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  • 1
    Article
    Article
    2017
    ISSN: 0020-7136 
    Language: English
    In: International journal of cancer, 2017-01-01, Vol.140 (1), p.9-9
    Subject(s): Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    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
    Article
    Article
    2016
    ISSN: 0020-7136 
    Language: English
    In: International journal of cancer, 2016-01-01, Vol.138 (1), p.9-9
    Subject(s): Humans ; Periodicals as Topic ; Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    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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  • 3
    Language: English
    In: Nature reviews. Genetics, 2013-11, Vol.14 (11), p.765-780
    Description: Malignancies are characterized by extensive global reprogramming of epigenetic patterns, including gains or losses in DNA methylation and changes to histone marks. Furthermore, high-resolution genome-sequencing efforts have discovered a wealth of mutations in genes encoding epigenetic regulators that have roles as 'writers', 'readers' or 'editors' of DNA methylation and/or chromatin states. In this Review, we discuss how these mutations have the potential to deregulate hundreds of targeted genes genome wide. Elucidating these networks of epigenetic factors will provide mechanistic understanding of the interplay between genetic and epigenetic alterations, and will inform novel therapeutic strategies.
    Subject(s): Neoplasms - metabolism ; Chromatin ; Epigenesis, Genetic ; Humans ; Computational Biology ; Neoplasm Proteins - metabolism ; DNA Methylation ; Histones - genetics ; Neoplasms - genetics ; Genes, Regulator ; Histones - metabolism ; Mutation ; Genome ; Neoplasm Proteins - genetics ; Epigenetic inheritance ; DNA ; Genetic aspects ; Research ; Genetic regulation ; Methylation ; Health aspects ; Mutation (Biology) ; Cancer ; Index Medicus
    ISSN: 1471-0056
    E-ISSN: 1471-0064
    Source: Academic Search Ultimate
    Source: Nature Journals Online
    Source: Nature Reviews
    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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  • 4
    Language: English
    In: International journal of cancer, 2016-05-15, Vol.138 (10), p.2322-2333
    Description: In 2011, a novel form of genome instability was reported by Stephens et al., characterized by tens to hundreds of locally clustered rearrangements affecting one or a few chromosome(s) in cancer cells. This phenomenon, termed chromothripsis, is likely due to a single catastrophic event leading to the simultaneous formation of multiple double‐strand breaks, which are repaired by error‐prone mechanisms. Since then, the occurrence of chromothripsis was detected in a wide range of tumor entities. In this review, we will discuss potential mechanisms of chromothripsis initiation in cancer and outline the prevalence of chromothripsis across entities. Furthermore, we will examine how chromothriptic events may promote cancer development and how they may affect cancer therapy.
    Subject(s): genome instability ; catastrophic genomic rearrangement ; chromothripsis ; Genomic Instability ; Neoplasms - therapy ; Animals ; Neoplasms - genetics ; Cell Transformation, Neoplastic - genetics ; Humans ; Chromosome Aberrations ; Genomics ; Cancer cells ; Cancer ; Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    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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  • 5
    Article
    Article
    2017
    ISSN: 0020-7136 
    Language: English
    In: International journal of cancer, 2017-09-01, Vol.141 (5), p.866-866
    Subject(s): Genetic Predisposition to Disease ; Neoplasms - genetics ; Humans ; Translational Medical Research ; Neoplasms - drug therapy ; Genes ; Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    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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  • 6
    Language: English
    In: Nature reviews. Cancer, 2014-02, Vol.14 (2), p.92-107
    Description: We have extended our understanding of the molecular biology that underlies adult glioblastoma over many years. By contrast, high-grade gliomas in children and adolescents have remained a relatively under-investigated disease. The latest large-scale genomic and epigenomic profiling studies have yielded an unprecedented abundance of novel data and provided deeper insights into gliomagenesis across all age groups, which has highlighted key distinctions but also some commonalities. As we are on the verge of dissecting glioblastomas into meaningful biological subgroups, this Review summarizes the hallmark genetic alterations that are associated with distinct epigenetic features and patient characteristics in both paediatric and adult disease, and examines the complex interplay between the glioblastoma genome and epigenome.
