ライフサイエンスコーパス: LOH

1 LOH at 8 loci, that is 3p12, 3p14.2, 5q21, 9p21, 9q, 13q

2 LOH events were commonly associated with acquired resist

3 LOH occurred in 54 out of 96 (56%) evaluable tumours, bu

4 LOH was by far the most common form of second hit.

5 LOH was present in 2.1% to 47.8% of all the preneoplasti

6 LOH was present in 28 out of 34 (82%) schwannomatosis-re

7 r probe for CN(-), (2F)LOH, (1F)LOH, and (0F)LOH acts as control molecules.

8 njugates, (5F)LOH, (2F)LOH, (1F)LOH, and (0F)LOH were synthesized and characterized.

9 11p15 LOH was identified in 19 (41%) of 46 evaluable VLRWTs an

10 WT1 mutation and 11p15 LOH are associated with relapse in patients with VLRWTs

11 mutation of WT1, CTNNB1, and WTX; for 11p15 LOH using microsatellite analysis; and for H19DMR and Kv

12 se (P = .004); all nine cases also had 11p15 LOH.

13 (unfavorable biology including 1p and/or 11q LOH [n = 7] or symptomatic with unknown biology [n = 4])

14 favorable biologic feature without 1p or 11q LOH) were assigned four cycles, and 11 patients (unfavor

15 In all, 65 of 124 LOH tested samples were available for CISH and 58 of tho

16 The randomized sample consisted of 150 LOH-positive patients.

17 of heterozygosity (LOH) using a panel of 16 LOH mutational markers associated with tumor suppressor

18 TP53 mutations and chromosome 17 LOH with selection against wild-type TP53 are observed i

19 did not show prognostic significance of 18q LOH.

20 In multivariate logistic regression, 18q LOH was independently associated with JC virus T antigen

21 positive tumors and 74% among those with 18q LOH-negative tumors (log-rank P = .80).

22 fic survival was 75% among patients with 18q LOH-positive tumors and 74% among those with 18q LOH-neg

23 d either loss of one copy of chromosome 19p (LOH, 40 of 65 cases, 62%) or both copies (HD 18 of 65 ca

24 characterized by a high percentage of 1p/19q LOH and IDH1 mutations), that especially benefits from P

25 Specific genetic changes (IDH1, 1p/19q LOH, and EGFR amplification) segregate into different su

26 Combining known molecular (1p/19q LOH, IDH1) prognostic parameters with intrinsic subtypes

27 as a molecular probe for CN(-), (2F)LOH, (1F)LOH, and (0F)LOH acts as control molecules.

28 opyranosyl conjugates, (5F)LOH, (2F)LOH, (1F)LOH, and (0F)LOH were synthesized and characterized.

29 LOH acts as a molecular probe for CN(-), (2F)LOH, (1F)LOH, and (0F)LOH acts as control molecules.

30 ked, glucopyranosyl conjugates, (5F)LOH, (2F)LOH, (1F)LOH, and (0F)LOH were synthesized and character

31 on deficiency subgroups: BRCA mutant (n=40), LOH high (n=82), or LOH low (n=70).

32 Analysing 22,392 and 74,415 LOH events in 363 glioblastoma and 513 ovarian cancer sa

33 3) x 10(-7) M (6 +/- 1 ppb) was shown by (5F)LOH for CN(-) in solution.

34 The conjugate (5F)LOH releases a fluorescent product upon reaction by CN(-

35 azole-linked, glucopyranosyl conjugates, (5F)LOH, (2F)LOH, (1F)LOH, and (0F)LOH were synthesized and

36 nzenesulfonyl reactive center present in (5F)LOH in the selectivity of CN(-) over other anions has be

37 The utility of (5F)LOH has been demonstrated by showing its reactivity towa

38 philic substitution reaction of CN(-) on (5F)LOH.

39 While the (5F)LOH acts as a molecular probe for CN(-), (2F)LOH, (1F)LO

40 The reactivity of CN(-) toward (5F)LOH has been elicited through the changes observed in NM

41 spects of the reactivity of CN(-) toward (5F)LOH were supported by DFT computational study.

42 an early event, as 62.5% of tumours showed a LOH pattern suggestive of HR defects.

