Tolerance of whole-genome doubling propagates chromosomal instability and accelerates cancer genome evolution. - Wikidata - wikimedia - TriplyDB

Tolerance of whole-genome doubling propagates chromosomal instability and accelerates cancer genome evolution.

Tolerance of whole-genome doubling propagates chromosomal instability and accelerates cancer genome evolution.

http://www.wikidata.org/entity/Q34946877

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Cell Fusion in the War on Cancer: A Perspective on the Inception of Malignancy The Dark Side of Cell Fusion Cancer Evolution and the Limits of Predictability in Precision Cancer Medicine Genome management and mismanagement--cell-level opportunities and challenges of whole-genome duplication BCL9L Dysfunction Impairs Caspase-2 Expression Permitting Aneuploidy Tolerance in Colorectal Cancer Transcriptome analysis of tetraploid cells identifies cyclin D2 as a facilitator of adaptation to genome doubling in the presence of p53 Clonal Evolutionary Analysis during HER2 Blockade in HER2-Positive Inflammatory Breast Cancer: A Phase II Open-Label Clinical Trial of Afatinib +/- Vinorelbine Can oncology recapitulate paleontology? Lessons from species extinctions Transient endoreplication down-regulates the kinesin-14 HSET and contributes to genomic instability.SAAS-CNV: A Joint Segmentation Approach on Aggregated and Allele Specific Signals for the Identification of Somatic Copy Number Alterations with Next-Generation Sequencing Data.Cyclin D mediates tolerance of genome-doubling in cancers with functional p53.Genomic landscape and evolution of metastatic chromophobe renal cell carcinoma.Uncoupling of the Hippo and Rho pathways allows megakaryocytes to escape the tetraploid checkpoint.The role of tumour heterogeneity and clonal cooperativity in metastasis, immune evasion and clinical outcome Spatial and temporal diversity in genomic instability processes defines lung cancer evolution.Glioblastoma adaptation traced through decline of an IDH1 clonal driver and macro-evolution of a double-minute chromosome.Chromosome mis-segregation and cytokinesis failure in trisomic human cells Polyploidy can drive rapid adaptation in yeast.APOBEC Enzymes: Mutagenic Fuel for Cancer Evolution and Heterogeneity.Cytokinetic Failure-induced Tetraploidy Develops into Aneuploidy, Triggering Skin Aging in Phosphovimentin-deficient Mice.Centrosome amplification induces high grade features and is prognostic of worse outcomes in breast cancer.Tracking the genomic evolution of esophageal adenocarcinoma through neoadjuvant chemotherapy.Paired exome analysis of Barrett's esophagus and adenocarcinoma.Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Intra-patient Inter-metastatic Genetic Heterogeneity in Colorectal Cancer as a Key Determinant of Survival after Curative Liver Resection.Identification of Selective Lead Compounds for Treatment of High-Ploidy Breast Cancer Morphometric analysis of immunoselection against hyperploid cancer cells Selective advantage of trisomic human cells cultured in non-standard conditions Whole-genome duplication increases tumor cell sensitivity to MPS1 inhibition.Tetraploid cells produced by absence of substrate adhesion during cytokinesis are limited in their proliferation and enter senescence after DNA replication Overexpression screens identify conserved dosage chromosome instability genes in yeast and human cancer The Zn-finger domain of MdmX suppresses cancer progression by promoting genome stability in p53-mutant cells.Linking genomic reorganization to tumor initiation via the giant cell cycle The PIDDosome activates p53 in response to supernumerary centrosomes.Heterogeneity in sarcoma cell lines reveals enhanced motility of tetraploid versus diploid cells.The Consequences of Chromosome Segregation Errors in Mitosis and Meiosis.Size Does Matter: Why Polyploid Tumor Cells are Critical Drug Targets in the War on Cancer.Evolutionary mechanism unifies the hallmarks of cancer.Genomic instability: Crossing pathways at the origin of structural and numerical chromosome changes.Stage-specific frequency and prognostic significance of aneuploidy in patients with sporadic colorectal cancer--a meta-analysis and current overview.

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P2860

Tolerance of whole-genome doubling propagates chromosomal instability and accelerates cancer genome evolution.

http://www.wikidata.org/entity/Q34946877

description

2014 nî lūn-bûn

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2014 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2014 թվականի հունվարին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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Tolerance of whole-genome doub ...... rates cancer genome evolution.

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Tolerance of whole-genome doub ...... rates cancer genome evolution.

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Tolerance of whole-genome doub ...... rates cancer genome evolution.

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type

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Tolerance of whole-genome doub ...... rates cancer genome evolution.

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Tolerance of whole-genome doub ...... rates cancer genome evolution.

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Tolerance of whole-genome doub ...... rates cancer genome evolution.

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Tolerance of whole-genome doub ...... rates cancer genome evolution.

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Tolerance of whole-genome doub ...... rates cancer genome evolution.

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Tolerance of whole-genome doub ...... rates cancer genome evolution.

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2159-8290.CD-13-0285

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Cancer Discovery

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Tolerance of whole-genome doub ...... erates cancer genome evolution

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Andrew J Rowan

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David Endesfelder

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Dmitri Mouradov

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Rebecca A Burrell

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Sally M Dewhurst

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Tejal Joshi

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P2860

Massive genomic rearrangement acquired in a single catastrophic event during cancer development

Intratumor Heterogeneity and Branched Evolution Revealed by Multiregion Sequencing

The life history of 21 breast cancers

A mechanism linking extra centrosomes to chromosomal instability

Cytokinesis failure generating tetraploids promotes tumorigenesis in p53-null cells

Examining the link between chromosomal instability and aneuploidy in human cells

Telomere-driven tetraploidization occurs in human cells undergoing crisis and promotes transformation of mouse cells.

DNA ploidy status and prognosis in colorectal cancer: a meta-analysis of published data.

PICNIC: an algorithm to predict absolute allelic copy number variation with microarray cancer data.

Proliferation of aneuploid human cells is limited by a p53-dependent mechanism.

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2

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Zoltan Szallasi

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Nicholas J. Hawkins

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