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  • 1
    Language: English
    In: EMBO molecular medicine, 2014-01, Vol.6 (1), p.16-26
    Description: Recent advances reveal mRNA 3′end processing as a highly regulated process that fine‐tunes posttranscriptional gene expression. This process can affect the site and/or the efficiency of 3′end processing, controlling the quality and the quantity of substrate mRNAs. The regulation of 3′end processing plays a central role in fundamental physiology such as blood coagulation and innate immunity. In addition, errors in mRNA 3′end processing have been associated with a broad spectrum of human diseases, including cancer. We summarize and discuss the paradigmatic shift in the understanding of 3′end processing as a mechanism of posttranscriptional gene regulation that has reached clinical medicine. By connecting human diseases with mRNA 3' end formation and process, this comprehensive review provides a timely and useful memento to biologists and clinicians that the deregulation of gene expression can terribly affect human health.
    Subject(s): post‐transcriptional gene regulation ; clinical importance of 3′ end mRNA processing ; regulation of 3′ end mRNA processing ; control of polyadenylation ; Proteins ; Post-transcription ; Blood coagulation ; Gene regulation ; Innate immunity ; Physiology ; RNA polymerase ; Mutation ; Gene expression ; Binding sites ; post-transcriptional gene regulation ; Reviews
    ISSN: 1757-4676
    E-ISSN: 1757-4684
    Source: HighWire Press (Free Journals)
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 2
    Language: English
    In: Molecular cancer research, 2007-12-01, Vol.5 (12), p.1232-1240
    Description: Glioblastomas, the most malignant of all brain tumors, are characterized by cellular resistance to apoptosis and a highly invasive growth pattern. These factors contribute to the poor response of glioblastomas to radiochemotherapy and prevent their complete neurosurgical resection. However, the driving force behind the distinct motility of glioma cells is only partly understood. Here, we report that in the absence of cellular stress and proapoptotic stimuli, human glioblastoma cells exhibit a constitutive activation of caspases in vivo and in vitro . The inhibition of caspases by various peptide inhibitors decreases the migration of cells in scrape motility assays and the invasiveness of cells in spheroid assays. Similarly, specific small interfering RNA– or antisense-mediated down-regulation of caspase-3 and caspase-8 results in an inhibition of the migratory potential of glioma cells. The constitutive caspase-dependent motility of glioblastoma cells is independent of CD95 activation and it is not mediated by mitogen-activated protein/extracellular signal-regulated kinase kinase signaling. The basal caspase activity is accompanied by a constant cleavage of the motility-associated gelsolin protein, which may contribute to the caspase-mediated promotion of migration and invasiveness in glioblastoma cells. Our results suggest that the administration of low doses of caspase inhibitors that block glioma cell motility without affecting the execution of apoptotic cell death may be exploited as a novel strategy for the treatment of glioblastomas. (Mol Cancer Res 2007;5(12):1232–40)
    Subject(s): migration ; apoptosis ; brain tumors ; invasion ; gliomas ; caspases ; Brain Neoplasms - enzymology ; Glioblastoma - enzymology ; MAP Kinase Signaling System - physiology ; Gelsolin - metabolism ; Neoplasm Invasiveness ; Humans ; Brain Neoplasms - pathology ; Caspase 3 - metabolism ; Caspase 8 - metabolism ; Enzyme Inhibitors - pharmacology ; fas Receptor - metabolism ; Caspase Inhibitors ; Cell Movement - physiology ; Caspase 8 - genetics ; Glioblastoma - pathology ; Caspase 3 - genetics ; Cell Line, Tumor ; RNA, Small Interfering ; Index Medicus
    ISSN: 1541-7786
    E-ISSN: 1557-3125
    Source: HighWire Press (Free Journals)
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 3
    Language: English
    In: Cancer biology & therapy, 2008-12-01, Vol.7 (12), p.1982-1990
    Description: Resistance to apoptosis is one reason for the poor response of malignant brain tumors to therapy. The PPARγ-modulating drug Troglitazone down-regulates the anti-apoptotic FLIP protein and sensitizes glioblastoma cells to apoptosis induced by the death ligand TRAIL. To investigate the molecular basis of an experimental combination therapy for malignant gliomas with TRAIL and Troglitazone, we investigated the Troglitazone-induced signaling cascades and the expression of TRAIL receptors and FLIP in malignant gliomas. Troglitazone down-regulated the FLIP protein through accelerated ubiquitin/proteasome-dependent degradation, which might be mediated by a Troglitazone-induced increase in reactive oxygen species. Moreover, Troglitazone induced the phosphorylation of the MAP kinase ERK1/2 as well as of the BAD protein. Inhibition of either PPARγ or MEK1/2 blocked the Troglitazone-mediated phosphorylation of BAD and further increased the synergistic induction of glioma cell death by TRAIL and Troglitazone. Immunohistochemical analysis demonstrated that FLIP and TRAIL-R2 were significantly higher expressed in anaplastic (WHO grade III) than in diffuse (WHO grade II) gliomas. High FLIP and low TRAIL-R2 expression levels were associated with a poor prognosis of patients. Our findings warrant a further pre-clinical evaluation of an experimental anti-glioma therapy with TRAIL and Troglitazone, potentially in conjunction with a MAP kinase inhibitor.
