free cellular environment. Our findings emphasize the importance of assessing potential viral activation in the treatment of MB patients with epigenetic drugs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process
[do] DOI:10.3892/ijo.2018.4286

  8 / 8145 MEDLINE  
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[PMID]: 29358733
[Au] Autor:Niklison-Chirou MV
[Ad] Address:Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London, E1 2AT, UK. m.niklison-chirou@qmul.ac.uk.
[Ti] Title:Glutamine metabolism, the Achilles heel for medulloblastoma tumor.
[So] Source:Cell Death Dis;9(2):74, 2018 Jan 22.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Pt] Publication type:NEWS
[Em] Entry month:1801
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-017-0117-1

  9 / 8145 MEDLINE  
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[PMID]: 29485447
[Au] Autor:Arunraj ST; Parida GK; Damle NA; Arora S; Reddy S; Chakraborty D; Prabhu M; Tripathi M; Bal C
[Ti] Title:68Ga-DOTANOC PET/CT in Medulloblastoma.
[So] Source:Clin Nucl Med;, 2018 Feb 27.
[Is] ISSN:1536-0229
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Medulloblastoma, also known as cerebellar primitive neuroectodermal tumor, is the most common brain tumor in children and arises in the posterior cranial fossa. We present the case of a patient with desmoplastic type of medulloblastoma, which showed recurrence more than once. When Ga-DOTANOC PET-CT was done, the lesions showed somatostatin receptor expression, opening another potential therapeutic option for this patient.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher
[do] DOI:10.1097/RLU.0000000000002021

  10 / 8145 MEDLINE  
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[PMID]: 29500296
[Ti] Title:Medulloblastoma Circulating Tumor Cells Form Leptomeningeal Metastases.
[So] Source:Cancer Discov;, 2018 Mar 02.
[Is] ISSN:2159-8290
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:NCAM CD45 medulloblastoma cells were shown to be medulloblastoma circulating tumor cells (CTC).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180303
[Lr] Last revision date:180303
[St] Status:Publisher
[do] DOI:10.1158/2159-8290.CD-RW2018-035


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