ライフサイエンスコーパス: CNA

1 CNA acquisition in PDXs was correlated with the tissue-s

2 CNA detection in tumors from single nucleotide polymorph

3 CNA number and length are linked to patient survival, su

4 CNAs of the CDKN2A-TP53-RB-E2F axis provide a structural

5 CNAs were detected in 94% of BIA-ALCLs, with losses at c

6 sembled pili, four domains of BcpA - CNA(1), CNA(2), XNA and CNA(3) - each acquire intramolecular lys

7 To investigate the relationship between 1q21 CNAs and DNA hypomethylation of the 1q12 pericentromeric

8 d an average of 16.3 somatic mutations and 4 CNAs per sample.

9 m 13 patients (training set), we generated a CNA-based classifier that we validated in 18 additional

10 Copy number abbreviation (CNA) is one type of genomic aberration that is often ind

11 Copy-number aberration (CNA) analysis identified recurrent alterations, includin

12 exome sequencing and copy number aberration (CNA) analysis, which showed an average of 16.3 somatic m

13 aring the cells' DNA copy number aberration (CNA) landscapes with those of the primary tumors and lym

14 ially determined the copy number aberration (CNA) profiles of 74 patients with index tumors of Gleaso

15 and the genome-wide copy number aberration (CNA) profiles of individual vitreous-isolated B cells we

16 enes on the basis of copy number aberration (CNA) regions of cancer genomes, by integrating publicly

17 fine multichromosome copy number aberration (CNA) signatures that can be used to evaluate risk.

18 st tumours that have copy number aberration (CNA), gene expression and long-term clinical follow-up d

19 copy number variants (CNV) and aberrations (CNA) from targeted sequencing data are based on the dept

20 he most significant copy number aberrations (CNA) and identified regions of peak and broad copy numbe

21 DNA copy number aberrations (CNA) are frequently observed in colorectal cancers (CRC)

22 s devoid of somatic copy-number aberrations (CNA-devoid) are consistently prognostic across several o

23 At diagnosis, 15 aberrations (CNAs, n = 10; UPDs, n = 5) were identified in 13 patient

24 ons and copy number alterations/aberrations (CNAs) in the two most common breast cancer histologies,

25 tic significance of copy-number aberrations (CNAs) and copy-neutral loss of heterozygosity (cnLOH) id

26 me-wide chromosomal copy number aberrations (CNAs) and mutational profiles for a subset (n = 7) were

27 Copy-number aberrations (CNAs) and whole-genome duplications (WGDs) are frequent

28 Somatic copy number aberrations (CNAs) have been implicated in the development and progre

29 isease, we examined copy-number aberrations (CNAs) in circulating tumor cells (CTCs) from pretreatmen

30 Studying recurrent copy number aberrations (CNAs) in human cancers would enable the elucidation of d

31 e analysis of large copy-number aberrations (CNAs) in individual cells.

32 ive allele-specific copy-number aberrations (CNAs) in these samples, including copy-neutral LOHs, who

33 uding the high-risk copy number aberrations (CNAs) of +1q21 and 17p(-).

34 nd acquired somatic copy number aberrations (CNAs) were associated with expression in ~40% of genes,

35 Copy number aberrations (CNAs), which are pathogenic copy number variations (CNVs

36 Copy number aberrations (CNAs), which delete or amplify large contiguous segments

37 variants (SNVs) and copy number aberrations (CNAs), while MutSigCV (SNVs) and GISTIC (CNAs) algorithm

38 t commonly shared copy number abnormalities (CNAs) in all types were losses at chromosomes 6q23-26 an

39 Copy number abnormalities (CNAs) such as somatically-acquired chromosomal deletions

40 clinically relevant copy number abnormality (CNA) profiles.

41 Accurate CNA determination is complicated by uneven genomic distr

42 ftware (PennCNV-tumor) for fast and accurate CNA detection using signal intensity data from SNP genot

43 arance on anaerobic colistin nalidixic acid (CNA) agar which likely facilitated its detection and ide

44 agar plate [BAP]), colistin-nalidixic acid (CNA), and MacConkey agars in 5% CO2 for 48 h.

45 d (CLA) and conjugated nonadecadienoic acid (CNA) have been previously shown to effectively reduce bo

46 s are used to form these click nucleic acid (CNA) polymers.

47 w synthetic DNA analog, click nucleic acids (CNAs).