    Subject(s): Binding ; Proteins ; Landes ; Calcium ; Bioscience ; Biology ; Cell ; Cycle ; Cancer ; Organogenesis ; Cell Line ; Phosphorylation ; Apoptosis - drug effects ; Humans ; Antineoplastic Agents - therapeutic use ; Mitogen-Activated Protein Kinase 1 - drug effects ; Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism ; Mitogen-Activated Protein Kinase 3 - drug effects ; Thiazolidinediones - therapeutic use ; Chromans - pharmacology ; Chromans - therapeutic use ; Mitogen-Activated Protein Kinase 3 - metabolism ; Glioma - pathology ; bcl-Associated Death Protein - drug effects ; Cell Line, Tumor ; bcl-Associated Death Protein - metabolism ; Antineoplastic Agents - pharmacology ; Receptors, TNF-Related Apoptosis-Inducing Ligand - genetics ; Proteasome Endopeptidase Complex - metabolism ; Thiazolidinediones - pharmacology ; CASP8 and FADD-Like Apoptosis Regulating Protein - metabolism ; Troglitazone ; Mitogen-Activated Protein Kinase 1 - metabolism ; Index Medicus
    ISSN: 1538-4047
    E-ISSN: 1555-8576
    Source: PubMed Central
    Source: Alma/SFX Local Collection
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  • 4
    Language: English
    In: Neuro-oncology (Charlottesville, Va.), 2019-04-23, Vol.21 (Supplement_2), p.ii82-ii82
    Description: Abstract There is a broad variety of CNS tumor entities that can affect children and adolescents, associated with divergent clinical outcomes. We have recently proposed a DNA methylation-based classification to distinguish biologically distinct CNS tumor classes within and across neuropathological entities. The Molecular Neuropathology 2.0 study integrates genome-wide (epi-)genetic diagnostics with reference neuropathological assessment for newly-diagnosed pediatric CNS tumors in Germany. From 04/2015 to 09/2017, 607 patients with sufficient tissue were enrolled from 51 German centers. A reference neuropathological diagnosis according to the WHO classification was established for 95% of tumors and reflected the distribution of known histological CNS tumor entities in a pediatric population. Using 10 FFPE sections for DNA extraction, a DNA methylation-based molecular diagnosis was established in 95% of cases, of which 83% were assigned to a distinct CNS tumor methylation class. The remaining 17% did not match any of 82 currently established classes, but revealed evidence for novel rare molecular entities. Gene panel sequencing of 〉130 genes performed for 88% of patients with matched blood samples indicated diagnostically, prognostically, or therapeutically relevant somatic alterations in 47%. Germline DNA sequencing indicated potential predisposition syndromes in ~10% of patients, leading to human genetic counselling of affected families. Discrepant results by neuropathological and (epi-)genetic classification (~20%) were discussed in a weekly multi-disciplinary tumor board including reference neuroradiological evaluation. The majority of clinically-relevant discrepancies (67%) involved tumors neuropathologically diagnosed as high-grade gliomas, of which 25% were showed discrepant results. Clinical follow-up of enrolled patients through the German HIT study centers is ongoing. The MNP 2.0 study adds a valuable layer of information to clinical neuropathological diagnostics and has expanded to an international registry for molecular data analysis for pediatric CNS tumors. The results provide insight into tumors with divergent neuropathological and molecular classification with potential implications for patient management.