43 also other NAT2 low activity variants after LOH respond to APA treatment.

44 rized a yeast clone isolated for carrying an LOH event at a specific chromosome site, and surprisingl

45 ratio 0.27, 95% CI 0.16-0.44, p<0.0001) and LOH high (0.62, 0.42-0.90, p=0.011) subgroups compared w

46 an fungal pathogen Candida albicans, CNV and LOH confer increased virulence and antifungal drug resis

47 eCNV, a statistical method to detect CNV and LOH using depth-of-coverage and B-allele frequencies, fr

48 Consistent deletion and LOH of genes on chromosome 3 occur in metastasizing diso

49 TP53 mutations and LOH have been linked, in many cases, with poor therapy r

50 Combined lymph node and LOH status was highly predictive of EFS and should be co

51 m the combined gene expression profiling and LOH analysis of 160 cases of RMS and non-RMS soft tissue

52 with combined positive lymph node status and LOH 1p or 16q.

53 ous germline or somatic), BRCA wild-type and LOH high (LOH high group), or BRCA wild-type and LOH low

54 ients with BRCA mutant or BRCA wild-type and LOH high platinum-sensitive ovarian carcinomas treated w

55 ients with BRCA mutant or BRCA wild-type and LOH high platinum-sensitive ovarian carcinomas treated w

56 high (LOH high group), or BRCA wild-type and LOH low (LOH low group).

57 completely eliminated any selection for Arf LOH.

58 and anti-PD1, respectively, we find that B2M LOH is enriched threefold in non-responders ( 30%) compa

59 is slightly decreased in the absence of BLM, LOH is increased by fivefold or more, implying significa

60 pinpointing the loci recurrently affected by LOH events across multiple tumors.

61 ven though Rpa1(L230P) is ultimately lost by LOH.

62 d with LOH profiles, and 254 were classified LOH positive.

63 hematologic malignancies exhibit abundant CN-LOH, often in the setting of a normal metaphase karyotyp

64 nal haematopoiesis with specific acquired CN-LOH mutations.

65 These observations suggest that acquired CN-LOH of chromosome 1p involving the MPL location may repr

66 mate recombination events such as iHR and CN-LOH.

67 on of candidate genes contained in common CN-LOH and deletion regions and have led to the discovery o

68 gous recombination (iHR), a precedent for CN-LOH.

69 acterized by recurrent chromosomal gains, CN-LOH, DAXX mutations, and ALT-positivity.

70 into the underlying mechanisms generating CN-LOH have great promise for elucidating general cancer me

71 and copy-neutral loss of heterozygosity (CN-LOH) in patients with diverse myeloid malignancies.

72 ired copy-neutral loss of heterozygosity (CN-LOH) of chromosome 1p in granulocytes, consistent with a

73 hree copy-neutral loss of heterozygosity (CN-LOH) regions greater than 1 Mb were observed and all wer

74 py number neutral loss of heterozygosity (CN-LOH) were identified by STR and SNP arrays.

75 and copy-neutral loss of heterozygosity (CN-LOH)) on all chromosomes(1,2,5,6,9), but the sources of

76 ect, copy neutral loss of heterozygosity (CN-LOH).

77 py number neutral loss of heterozygosity (CN-LOH).

78 Acquired copy neutral LOH (CN-LOH) is a frequent occurrence in myeloid malignancies an

79 In myeloid malignancies, CN-LOH has been associated with the duplication of oncogeni

80 that further detailed characterization of CN-LOH lesions will probably facilitate our discovery of a

81 merging biologic and clinical features of CN-LOH relevant to hematologic malignancies.

82 In addition, we found that CN-LOH mutations across the genome tended to cause chromoso

83 Moreover, resistance was associated with CN-LOH at the TK locus.

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

85 s that TNFRSF14 mutations accompanied by CNN-LOH of the 1p36 locus in over 70% of mutated cases, as a

86 y number neutral loss of heterozygosity (CNN-LOH) can also be detected using approaches that take adv

87 y-number neutral loss of heterozygosity (CNN-LOH) of this locus was more frequently observed in PTFL

88 y number-neutral loss of heterozygosity (CNN-LOH) on either 7q or 9p including homozygous JAK2V617F w

89 s (65-6499 bp) that are associated with CNV, LOH, and chromosomal inversions.