48 An average of 1.14 somatically acquired CNAs per patient were observed.

49 landscape dominated by cis- and trans-acting CNAs.

50 ations detected at diagnosis plus additional CNAs that emerged at the MRD stage, whereas in the remai

51 on blood agar, colistin-nalidixic acid agar (CNA), and mannitol salt agar (MSA); and 25 enteric isola

52 r web-interface) for copy-number alteration (CNA) analysis and tumor purity estimation of paired tumo

53 ion profiles and DNA copy number alteration (CNA) data from 29 normal prostate tissue samples, 127 pr

54 d the pattern of DNA copy number alteration (CNA) in 168 primary tumors, raising the possibility of C

55 Copy number alteration (CNA) is a major contributor to genome instability, a hal

56 es the estimation of copy number alteration (CNA) possible, even at very low coverage.

57 Specifically, copy number alteration (CNA) profiles generated by next-generation sequencing (N

58 or detecting somatic copy-number alteration (CNA) using whole-genome sequencing (WGS) data.

59 matic mutations and copy number alterations (CNA) across a 641 cancer-associated-gene panel in a sing

60 Somatic copy number alterations (CNA) are found in most aggressive primary human prostate

61 rofiles and somatic copy number alterations (CNA) information on the same patients identified using m

62 tified differential copy-number alterations (CNA), mutations, DNA methylation, and miRNA expression b

63 port the spectrum of genomic CN alterations (CNAs) detected at 9p21, the major site of CN change in m

64 whereas at relapse, 56 genomic alterations (CNAs, n = 46; UPDs, n = 10) were detected in 29 patients

65 re used to evaluate copy-number alterations (CNAs) and determine their associations with treatment ou

66 elapse for selected copy number alterations (CNAs) and mutations.

67 WGS also delineated copy number alterations (CNAs) and structural variants in the 10 paired patients.

68 profiling to detect copy number alterations (CNAs) and uniparental disomies (UPDs) and performed comp

69 Whether somatic copy number alterations (CNAs) are a frequent cause of altered miRNA gene express

70 Somatic copy number alterations (CNAs) are a hallmark of cancer, but their role in tumori

71 Aneuploidy and copy-number alterations (CNAs) are a hallmark of human cancer.

72 in vivo results in copy-number alterations (CNAs) associated with DNA damage response and modulation

73 ered six cases with copy number alterations (CNAs) at the IDH1 locus at recurrence.

74 me chromosome-scale copy-number alterations (CNAs) but little-to-no single-nucleotide variants.

75 part by increasing copy number alterations (CNAs) during disease progression.

76 analysis of somatic copy number alterations (CNAs) has broad applications in cancer research.

77 on levels (GEs) and copy number alterations (CNAs) have important biological implications.

78 red the dynamics of copy number alterations (CNAs) in 1,110 PDX samples across 24 cancer types.

79 Copy number alterations (CNAs) in cancer patients show a large variability in the

80 matic mutations and copy number alterations (CNAs) in exome data from tumor-normal pairs.

81 curate detection of copy number alterations (CNAs) in human genomes is important for understanding su

82 tected somatic gene copy number alterations (CNAs) in mantle cell lymphoma (MCL) patients treated fir

83 e hypothesized that copy number alterations (CNAs) of intergenic nonprotein-coding domains could help

84 with a median of 9 copy number alterations (CNAs) per case, many of such CNAs being similar to those

85 Copy number alterations (CNAs) play an important role in molding the genomes of b

86 omprehensive set of copy number alterations (CNAs) that decreased p53 activity and perturbed cell cyc

87 DNA copy number alterations (CNAs) were defined by using array comparative genomic hy

88 DNA samples without copy number alterations (CNAs), almost all of these algorithms are not designed f

89 deletions (indels), copy number alterations (CNAs), and a wide range of gene fusions; no current clin

90 mal rearrangements, copy number alterations (CNAs), and associated driver genes, and compared these c

91 ecurrent arm-length copy number alterations (CNAs), and focal alterations such as deletion of 3p21 or

92 onship between SVs, copy number alterations (CNAs), and mRNA expression.

93 l, known as somatic copy number alterations (CNAs), can drive tumorigenesis.

94 a higher number of copy number alterations (CNAs), compared to the R337H-.

95 alterations (SNAs), copy number alterations (CNAs), DNA methylation, and RNA expression data.