    Subject(s): Epigentics ; Genetics
    ISSN: 1522-8517
    E-ISSN: 1523-5866
    Source: PubMed Central
    Source: Alma/SFX Local Collection
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  • 5
    Language: English
    In: Neuro-oncology (Charlottesville, Va.), 2018-06-22, Vol.20 (suppl_2), p.i181-i181
    Description: Abstract Children can be affected by a large variety of CNS tumor entities with very divergent outcomes, some of which are exceedingly rare. DNA methylation analysis is a powerful tool to distinguish biologically distinct CNS tumor classes within and across histological entities. The Molecular Neuropathology 2.0 study aims to integrate genome wide (epi-)genetic diagnostics with reference neuropathological assessment for all newly-diagnosed pediatric CNS tumors in Germany. In the first 2 ½ years, 675 patients with sufficient tissue were enrolled from 55 centers. For 〉95% of patients, a diagnosis according to the WHO classification was assigned by reference neuropathology. Using 10 FFPE sections as input, a DNA methylation-based molecular diagnosis was established in 95% of cases, of which 84% were assigned to a distinct CNS tumor methylation class. The remaining 16% did not match any of 82 currently established classes, with evidence for novel rare entities. Targeted gene panel sequencing of 〉130 genes performed for 88% of patients with matched blood samples indicated diagnostically, prognostically, or therapeutically relevant somatic alterations in 47%. Germline DNA sequencing data indicated potential predisposition syndromes in ~10% of patients. Discrepant results by neuropathological and molecular classification (~20%) were discussed in a weekly multi-disciplinary tumor board including reference neuroradiological evaluation. Clinical follow-up data for all patients is being collected by the HIT study centers. This ongoing study adds a valuable layer of information to clinical neuropathological diagnostics in Germany and will provide insight into CNS tumors with divergent neuropathological and molecular classification with potential implications for future patient management.
    Subject(s): Abstracts
    ISSN: 1522-8517
    E-ISSN: 1523-5866
    Source: PubMed Central
    Source: Alma/SFX Local Collection
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  • 6
    Language: English
    Description: BACKGROUND Medulloblastoma is associated with rare hereditary cancer predisposition syndromes; however, consensus medulloblastoma predisposition genes have not been defined and screening guidelines for genetic counselling and testing for paediatric patients are not available. We aimed to assess and define these genes to provide evidence for future screening guidelines. METHODS In this international, multicentre study, we analysed patients with medulloblastoma from retrospective cohorts (International Cancer Genome Consortium [ICGC] PedBrain, Medulloblastoma Advanced Genomics International Consortium [MAGIC], and the CEFALO series) and from prospective cohorts from four clinical studies (SJMB03, SJMB12, SJYC07, and I-HIT-MED). Whole-genome sequences and exome sequences from blood and tumour samples were analysed for rare damaging germline mutations in cancer predisposition genes. DNA methylation profiling was done to determine consensus molecular subgroups: WNT (MB), SHH (MB), group 3 (MB), and group 4 (MB). Medulloblastoma predisposition genes were predicted on the basis of rare variant burden tests against controls without a cancer diagnosis from the Exome Aggregation Consortium (ExAC). Previously defined somatic mutational signatures were used to further classify medulloblastoma genomes into two groups, a clock-like group (signatures 1 and 5) and a homologous recombination repair deficiency-like group (signatures 3 and 8), and chromothripsis was investigated using previously established criteria. Progression-free survival and overall survival were modelled for patients with a genetic predisposition to medulloblastoma. FINDINGS We included a total of 1022 patients with medulloblastoma from the retrospective cohorts (n=673) and the four prospective studies (n=349), from whom blood samples (n=1022) and tumour samples (n=800) were analysed for germline mutations in 110 cancer predisposition genes. In our rare variant burden analysis, we compared these against 53 105 sequenced controls from ExAC and identified APC, BRCA2, PALB2, PTCH1, SUFU, and TP53 as consensus medulloblastoma predisposition genes according to our rare variant burden analysis and estimated that germline mutations accounted for 6% of medulloblastoma diagnoses in the retrospective cohort. The prevalence of genetic predispositions differed between molecular subgroups in the retrospective cohort and was highest for patients in the MB subgroup (20% in the retrospective cohort). These estimates were replicated in the prospective clinical cohort (germline mutations accounted for 5% of medulloblastoma diagnoses, with the highest prevalence [14%] in the MB