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1 ferentially methylated regions and detecting copy number aberrations.
2 er genes are targeted by regional chromosome copy number aberrations.
3 led similar frequencies of recurrent genomic copy number aberrations.
4 few driver point mutations but abundant DNA copy number aberrations.
5 predominantly nonsilent mutations, and fewer copy number aberrations.
6 ng the statistical significance of recurrent copy number aberrations.
7 troduced for identifying common regions with copy number aberrations.
8 o distinguish between recurrent and sporadic copy number aberrations.
9 f cross-species overlap in cancer-associated copy number aberrations.
10 We also observe biases in chromosome copy number aberrations.
11 profiles revealed numerous recurrent genomic copy number aberrations.
12 omas had a significantly higher frequency of copy number aberrations (67%) than other subgroups (P =
13 .0 array-based genomic profiling of acquired copy number aberrations (aCNA) and copy neutral LOH (cnL
14 genesis of CLL as recurrent acquired genomic copy number aberrations (aCNA) and recurrent gene mutati
15 m 255 patients with CLL for acquired genomic copy number aberrations (aCNAs) with the use of ultra-hi
18 nitiating cells have uncovered multiple gene copy number aberrations and have yielded new insight int
19 relationships of protein expression with DNA copy number aberrations and signatures of post-transcrip
20 variations, small insertions and deletions, copy number aberrations and structural variations in bot
22 omatic mutations (up to 50 bases in length), copy number aberrations, and structural rearrangements i
23 tumours were characterised by an absence of copy-number aberrations apart from LOH chromosome 16q, t
24 dual evolution, showing that the majority of copy number aberrations are acquired at the earliest sta
26 ic landscape of mCRC reveals a number of DNA copy number aberrations associated with response to drug
30 el approach for finding regions of recurrent copy number aberrations, called CNAnova, from Affymetrix
32 CLLs by combining whole-exome sequencing and copy number aberration (CNA) analysis, which showed an a
36 ntify potential driver genes on the basis of copy number aberration (CNA) regions of cancer genomes,
37 of metastasis, and to define multichromosome copy number aberration (CNA) signatures that can be used
38 es in 2,433 primary breast tumours that have copy number aberration (CNA), gene expression and long-t
39 se approach to identify the most significant copy number aberrations (CNA) and identified regions of
40 s, we performed a genome-wide search for DNA copy number aberrations (CNA) in a panel of 33 tumors en
41 erived from breast tumours devoid of somatic copy-number aberrations (CNA-devoid) are consistently pr
44 ymorphism (SNP) arrays allows measurement of copy number aberrations (CNAs) in cancer at more than on
47 -derived from real data-that contain somatic copy number aberrations (CNAs) of various lengths and fr
48 cleotide polymorphisms) and acquired somatic copy number aberrations (CNAs) were associated with expr
49 humans by comparing all D. rerio genes with copy number aberrations (CNAs) with a cohort of 75 publi
52 ve from chemorefractory disease, we examined copy-number aberrations (CNAs) in circulating tumor cell
54 ype, or G-CIMP tumors, have distinct genomic copy number aberrations, DNA methylation patterns, and (
55 ofiles to identify relationships between DNA copy number aberrations, gene expression alterations, an
56 q24 and a total number of independent genome copy number aberrations >7 are associated with reduced s
57 profiling remains difficult because true DNA copy-number aberrations have to be discriminated from WG
58 t cancer-specific survival (METABRIC cohort [copy number aberration]: hazard ratio [HR] 1.50, 95% CI
60 eletions of 360 cancer genes and genome-wide copy number aberrations in 413 and 170 ILBC samples, res
61 We studied 282 females with SBC, focusing on copy number aberrations in cancer-free breast tissue (un
62 sistent with previous studies, such as large copy number aberrations in chromosome 8 and complex rear
63 enomic hybridization to identify and compare copy number aberrations in five mouse models of breast c
66 that triple-negative breast cancers acquire copy number aberrations in short punctuated bursts in th
68 allows quantitative detection and mapping of copy number aberrations in tumors and subsequent associa
70 arrays, we conducted an analysis of somatic copy-number aberrations in 486 gastrointestinal adenocar
71 verely retarded patients, were found to have copy-number aberrations in addition to the 5p deletion.
74 clinicopathological relevance of SPAG5 gene copy number aberrations, mRNA transcript expression, and
75 comparative genomic hybridization to analyse copy number aberrations occurring in FTC in order to obt
78 current single nucleotide variants and focal copy number aberrations, poor-prognosis hindbrain ependy
79 University Hospital to identify genome-wide copy number aberrations, putative driver genes, deregula
80 olution across the genome to map genomic DNA copy number aberrations quantitatively from 14 FTC onto
81 ion sites were enriched in recurrent somatic copy-number aberration regions from multiple cancer type
82 sed by a large number of somatic chromosomal copy number aberrations (SCNA) that frequently affect on
84 rmal melanocytic proliferations that exhibit copy number aberrations should undergo careful clinical
85 without chronic sun-induced damage) for DNA copy number aberrations specific to melanoma subtypes wh
86 some breaks, inversions, deletions and micro copy number aberrations, specifically in BRCA1-deficient
87 cleotide variants, insertions and deletions, copy-number aberrations, structural variants and gene fu
88 ssion and analysed the associations of SPAG5 copy number aberrations, transcript expression, and prot
90 6 esophageal adenocarcinoma was analyzed for copy number aberrations using Affymetrix SNP 6.0 arrays.
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