96 rom the presence of copy number alterations (CNAs), for which analysis of the expression of the under

97 compared mutations, copy number alterations (CNAs), gene expression and drug response to BCa patient

98 em showed identical copy number alterations (CNAs), in another 3 cases, MRD clonal PCs displayed all

99 underwent recurrent copy number alterations (CNAs), particularly deletion of the RAS inhibitor Neurof

100 ates typically lack copy number alterations (CNAs).

101 genes (mRNA, miRNA, copy number alterations [CNAs], SNPs, single nucleotide variants [SNVs], CpG meth

102 nd allele-specific copy number alternations (CNA) from cancer whole exome sequencing data based on Lo

103 The correlations among GEs and among CNAs make the analysis even more complicated.

104 ibe the interconnections among GEs and among CNAs.

105 BA) and the central nucleus of the amygdala (CNA) and recorded sleep and wakefulness.

106 CLA and CNA significantly reduced body weight and fat mass by in

107 CLA and CNA significantly reduced serum leptin and tumour necros

108 The CXCR4 and CNA findings were validated in independent expansion coh

109 analysis combining both gene expression and CNA data from The Cancer Genome Atlas.

110 ify significant predictors of metastasis and CNA signatures.

111 rmance of VarScan 2 for somatic mutation and CNA detection and shed new light on the landscape of gen

112 nt predictors of poor metastatic outcome and CNA signatures were identified that can add a specific H

113 WES, clonal PCs in AL display phenotypic and CNA profiles similar to MM, but their transcriptome is r

114 ur domains of BcpA - CNA(1), CNA(2), XNA and CNA(3) - each acquire intramolecular lysine-asparagine i

115 etween the number of mutational hotspots and CNAs generated from these platforms highlight a number o

116 for the simultaneous formation of anomalous CNAs in multiple chromosome regions.

117 Many methods exist for assessing CNAs using microarrays, but considerable technical issue

118 hanism cannot apply to CNAbeta1, an atypical CNA isoform generated by alternative 3'-end processing,

119 Exome-based CNA analysis identified 29 large-scale alterations and 6

120 ples compared to 15 found by CGI's HMM-based CNA model.

121 sed methods and outperforms sequencing-based CNA detection tools.

122 tory or chemosensitive by using the baseline CNA classifier.

123 ithin assembled pili, four domains of BcpA - CNA(1), CNA(2), XNA and CNA(3) - each acquire intramolec

124 ble antagonist, beta-chlornaltrexamine (beta-CNA).

125 partial irreversible block of MORs with beta-CNA, there was an increase in the time it took to reach

126 An association between CNAs and high grade and advanced stage was observed in M

127 nd microsatellite instability based on broad CNA scores and discrete genomic imbalances.

128 e percentage of the tumor genome affected by CNA, was associated with biochemical recurrence and meta

129 ng expression outlier genes driven in cis by CNAs, we identified putative cancer genes, including del

130 GEs are partly regulated by CNAs, and much effort has been devoted to understanding

131 rehensively and systematically characterized CNAs and the accompanying gene expression changes in tum

132 disease did not switch to a chemorefractory CNA profile, which suggests that the genetic basis for i

133 Genome Atlas datasets, we find that combined CNA/SNA data divide gliomas into three highly distinct m

134 The most common CNA was a gain in chromosome 6p.

135 A comparative CNA analysis of fusion-positive and fusion-negative ACCs

136 For comparison, CNAs for anaplastic lymphoma kinase (ALK)- nodal anaplas

137 for organogel formation where complementary CNA-based polymers form reversible crosslinks.

138 App generates genome-wide profiles, computes CNA scores for broad, focal and global CNA burdens, and

139 Moreover, VCF2CNA achieved highly consistent CNA profiles between WGS and WXS platforms (mean F1 scor

140 a total of 48 somatic miRNA gene-containing CNAs that were not identified by routine cytogenetics in

141 Notably, CTC CNA profiles obtained at relapse from five patients with

142 considerable technical issues limit current CNA calling based upon DNA sequencing.

143 We conclude that MLPA defined CNA profiles can be accurately mirrored by SNP6.0 or sim

144 re required when characterizing high density CNAs data.

145 proaches, where the low-coverage WGS-derived CNA segments were highly accordant (PCC >0.95) with thos

146 present SynthEx, a novel tool for detecting CNAs from whole exome and genome sequencing.