subgroup). Patients with germline APC mutations developed MB and accounted for most (five [71%] of seven) cases of MB that had no somatic CTNNB1 exon 3 mutations. Patients with germline mutations in SUFU and PTCH1 mostly developed infant MB. Germline TP53 mutations presented only in childhood patients in the MB subgroup and explained more than half (eight [57%] of 14) of all chromothripsis events in this subgroup. Germline mutations in PALB2 and BRCA2 were observed across the MB, MB, and MB molecular subgroups and were associated with mutational signatures typical of homologous recombination repair deficiency. In patients with a genetic predisposition to medulloblastoma, 5-year progression-free survival was 52% (95% CI 40-69) and 5-year overall survival was 65% (95% CI 52-81); these survival estimates differed significantly across patients with germline mutations in different medulloblastoma predisposition genes. INTERPRETATION Genetic counselling and testing should be used as a standard-of-care procedure in patients with MB and MB because these patients have the highest prevalence of damaging germline mutations in known cancer predisposition genes. We propose criteria for routine genetic screening for patients with medulloblastoma based on clinical and molecular tumour characteristics. FUNDING German Cancer Aid; German Federal Ministry of Education and Research; German Childhood Cancer Foundation (Deutsche Kinderkrebsstiftung); European Research Council; National Institutes of Health; Canadian Institutes for Health Research; German Cancer Research Center; St Jude Comprehensive Cancer Center; American Lebanese Syrian Associated Charities; Swiss National Science Foundation; European Molecular Biology Organization; Cancer Research UK; Hertie Foundation; Alexander and Margaret Stewart Trust; V Foundation for Cancer Research; Sontag Foundation; Musicians Against Childhood Cancer; BC Cancer Foundation; Swedish Council for Health, Working Life and Welfare; Swedish Research Council; Swedish Cancer Society; the Swedish Radiation Protection Authority; Danish Strategic Research Council; Swiss Federal Office of Public Health; Swiss Research Foundation on Mobile Communication; Masaryk University; Ministry of Health of the Czech Republic; Research Council of Norway; Genome Canada; Genome BC; Terry Fox Research Institute; Ontario Institute for Cancer Research; Pediatric Oncology Group of Ontario; The Family of Kathleen Lorette and the Clark H Smith Brain Tumour Centre; Montreal Children's Hospital Foundation; The Hospital for Sick Children: Sonia and Arthur Labatt Brain Tumour Research Centre, Chief of Research Fund, Cancer Genetics Program, Garron Family Cancer Centre, MDT's Garron Family Endowment; BC Childhood Cancer Parents Association; Cure Search Foundation; Pediatric Brain Tumor Foundation; Brainchild; and the Government of Ontario.
    Subject(s): Medicine & health ; Medical Clinic
    ISSN: 1470-2045
    E-ISSN: 1474-5488
    Source: ZORA
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  • 7
    Language: English
    In: Neuro-oncology (Charlottesville, Va.), 2018-06-22, Vol.20 (suppl_2), p.i182-i182
    Description: Abstract Precise diagnosis and robust detection of actionable alterations is required for individualized treatments. The Pediatric Targeted Therapy (PTT) 2.0 program aims at improvement of diagnostic accuracy and detection of targetable alterations by extended molecular diagnostics. The impact of these analyses on clinical management is being evaluated. Pediatric patients with relapsed or progressive tumors after treatment according to standard protocols are included, independent of the histological diagnosis. Formalin fixed paraffin embedded material and a blood sample for germline correction are requested. The methods employed are DNA methylation array, customized targeted gene panel sequencing (130 genes), RNA and Sanger sequencing in selected cases, and immunohistochemistry (IHC) of selected markers. A questionnaire-based follow-up is used to determine the clinical impact of the analysis. We have included n=111 cases from 22.02.2017.-31.12.2017, analysis was completed for n=83 cases (75%) at the time of abstract submission. The most common entities were brain tumors (n=56/83, 67%). DNA methylation array alone allowed diagnostic classification in n=45/83 cases (54.2%) and n=34/56 brain tumor cases (60,7%), respectively. Actionable targets as detected by copy number calculation, gene panel sequencing, RNA sequencing and IHC were found in n=47/83 cases (56.6%). Pathogenic germline alterations with clinical relevance were identified in n=7/83 cases (8.4%) and were confirmed by Sanger sequencing. Follow-up analyses are ongoing. In conclusion, combination of next-generation diagnostics such as methylation arrays and targeted sequencing in addition to selected IHC markers added robust information concerning diagnosis and targetable alterations. The impact on clinical decision-making and on outcome is currently being evaluated.