    Subject(s): Epigenomics ; Neoplasms, Nerve Tissue - genetics ; Age Factors ; Glioblastoma - genetics ; Humans ; Genetic research ; Epigenetic inheritance ; Genetic aspects ; Research ; Genetic susceptibility ; Glioblastoma multiforme ; Index Medicus
    ISSN: 1474-175X
    E-ISSN: 1474-1768
    Source: Academic Search Ultimate
    Source: Nature Journals Online
    Source: Nature Reviews
    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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  • 7
    Language: English
    In: Nature reviews. Cancer, 2012-12, Vol.12 (12), p.818-834
    Description: The division of medulloblastoma into different subgroups by microarray expression profiling has dramatically changed our perspective of this malignant childhood brain tumour. Now, the availability of next-generation sequencing and complementary high-density genomic technologies has unmasked novel driver mutations in each medulloblastoma subgroup. The implications of these findings for the management of patients are readily apparent, pinpointing previously unappreciated diagnostic and therapeutic targets. In this Review, we summarize the 'explosion' of data emerging from the application of modern genomics to medulloblastoma, and in particular the recurrent targets of mutation in medulloblastoma subgroups. These data are currently making their way into clinical trials as we seek to integrate conventional and molecularly targeted therapies.
    Subject(s): Genome-Wide Association Study ; Signal Transduction ; Humans ; Cyclin-Dependent Kinase 6 - genetics ; Hedgehog Proteins - metabolism ; Male ; Medulloblastoma - metabolism ; Cerebellar Neoplasms - genetics ; beta Catenin - genetics ; Tetraploidy ; Animals ; Hedgehog Proteins - genetics ; DNA Mutational Analysis ; Female ; Mice ; Histones - metabolism ; Mutation ; Genomics - methods ; Medulloblastoma - genetics ; Child ; Cerebellar Neoplasms - metabolism ; Care and treatment ; Prognosis ; Demographic aspects ; Medulloblastoma ; Genomics ; Central nervous system diseases ; Genetic aspects ; Research ; Index Medicus
    ISSN: 1474-175X
    E-ISSN: 1474-1768
    Source: Academic Search Ultimate
    Source: Nature Journals Online
    Source: Nature Reviews
    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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  • 8
    Language: English
    In: The New England journal of medicine, 2014-06-12, Vol.370 (24), p.2286-2294
    Description: In some patients with CLL, resistance to the BTK inhibitor ibrutinib develops. Two classes of resistance mutations have been found: the more common involves alteration of the drug-binding site to make binding reversible; the less common activates a downstream kinase that effectively bypasses BTK. The development of B-cell–receptor antagonists has been a therapeutic advance in chronic lymphocytic leukemia (CLL). Although B-cell–receptor ligation in normal cells induces proliferation, apoptosis, or anergy, 1 pathway dysregulation in CLL results in the propagation of proliferative and prosurvival signals. 2 , 3 Several agents targeting the B-cell–receptor pathway are in development, including the Bruton's tyrosine kinase (BTK) inhibitor ibrutinib. Although BTK is not recurrently mutated in CLL, 4 , 5 it is up-regulated at the transcript level and is constitutively active. 6 , 7 Ibrutinib irreversibly binds BTK at the C481 residue, rendering it kinase-inactive, inducing modest CLL-cell apoptosis, and abolishing proliferation and B-cell–receptor signaling in . . .
