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 analysis discovered CNAs that were shared at diagnos

3 CNA detection in tumors from single nucleotide polymorph

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

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

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

7 An average of 5.1 (range 3-11) CNAs (excluding immunoglobulin/T-cell receptor alteratio

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

9 7 genomes containing the most changes (10-29 CNAs per genome).

10 were found in the 86 AML genomes (mean, 2.34 CNAs per genome), with French-American-British system M6

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

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

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

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

15 DNA copy number aberration (CNA) is a hallmark of genomic abnormality in tumor cells

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

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

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

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

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

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

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

23 wide search for DNA copy number aberrations (CNA) in a panel of 33 tumors encompassing grade 1 throug

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

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

26 lows measurement of copy number aberrations (CNAs) in cancer at more than one million locations in th

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

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

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

30 hat contain somatic copy number aberrations (CNAs) of various lengths and frequencies over germline s

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

32 D. rerio genes with copy number aberrations (CNAs) with a cohort of 75 published human T-ALLs analyze

33 riations (CNVs) and copy number aberrations (CNAs).

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

35 d those harboring copy number abnormalities (CNAs) of potential prognostic significance (MYC/MYCN amp

36 Copy number abnormalities (CNAs) represent an important type of genetic mutation th

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

38 gene expression, copy number abnormalities (CNAs), and DNA methylation.

39 H) to investigate copy number abnormalities (CNAs), one of the most prominent lesion types reported f

40 Accurate CNA determination is complicated by uneven genomic distr

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

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

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

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

45 Circulating nucleic acid (CNA) has been the focus of recent research as a noninvas

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 ts with an abnormal karyotype had additional CNA detected by SNP array, and several CNA regions were

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

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

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

60 iling of chromosome copy number alterations (CNA) in gliomas, and now present our findings on how tho

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 variation (CNV) and copy number alterations (CNA).

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 tion of somatic DNA copy number alterations (CNAs) and significant consensus events (SCEs) in cancer

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

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

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

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

72 imately 6 per case) copy number alterations (CNAs) as revealed by genome-wide single-nucleotide polym

73 Copy number alterations (CNAs) associated with cancer are known to contribute to

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

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

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

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 permit detection of copy number alterations (CNAs) of less than 5 Mb in size.

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

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

87 Acquired copy number alterations (CNAs) were confirmed using an ultra-dense array comparat

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

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

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

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

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

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

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

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

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

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

98 nce of regional DNA copy number alterations (CNAs), which may lead to deletion or over-expression of

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

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

101 ibe the interconnections among GEs and among CNAs.

102 nostic significance (MYC/MYCN amplification, CNAs of chromosome 6 and 17), we evaluated clinical, pat

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

104 precursor encompasses 2 Ig folds (CNA(2) and CNA(3)) and one jelly-roll domain (XNA) each of which sy

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

106 CLA and CNA significantly reduced serum leptin and tumour necros

107 s, genoCNV and genoCNA, designed for CNV and CNA studies, respectively.

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

109 ify significant predictors of metastasis and CNA signatures.

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

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

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

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

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

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

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

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

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

119 tory or chemosensitive by using the baseline CNA classifier.

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

121 ioid antagonist beta-chlornaltrexamine (beta-CNA) but was not reversed by a saturating concentration

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

123 f etorphine, methadone, oxymorphone, or beta-CNA also reduced the current induced by ME but did not b

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

125 quantitative relationships observed between CNA and gene expression in multiple cancer types and bio

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

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

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

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

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

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

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

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

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

135 We identified and compared CNAs in 5 pairs of monozygotic twins with concordant ETV

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

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

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

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

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

141 CNA analysis discovered CNAs that were shared at diagnosis and relapse and other

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

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

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

145 "Driver" CNAs in another twin with ALL were all absent in the sha

146 All "driver" CNAs (total of 32) were distinct within each of the 5 tw

147 These data place all "driver" CNAs secondary to the prenatal gene fusion event and mos

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

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

150 at relapse, integration of gene expression, CNA, and methylation data suggest a possible convergence

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

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

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

154 The BcpA precursor encompasses 2 Ig folds (CNA(2) and CNA(3)) and one jelly-roll domain (XNA) each

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

156 ods that have been used near exclusively for CNA analysis.

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

158 e direct method was 95% from blood, 75% from CNA, and 95% from MSA.

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

160 We also compared genes from CNAs of passaged zebrafish malignancies with aCGH result

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

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

163 thelial neoplasia and did not harbor genomic CNAs.