    Subject(s): Abstracts
    ISSN: 1522-8517
    E-ISSN: 1523-5866
    Source: PubMed Central
    Source: Alma/SFX Local Collection
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  • 8
    Language: Norwegian
    In: The lancet oncology, 2018
    Description: Background Medulloblastoma is associated with rare hereditary cancer predisposition syndromes; however, consensus medulloblastoma predisposition genes have not been defined and screening guidelines for genetic counselling and testing for paediatric patients are not available. We aimed to assess and define these genes to provide evidence for future screening guidelines. Methods In this international, multicentre study, we analysed patients with medulloblastoma from retrospective cohorts (International Cancer Genome Consortium [ICGC] PedBrain, Medulloblastoma Advanced Genomics International Consortium [MAGIC], and the CEFALO series) and from prospective cohorts from four clinical studies (SJMB03, SJMB12, SJYC07, and I-HIT-MED). Whole-genome sequences and exome sequences from blood and tumour samples were analysed for rare damaging germline mutations in cancer predisposition genes. DNA methylation profiling was done to determine consensus molecular subgroups: WNT (MBWNT), SHH (MBSHH), group 3 (MBGroup3), and group 4 (MBGroup4). Medulloblastoma predisposition genes were predicted on the basis of rare variant burden tests against controls without a cancer diagnosis from the Exome Aggregation Consortium (ExAC). Previously defined somatic mutational signatures were used to further classify medulloblastoma genomes into two groups, a clock-like group (signatures 1 and 5) and a homologous recombination repair deficiency-like group (signatures 3 and 8), and chromothripsis was investigated using previously established criteria. Progression-free survival and overall survival were modelled for patients with a genetic predisposition to medulloblastoma. Findings We included a total of 1022 patients with medulloblastoma from the retrospective cohorts (n=673) and the four prospective studies (n=349), from whom blood samples (n=1022) and tumour samples (n=800) were analysed for germline mutations in 110 cancer predisposition genes. In our rare variant burden analysis, we compared these against 53 105 sequenced controls from ExAC and identified APC, BRCA2, PALB2, PTCH1, SUFU, and TP53 as consensus medulloblastoma predisposition genes according to our rare variant burden analysis and estimated that germline mutations accounted for 6% of medulloblastoma diagnoses in the retrospective cohort. The prevalence of genetic predispositions differed between molecular subgroups in the retrospective cohort and was highest for patients in the MBSHH subgroup (20% in the retrospective cohort). These estimates were replicated in the prospective clinical cohort (germline mutations accounted for 5% of medulloblastoma diagnoses, with the highest prevalence [14%] in the MBSHH subgroup). Patients with germline APC mutations developed MBWNT and accounted for most (five [71%] of seven) cases of MBWNT that had no somatic CTNNB1 exon 3 mutations. Patients with germline mutations in SUFU and PTCH1 mostly developed infant MBSHH. Germline TP53 mutations presented only in childhood patients in the MBSHH subgroup and explained more than half (eight [57%] of 14) of all chromothripsis events in this subgroup. Germline mutations in PALB2 and BRCA2 were observed across the MBSHH, MBGroup3, and MBGroup4 molecular subgroups and were associated with mutational signatures typical of homologous recombination repair deficiency. In patients with a genetic predisposition to medulloblastoma, 5-year progression-free survival was 52% (95% CI 40–69) and 5-year overall survival was 65% (95% CI 52–81); these survival estimates differed significantly across patients with germline mutations in different medulloblastoma predisposition genes. Interpretation Genetic counselling and testing should be used as a standard-of-care procedure in patients with MBWNT and MBSHH because these patients have the highest prevalence of damaging germline mutations