147 thods that have been developed for detecting CNAs in scDNAseq data, and categorize them according to

148 f 143 patients being assigned to a different CNA risk group and eight patients using the automated pi

149 s a substantial challenge, because different CNAs may overlap with one another on the genome.

150 nstrate its utility for discovering distinct CNA events and for deriving ancillary information such a

151 s, identifies the genes most likely to drive CNA formation using the cghMCR method and identifies rec

152 rmine associations between mutations, driver CNA profiles, clinical-pathological parameters and survi

153 orithm (extended-common neighbor analysis (E-CNA)) is developed that allows for an efficient identifi

154 er local orientation analysis methods, the E-CNA method allows for atomic scale characterization of t

155 , and with a newly developed high-efficiency CNA profiling protocol.

156 We assess whether equivalent CNA profiles are called using SNP arrays, ensuring platf

157 -cell DNA sequencing data and helps estimate CNA rates in a large pan-cancer dataset.

158 However, estimating CNA from patients' tumour samples poses considerable cha

159 line in situations with branching evolution, CNA gain, and neutral mutations.

160 d single, concurrent, and mutually exclusive CNAs that could be the driving events in cancer metastas

161 In summary, CNApp facilitates CNA-driven research by providing a unique framework to i

162 ype shows specific ranges of broad and focal CNA scores.

163 Focal CNAs affecting the MYC gene and the PTEN gene were obser

164 tens or even hundreds of large and/or focal CNAs, a major difficulty is differentiating between impo

165 We searched for additional recurrent focal CNAs using the correlation matrix diagonal segmentation

166 e a helpful complement to the read depth for CNA analysis for two reasons.

167 rch directions for computational methods for CNA detection from scDNAseq data.

168 A wide array of methods for CNA detection has been either developed specifically for

169 Standard methods for CNA inference analyze tumor samples individually; howeve

170 There is an urgent need for CNA-based biomarkers in clinics,.

171 valuate the use of sequencing techniques for CNA analysis, especially with the rapid growth of the di

172 efficient and platform-independent tool for CNA and tumor purity analyses without accessing raw sequ

173 Notably, Staphylococci spp. from CNA exhibit low identification rates.

174 These results demonstrate the power of GEMM CNA analysis to inform the pathogenesis of human cancer.

175 ith distant metastases and widespread genome CNAs that were independent of forced disruption of Tp53

176 thelial neoplasia and did not harbor genomic CNAs.

177 ns (CNAs), while MutSigCV (SNVs) and GISTIC (CNAs) algorithms estimated the significance of recurrent

178 putes CNA scores for broad, focal and global CNA burdens, and uses machine learning-based predictions

179 "aberrant cells of unknown origin" that have CNA landscapes discordant from the tumor.

180 nificantly more common in tumors with a high CNA burden (P < .001 and P < .003, respectively).

181 These overlap with human CNAs including NF1, which is deleted or mutated in 27.7%

182 SynthEx robustly identifies CNAs using sequencing data without the additional costs

183 Tumors and cultures with IDH1 CNA had decreased 2HG, maintenance of G-CIMP, and DNA me

184 in turn, identify the functionally important CNAs that are under natural selection on the parental al

185 rigenesis, and observe marked differences in CNA prevalence between mouse mammary tumours initiated w

186 nd human tumours narrows critical regions in CNAs, thereby identifying candidate driver genes.

187 g reliably identifies substitutions, indels, CNAs, and gene fusions, with similar accuracy to lower-t

188 ere we use gene expression profiles to infer CNAs in 3,108 samples from 45 mouse models, providing th

189 ies produce data that is ideal for inferring CNAs.

190 Integrative CNA analyses of 97 CTCs from 23 patients confirmed the c

191 Microinjections of LY37 or LY34 into CNA had no significant impact on sleep.

192 Microinjections into CNA were conducted at one dosage range for LY37 (0.1 nM,

193 d PTLs also have frequent 9p24.1/PD-L1/PD-L2 CNAs and additional translocations of these loci, struct

194 1A-mutated tumors display significantly less CNAs across multiple cancer types.