90 We also measured the rates of coincident LOH at two different chromosomes and found that double L

91 ble patients (n = 5) and those with combined LOH 1p/16q (n = 40) were excluded.

92 Consistently, LOH for hDMP1 was associated with luminal A category and

93 Conversely, LOH for hDMP1 was found in mutually exclusive fashion wi

94 raightforward principle that, by definition, LOH depletes heterozygotes, thereby disrupting Hardy-Wei

95 ative cases showed somatic allelic deletion; LOH of RBBP8 was associated with a significantly worse p

96 mutations in 8 patients (62%) and discordant LOH profiles in 7 patients (54%); independent genetic al

97 th histologic types of sporadic GC displayed LOH in 7.5%, mutations in 1.7%, and hypermethylation in

98 re also heterozygous, yet multiple, distinct LOH tracts were present in each isolate.

99 different chromosomes and found that double LOH formed at rates 14- to 150-fold higher than expected

100 To examine LOH associated with DSB-induced interhomolog recombinati

101 mice and Men1(+/-); Cdk2(-/-) mice exhibited LOH.

102 ose of human MHE, suggesting a role for Ext1 LOH in MHE.

103 nation (HR) repair and suppressing extensive LOH and chromosomal rearrangements in response to a DSB.

104 romosome loss, thereby suppressing extensive LOH.

105 For LOH profiles, the package contains significance tests.

106 This accounts for LOH in both its hemizygous deletion and copy-neutral for

107 A wild-type, but could not be classified for LOH, because of insufficient neoplastic nuclei in the sa

108 fied a cutoff of 14% or more genomic LOH for LOH high.

109 The 3-year CFS was significantly lower for LOH-positive compared with LOH-negative groups (74% vs 8

110 Examining clinical SMN samples, we found LOH of NF1 in SMNs from non-NF1 patients.

111 bsence of copy-number aberrations apart from LOH chromosome 16q, the genomic location of the CYLD gen

112 prespecified a cutoff of 14% or more genomic LOH for LOH high.

113 2, we assessed the ability of tumour genomic LOH, quantified with a next-generation sequencing assay,

114 75H mutation in TP53, whereas TOSE cells had LOH at the TP53 locus with a new R273H mutation at the p

115 creased frequency of loss of heterozygosity (LOH) across the genome (median 913 vs. 460 Mb in LOH, P

116 two of these genes, loss of heterozygosity (LOH) analysis of tSNPs in 314 ovarian tumours was used t

117 S pyrosequencing and loss of heterozygosity (LOH) analysis on chromosomes 6q and 17p.

118 ncreased spontaneous loss of heterozygosity (LOH) and chromosome mis-segregation in the mus81Delta ye

119 r variations (CNVs), loss of heterozygosity (LOH) and complex rearrangements, such as in chromothrips

120 copy number-neutral loss of heterozygosity (LOH) and deletions of chromosome 4q24 in a large cohort

121 variation (CNV) and loss of heterozygosity (LOH) are frequently observed during the somatic evolutio

122 their tumors due to loss of heterozygosity (LOH) at 8p22.

123 h a common region of loss of heterozygosity (LOH) at chr8p22 locus.

124 HWT without combined loss of heterozygosity (LOH) at chromosomes 1p and 16q treated in the Children's

125 amplifications, and loss of heterozygosity (LOH) at high resolution.

126 ring the presence of loss of heterozygosity (LOH) at selected genetic locations of tumor samples, or

127 stoma, with frequent loss of heterozygosity (LOH) at the Arf locus.

128 ated and altered and loss of heterozygosity (LOH) at the Trp53 wild-type locus is selected against, w

129 TOSE cells showed loss of heterozygosity (LOH) at TP53, increased nuclear p53 immunoreactivity and

130 del and show that 8p loss of heterozygosity (LOH) attenuates the action of several genes that collect

131 ypermethylation, and loss of heterozygosity (LOH) by polymerase chain reaction sequencing.