    Subject(s): Biological and medical sciences ; General aspects ; Medical sciences ; Recurrence ; Phospholipase C gamma - metabolism ; Pyrazoles - therapeutic use ; Humans ; Middle Aged ; Binding Sites - genetics ; Leukemia, Lymphocytic, Chronic, B-Cell - genetics ; Pyrimidines - pharmacology ; Receptors, Antigen, B-Cell - metabolism ; Sequence Analysis, DNA ; Exome ; Point Mutation ; Drug Resistance, Neoplasm - genetics ; Protein-Tyrosine Kinases - genetics ; Pyrimidines - therapeutic use ; Agammaglobulinaemia Tyrosine Kinase ; Phospholipase C gamma - genetics ; Aged ; Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy ; Protein-Tyrosine Kinases - antagonists & inhibitors ; Pyrazoles - pharmacology ; Tyrosine ; Cysteine ; Chronic lymphatic leukemia ; Serine ; Leukemia ; Genomes ; Lymphatic leukemia ; Kinases ; Bruton's tyrosine kinase ; Lymphocytes B ; Mutation ; Lymphocytosis ; Protein-tyrosine kinase ; Deoxyribonucleic acid--DNA ; Apoptosis ; Index Medicus ; Abridged Index Medicus
    ISSN: 0028-4793
    E-ISSN: 1533-4406
    Source: Single 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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  • 9
    Language: English
    In: Acta neuropathologica, 2012-04, Vol.123 (4), p.465-472
    Description: Medulloblastoma, a small blue cell malignancy of the cerebellum, is a major cause of morbidity and mortality in pediatric oncology. Current mechanisms for clinical prognostication and stratification include clinical factors (age, presence of metastases, and extent of resection) as well as histological subgrouping (classic, desmoplastic, and large cell/anaplastic histology). Transcriptional profiling studies of medulloblastoma cohorts from several research groups around the globe have suggested the existence of multiple distinct molecular subgroups that differ in their demographics, transcriptomes, somatic genetic events, and clinical outcomes. Variations in the number, composition, and nature of the subgroups between studies brought about a consensus conference in Boston in the fall of 2010. Discussants at the conference came to a consensus that the evidence supported the existence of four main subgroups of medulloblastoma (Wnt, Shh, Group 3, and Group 4). Participants outlined the demographic, transcriptional, genetic, and clinical differences between the four subgroups. While it is anticipated that the molecular classification of medulloblastoma will continue to evolve and diversify in the future as larger cohorts are studied at greater depth, herein we outline the current consensus nomenclature, and the differences between the medulloblastoma subgroups.
    Subject(s): Pathology ; Neurosciences ; SHH ; Medicine & Public Health ; Medulloblastoma ; Group 4 ; Group 3 ; WNT ; Consensus ; Subgroups ; Hedgehog Proteins ; Cerebellar Neoplasms - diagnosis ; Humans ; Transcriptome ; Medulloblastoma - diagnosis ; Gene Expression Profiling ; Wnt Proteins ; Cerebellar Neoplasms - genetics ; Cerebellar Neoplasms - classification ; Medulloblastoma - genetics ; Medulloblastoma - classification ; Index Medicus ; Consensus Paper
    ISSN: 0001-6322
    E-ISSN: 1432-0533
    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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  • 10
    Language: English
    In: Nature medicine, 2015-08, Vol.21 (8), p.846-853
    Description: The extent of tumor heterogeneity is an emerging theme that researchers are only beginning to understand. How genetic and epigenetic heterogeneity affects tumor evolution and clinical progression is unknown. The precise nature of the environmental factors that influence this heterogeneity is also yet to be characterized. Nature Medicine, Nature Biotechnology and the Volkswagen Foundation organized a meeting focused on identifying the obstacles that need to be overcome to advance translational research in and tumor heterogeneity. Once these key questions were established, the attendees devised potential solutions. Their ideas are presented here.
    Subject(s): Epigenomics ; Neoplasms - genetics ; Humans ; Tumor Microenvironment ; Benchmarking ; High-Throughput Nucleotide Sequencing ; Neoplasms - pathology ; Neoplasms - drug therapy ; Epigenetic inheritance ; Genetic aspects ; Research ; Spontaneous generation ; Risk factors ; Tumors ; Index Medicus ; Epigenetics ; Epigenètica
    ISSN: 1078-8956
    E-ISSN: 1546-170X
    Source: Single Journals
    Source: Academic Search Ultimate
    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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