195 tive ACCs and MECs revealed relatively lower CNAs in fusion-positive tumors than in fusion-negative t

196 be mutated in samples that have few or many CNAs, which we term CONIM genes (COpy Number Instability

197 ny genomic region juxtaposed to it and mimic CNAs found in the bone marrow of patients with high-risk

198 onstrate concordance between SNP6.0 and MLPA CNA calling on 143 leukaemia samples from two UK trials;

199 Moreover, CNA analysis may serve as a parameter for future diagnos

200 Moreover, CNA burden was associated with biochemical recurrence in

201 ne expression possibly regulated by multiple CNAs and one CNA potentially regulating the expressions

202 It jointly models the effects of multiple CNAs on multiple GEs.

203 We find that 34% of CNA breakpoints can be clarified structurally and that m

204 modulatory role for miRNAs in the biology of CNA-devoid breast cancers, a common subtype in which the

205 ond, this knowledge enables deconvolution of CNA patterns in complex genomic regions.

206 ast cancers, and the potential importance of CNA heterogeneity in phenomena such as therapeutic resis

207 lk tumor and DTC genomes enables ordering of CNA events in molecular pseudo-time and traced the origi

208 A heterogeneous population of CNA-positive cells is present in the bone marrow of non-

209 tissue-of-origin influences the position of CNA breakpoints and the properties of the resulting CNAs

210 8 primary tumors, raising the possibility of CNA as a prognostic biomarker.

211 Regions of CNA encompassed genes involved in the JAK/STAT pathway a

212 uired to test the prognostic significance of CNA presence in disease relapse in patients with AML.

213 he mechanisms underlying the accumulation of CNAs and resulting subclonal heterogeneity in high-risk

214 We observed rapid accumulation of CNAs during PDX passaging, often due to selection of pre

215 els and methods for evolutionary analyses of CNAs from scDNAseq data and highlight advances and futur

216 rovide insights into the structural basis of CNAs as well as the impact of SVs on gene expression in

217 Unsupervised clustering of CNAs defined two distinct classes of bladder tumors that

218 rom 23 patients confirmed the convergence of CNAs and revealed single, concurrent, and mutually exclu

219 t allows the cost-effective determination of CNAs.

220 nd a favourable prognosis subgroup devoid of CNAs.

221 l that allows a comprehensive exploration of CNAs by using purity-corrected segmented data from multi

222 orms, intra-tumoral genetic heterogeneity of CNAs, the magnitude with which CNA heterogeneity affects

223 cRCC genome by better defining the impact of CNAs in conjunction with methylation changes on the expr

224 hysical maps to make posterior inferences of CNAs.

225 hylation changes and mutations and a lack of CNAs.

226 contributes to the recurrence and length of CNAs in the respective cancer type.

227 tability, as evidenced by a higher number of CNAs in the R337H+ cases compared to the R337H-.

228 regions were identified, and the presence of CNAs was found to be associated with decreased 3-year ov

229 gle-cell genome evolution in the presence of CNAs.

230 lly; however, it is well known that rates of CNAs vary by length, genomic position and type (amplific

231 ples that are known to have large regions of CNAs.

232 and adult patients revealed novel oncogenic CNAs, complex rearrangements and subclonal CNAs missed b

233 possibly regulated by multiple CNAs and one CNA potentially regulating the expressions of multiple g

234 amolecular isopeptide bonds in the CNA(2) or CNA(3) domains retain the ability to form pilus bundles.

235 However, the particular CNAs acquired during PDX passaging differed from those a

236 DLBCLs with p53 and cell cycle pathway CNAs had decreased abundance of p53 target transcripts a

237 We also identified genes located in peak CNAs with concordant methylation changes (hypomethylated

238 First, triblock copolymers of PEG-CNA-PLGA are synthesized and then formulated into polyme

239 rands do not get encapsulated within the PEG-CNA-PLGA nanoparticles.

240 Prognostic CNAs/cnLOH were identified: whereas early progression wa

241 y suitable for determination of high-quality CNA profile.

242 ware also allows users to identify recurrent CNA regions that may be associated with differential sur

243 Moreover, CNApp reproduces recurrent CNAs in hepatocellular carcinoma and predicts colon canc

244 akpoints and the properties of the resulting CNAs.

245 novel driver genes were detected by scanning CNAs of breast cancer, melanoma and liver carcinoma.

246 ooth-segmented and circular binary-segmented CNA profiles.

247 Several CNAs recurrently observed in primary tumors gradually di

248 y a phasing strategy to test if those shared CNAs are identical by descent.