132 nd cell line for raw loss of heterozygosity (LOH) calls was 96% (range, 91-99%) and for raw copy numb

133 driver genes undergo loss of heterozygosity (LOH) events per tumor, generating discrete differences b

134 Nevertheless, loss of heterozygosity (LOH) for either Pdcd10 or Ccm2 resulted in CCMs in mice.

135 of cHL, we detected loss of heterozygosity (LOH) for KLHDC8B in RS cells, but not reactive T lymphoc

136 zebrafish displayed loss of heterozygosity (LOH) for the wildtype tp53 locus.

137 variation (CNV) and loss of heterozygosity (LOH) from exome sequencing data extends the utility of t

138 analysis of CNV and loss of heterozygosity (LOH) in 25 primary seminomas, we confirmed several previ

139 ations, deletions or loss of heterozygosity (LOH) in beta-2-microglobulin (B2M), an essential compone

140 such as copy-neutral loss of heterozygosity (LOH) in cancer-are missed.

141 d a method to induce loss of heterozygosity (LOH) in developing lymphocytes through chromosome deleti

142 e showed no signs of loss of heterozygosity (LOH) in the Men1 locus, whereas tumors in Men1(+/-) mice

143 ; and BRCA wild-type/loss of heterozygosity (LOH) low patient subgroup (107 rucaparib v 54 placebo; 2

144 ression and/or 11p15 loss of heterozygosity (LOH) may have increased risk of relapse.

145 A) mutations genomic loss of heterozygosity (LOH) might also represent homologous recombination defic

146 ost cases (91%) show loss of heterozygosity (LOH) of chromosome 11p, with uniform selection against t

147 owed by deletions or loss of heterozygosity (LOH) of chromosomes carrying TP53, BRCA1 or BRCA2.

148 events often lead to loss of heterozygosity (LOH) of SNPs that are centromere distal to the crossover

149 Loss of heterozygosity (LOH) of the hDMP1 locus was found in 42% of human breast

150 es and 16 genes with loss of heterozygosity (LOH) on chromosome 3 in the disomy 3 metastasizing UMs t

151 mice showed frequent loss of heterozygosity (LOH) on chromosome 6.

152 mosome arm 1p or 11q loss of heterozygosity (LOH) status, and symptoms.

153 mber alterations and loss of heterozygosity (LOH) to define the spectrum of minimally deleted regions

154 ets and analyzed for loss of heterozygosity (LOH) using a panel of 16 LOH mutational markers associat

155 ce of locus-specific loss of heterozygosity (LOH)) is observed in 7% of BRCA1 ovarian, 16% of BRCA2 o

156 copy number status, loss of heterozygosity (LOH), and event break points, which is essential for dev

157 eric hypervariation, loss of heterozygosity (LOH), and whole or partial chromosome aneuploidies.

158 genotype of somatic loss of heterozygosity (LOH), by conditionally inactivating Ext1 via head-to-hea

159 ariations (CNVs) and loss of heterozygosity (LOH), comparing 138 cfDNA samples with matched primary t

160 ements and extensive loss of heterozygosity (LOH), hallmarks of cancer cells.

161 ell with concomitant loss of heterozygosity (LOH), supporting a tumor suppressor function for BHD in

162 ur shared regions of loss of heterozygosity (LOH).

163 nation (HR) leads to loss of heterozygosity (LOH).

164 ation often leads to loss of heterozygosity (LOH).

165 terations leading to loss of heterozygosity (LOH).

166 e of 65% (80 of 124) loss of heterozygosity (LOH).

167 t have undergone p53 loss of heterozygosity (LOH).

168 ntal copy number and loss of heterozygosity (LOH).

169 nd point mutation or loss of heterozygosity (LOH).

170 phenomenon known as loss of heterozygosity (LOH).

171 gains, copy-neutral loss-of-heterozygosity (LOH) and tetraploidy.

172 ency and location of loss-of-heterozygosity (LOH) events on chromosome III in Saccharomyces cerevisia

173 ers are initiated by loss-of-heterozygosity (LOH) events that lead to the replacement of single, func

174 umber variations and loss-of-heterozygosity (LOH) events.

175 entifying regions of loss-of-heterozygosity (LOH) in a tumor sample is a challenging problem.