in known cancer predisposition genes. We propose criteria for routine genetic screening for patients with medulloblastoma based on clinical and molecular tumour characteristics. Funding German Cancer Aid; German Federal Ministry of Education and Research; German Childhood Cancer Foundation (Deutsche Kinderkrebsstiftung); European Research Council; National Institutes of Health; Canadian Institutes for Health Research; German Cancer Research Center; St Jude Comprehensive Cancer Center; American Lebanese Syrian Associated Charities; Swiss National Science Foundation; European Molecular Biology Organization; Cancer Research UK; Hertie Foundation; Alexander and Margaret Stewart Trust; V Foundation for Cancer Research; Sontag Foundation; Musicians Against Childhood Cancer; BC Cancer Foundation; Swedish Council for Health, Working Life and Welfare; Swedish Research Council; Swedish Cancer Society; the Swedish Radiation Protection Authority; Danish Strategic Research Council; Swiss Federal Office of Public Health; Swiss Research Foundation on Mobile Communication; Masaryk University; Ministry of Health of the Czech Republic; Research Council of Norway; Genome Canada; Genome BC; Terry Fox Research Institute; Ontario Institute for Cancer Research; Pediatric Oncology Group of Ontario; The Family of Kathleen Lorette and the Clark H Smith Brain Tumour Centre; Montreal Children's Hospital Foundation; The Hospital for Sick Children: Sonia and Arthur Labatt Brain Tumour Research Centre, Chief of Research Fund, Cancer Genetics Program, Garron Family Cancer Centre, MDT's Garron Family Endowment; BC Childhood Cancer Parents Association; Cure Search Foundation; Pediatric Brain Tumor Foundation; Brainchild; and the Government of Ontario.
    ISSN: 1470-2045
    E-ISSN: 1474-5488
    Source: NORA - Norwegian Open Research Archives
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  • 9
    Language: English
    In: EMBO molecular medicine, 2014-01, Vol.6 (1), p.16-26
    Description: Recent advances reveal mRNA 3'end processing as a highly regulated process that fine-tunes posttranscriptional gene expression. This process can affect the site and/or the efficiency of 3'end processing, controlling the quality and the quantity of substrate mRNAs. The regulation of 3'end processing plays a central role in fundamental physiology such as blood coagulation and innate immunity. In addition, errors in mRNA 3'end processing have been associated with a broad spectrum of human diseases, including cancer. We summarize and discuss the paradigmatic shift in the understanding of 3'end processing as a mechanism of posttranscriptional gene regulation that has reached clinical medicine.
    Subject(s): Neoplasms - metabolism ; RNA Processing, Post-Transcriptional ; Poly(A)-Binding Proteins - genetics ; mRNA Cleavage and Polyadenylation Factors - metabolism ; Hematologic Diseases - metabolism ; Humans ; Neurodegenerative Diseases - genetics ; Neurodegenerative Diseases - metabolism ; RNA, Messenger - metabolism ; Animals ; Hematologic Diseases - physiopathology ; Neurodegenerative Diseases - physiopathology ; Neoplasms - genetics ; Poly(A)-Binding Proteins - metabolism ; Hematologic Diseases - genetics ; Neoplasms - physiopathology ; 3' Untranslated Regions ; Index Medicus
    E-ISSN: 1757-4684
    Source: Directory of Open Access Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 10
    Language: English
    Subject(s): Predictive Value of Tests ; Prospective Studies ; Genetic Testing ; Humans ; Transcriptome ; Child, Preschool ; Infant ; Male ; Gene Expression Profiling ; Biomarkers, Tumor ; Young Adult ; DNA Methylation ; DNA Mutational Analysis ; Germ-Line Mutation ; Adult ; Female ; Retrospective Studies ; Child ; Genetic Predisposition to Disease ; Reproducibility of Results ; Risk Factors ; Heredity ; Whole Exome Sequencing ; Phenotype ; Cerebellar Neoplasms ; Pedigree ; Medulloblastoma ; Progression-Free Survival ; Adolescent ; Models, Genetic
    Source: Cambridge University Library IR - DSpace@Cambridge
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