164 of AML patients with normal cytogenetics had CNA, whereas 40% of patients with an abnormal karyotype

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

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

167 und significant overlap (67%) with the human CNA dataset.

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

169 Second, when mapping the identified CNAs onto syntenic regions of the human genome, we noted

170 Our model not only identifies CNAs driving gene expression changes, but at the same ti

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

172 a novel approach, called CNAseg, to identify CNAs from second-generation sequencing data.

173 Additionally, we were able to identify CNAs whose gene expression correlation suggests possible

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

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

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

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

178 ge by altering a real dataset with spiked-in CNAs.

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

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

181 Integrating CNAs with gene expression helps to elucidate the mechani

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

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

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

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

186 idually count and size fluorescently-labeled CNA molecules as they are driven through a microfluidic

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

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

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

190 Moreover, CNA burden was associated with biochemical recurrence in

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

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

193 Cancers acquired an average of 34 new CNAs during passaging.

194 Of 86 genomes, 43 (50%) had no CNA or UPD at this level of resolution.

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

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

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

198 urth amide bond, derived from the Ig fold of CNA(1), is formed only after pilin subunits have been in

199 Injection of CNA-35 micelles resulted in a significantly higher magne

200 oscopy proved the precise co-localization of CNA-35 micelles with type I collagen.

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

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

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

204 8 primary tumors, raising the possibility of CNA as a prognostic biomarker.

205 ept experiment, we reported the potential of CNA-35 micelles to discriminate between stable AAA lesio

206 and successfully identified known regions of CNA associated with EGFR, KRAS and other important oncog

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

208 s shown promise for discerning the source of CNA molecules in cancer and prenatal diagnostics.

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

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

211 ignificantly confound downstream analysis of CNAs and affect the power to detect SCEs in clinical sam

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

213 es promise comprehensive characterization of CNAs.

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

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

216 t allows the cost-effective determination of CNAs.

217 nd a favourable prognosis subgroup devoid of CNAs.

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

219 hysical maps to make posterior inferences of CNAs.

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

221 st, we observed a significant overlapping of CNAs between human and canine tumors, and tumors from th

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

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

224 fy the transcriptional downstream targets of CNAs.

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

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

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

228 Fifty-five percent of original CNAs were preserved after serial transplantation, demons

229 was associated with poor outcome, but other CNAs were not.

230 We compared, within each pair, CNAs classified as potential "driver" or "passenger" mut

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

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

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

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

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

236 scrimination between true and false positive CNAs becomes an important issue.

237 ctionalized with a collagen-binding protein (CNA-35) were intravenously administered.

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

239 Recurrent CNA (RCNA) occurs in multiple cancer samples across the

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

241 the CNAnova framework to identify recurrent CNA regions with intra-tumour heterogeneity, present in

242 Recurrent CNAs are probably "driver" events contributing criticall

243 used methods for RCNA identification require CNA calling for individual samples before cross-sample a

244 Within all D. rerio CNAs, we identified 893 genes with human homologues and

245 akpoints and the properties of the resulting CNAs.

246 of CMDS is higher than that of single-sample CNA calling based two-step approaches.

247 Most research has focused on single-sample CNA discovery, the so-called segmentation problem.

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

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

250 ional CNA detected by SNP array, and several CNA regions were recurrent.

251 Several CNAs recurrently observed in primary tumors gradually di

252 Significantly, compared with the shared CNAs, we found that species-specific (especially human-s

253 Prognostically significant CNAs accumulate during clonal evolution and include gain

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

255 A total of 201 somatic CNAs were found in the 86 AML genomes (mean, 2.34 CNAs p

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

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

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

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

260 species-specific (especially human-specific) CNAs localize to evolutionarily unstable regions that ha

261 e calls from normal tissue are used to study CNAs in tumor tissue.

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

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

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

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

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

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

268 These findings indicate that CNAs recurrent between human and dog CRCs may have a hig

269 Recent studies suggest that CNAs and CNN-LOH occur frequently in AML.

270 The CNA-containing particles show high encapsulation of DNA

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

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

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

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

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

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

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

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

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

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

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

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

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

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

285 However, the way CNAs affect gene expression can vary in different cellul

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

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

291 n helps to elucidate the mechanisms by which CNAs act and to identify the transcriptional downstream

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

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

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

295 errant expression was rarely associated with CNAs.

296 ity of being cancer-causative, compared with CNAs found in one species only.

297 sparsely located in the genome compared 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.