249 Prognostically significant CNAs accumulate during clonal evolution and include gain

250 neous for single-nucleotide variants (SNVs), CNAs and genomic rearrangements.

251 ole-genome sequence data to identify somatic CNAs involving miRNA genes in 113 cases of AML, includin

252 pulation, derived from the impact of somatic CNAs on the transcriptome.

253 These data show that somatic CNAs specifically targeting miRNA genes are uncommon in

254 These allele-specific CNAs affect genomic regions containing well-known breast

255 n of tumor evolution, timing allele-specific CNAs before and after WGDs, identifying low-frequency su

256 rithm that infers allele- and clone-specific CNAs and WGDs jointly across multiple tumor samples from

257 Subtype-specific CNAs included a loss at 12q11-12 in ACC and a gain at 17

258 c CNAs, complex rearrangements and subclonal CNAs missed by alternative approaches.

259 creas cancer patients, we identify subclonal CNAs and WGDs that are more plausible than previously pu

260 e duplications (WGDs) and mirrored-subclonal CNAs.

261 eve autoinhibition of the catalytic subunit (CNA) by its C terminus.

262 er alterations (CNAs) per case, many of such CNAs being similar to those found in MM.

263 purity estimates for samples with sufficient CNAs.

264 In summary, we combine SV, CNA, and expression data to provide insights into the st

265 We further demonstrate that CNA burden can be measured in diagnostic needle biopsies

266 We find that CNA burden across the genome, defined as the percentage

267 ancer dataset of 10,635 genomes showing that CNAs classify cancer types according to their tissue-of-

268 The CNA-containing particles show high encapsulation of DNA

269 We have demonstrated that characterizing the CNA landscape in HCC will facilitate the understanding o

270 m the intramolecular isopeptide bonds in the CNA(2) or CNA(3) domains retain the ability to form pilu

271 A mutant lacking the CNA(1) isopeptide bond assembled deformed pilin subunits

272 Thus, structural integrity of the CNA(1) and XNA domains are determinants for the associat

273 , demonstrating the potential utility of the CNA-containing particles as carriers for chemotherapy ag

274 at contains an overhang complementary to the CNA can also be encapsulated, demonstrating the potentia

275 gh encapsulation of DNA complementary to the CNA sequence, whereas PEG-PLGA alone shows minimal DNA l

276 rather than abruptly, converging toward the CNA in CTCs.

277 n BA that control descending output (via the CNA or bed nucleus of the stria terminalis) that in turn

278 on-mediated adaptive immune response in the 'CNA-devoid' subgroup and a basal-specific chromosome 5 d

279 nction of the patients' covariates and their CNA profiles, in a mixed model framework.

280 tumors that differed in the degree of their CNA burden.

281 These CNAs affected genes and miRNAs that regulate critical ca

282 All these CNAs also included one or more protein coding genes.

283 Validated gene losses due to CNAs involved PRDM2 (93%), BTG1 (87%), HIVEP2 (77%), MKL

284 promising for elucidating and understanding CNAs, our findings show that even the best existing meth

285 uency subpopulations distinguished by unique CNAs and uncovering evidence of convergent evolution.

286 reas in the remaining 6 patients, there were CNAs present at diagnosis that were undetectable in MRD

287 When CNAs exist in the samples, accuracy can be dramatically

288 thout using reference/training samples, when CNAs do not exist.

289 netic reconstruction on simulated data where CNAs occur with varying probabilities, aids in the deriv

290 ), similarly in both treatment arms, whereas CNAs in MYC, ATM, CDK2, CDK4, and MDM2 had no prognostic

291 both samples occurred sporadically, whereas CNAs among primary tumor cells emerged accumulatively ra

292 erogeneity of CNAs, the magnitude with which CNA heterogeneity affects the genomes of breast cancers,

293 While CNAs are useful markers in cancer studies, single-nucleo

294 Determination of the genome-wide CNA profile is an important step in identifying the unde

295 ered as fixed predictors and the genome-wide CNA profiles are considered as random predictors.

296 he patients covariates and their genome-wide CNA profiles from NGS data.

297 errant expression was rarely associated with CNAs.

298 rate genotyping calls for tumor samples with CNAs.

299 t can accurately genotype tumor samples with CNAs.

300 ne sets significantly altered in tumors with CNAs compared with tumors without aberration.