176 ursts of genome-wide loss-of-heterozygosity (LOH) in Saccharomyces cerevisiae, providing support for

177 diverse spectrum of loss-of-heterozygosity (LOH) signatures characterized by interstitial and termin

178 large copy-number or loss-of-heterozygosity (LOH) variants involving multiple Shh genes, as well as o

179 signal measures the loss-of-heterozygosity (LOH) which is valuable for CNV identification.

180 etions, copy-neutral loss-of-heterozygosity (LOH), allele-specific gains/amplifications.

181 lele are followed by loss-of-heterozygosity (LOH), so tumors express only mutant p53.

182 e genomic regions of loss-of-heterozygosity (LOH), suggesting that mitotic recombination has a signif

183 ells can lead to the loss-of-heterozygosity (LOH), which is potentially carcinogenic.

184 ies and copy-neutral loss-of-heterozygosity (LOH).

185 ), molecular (1p/19q loss of heterozygosity [LOH], IDH1 mutation, and MGMT methylation), and histolog

186 ne or somatic), BRCA wild-type and LOH high (LOH high group), or BRCA wild-type and LOH low (LOH low

187 Characterizing HLA LOH with LOHHLA refines neoantigen prediction and may ha

188 The focal nature of HLA LOH alterations, their subclonal frequencies, enrichment

189 urrence as parallel events suggests that HLA LOH is an immune escape mechanism that is subject to str

190 Using LOHHLA, we find that HLA LOH occurs in 40% of non-small-cell lung cancers (NSCLCs

191 t how TP53 point mutations are acquired, how LOH occurs, or the cells involved.

192 a BRCA1/2 mutation, but with an elevated HRD-LOH score, who achieved a favorable pathologic response.

193 was assessed by loss of heterozygosity (HRD-LOH) in pretreatment core breast biopsies.

194 Mean HRD-LOH scores were higher in responders compared with nonre

195 The HRD-LOH assay was able to identify patients with sporadic tr

196 eficiency-large-scale state transitions [HRD-LOH/HRD-LST] scores were 12.68 and 5.11, respectively),

197 ons, and two of them had increased tumor HRD-LOH/HRD-LST scores.

198 In this study, we were able to identify LOH events although they occur only rarely in wild-type

199 across the genome (median 913 vs. 460 Mb in LOH, P < 0.05), with significant recurrent LOH on chromo

200 th UV and gamma-radiation efficiently induce LOH at doses of radiation that cause no significant loss

201 We used the recombination system to induce LOH at the E2A locus in developing B cells.

202 n genome-wide analysis of DNA damage-induced LOH events performed in any eukaryote.

203 f-the-art computational approaches can infer LOH from single-nucleotide polymorphism (SNP) array data

204 Inferred LOH rates are quite concordant across platforms/laborato

205 Here, we propose a method that infers LOH rates across an entire sample set on an SNP-by-SNP b

206 results suggest that wildtype Ewsa inhibits LOH induction, possibly by maintaining chromosomal stabi

207 Here we interrogate LOH of polymorphisms in essential genes as a novel class

208 We found our model (which we term J-LOH) to be superior for localizing rare aberrations in a

209 high group), or BRCA wild-type and LOH low (LOH low group).

210 etic criteria for high sensitivity to a NAT2 LOH therapy and their eligibility can be assessed by cli

211 Acquired copy neutral LOH (CN-LOH) is a frequent occurrence in myeloid maligna

212 y number aberrations (aCNA) and copy neutral LOH (cnLOH) together with sequence analysis of recurrent

213 hidden Markov model to identify copy-neutral LOH (loss of heterozygosity) events as short as 11 Mb in

214 Chromosomes 11p and 17 undergo copy-neutral LOH early during tumorigenesis, suggesting tumour-driver

215 esting genomic regions, such as copy-neutral LOH.

216 g loss of DNA copies, so-called copy-neutral LOH.

217 In addition, copy number-neutral LOH, or uniparental disomy, was also prevalent on 1q (8%

218 As) in these samples, including copy-neutral LOHs, whole-genome duplications (WGDs) and mirrored-subc

219 lymph node status ( P < .01) and absence of LOH 1p or 16q ( P < .01), but not with gross residual di

220 of preneoplastic lesions and accumulation of LOH at various tumor suppressor genes, suggesting a poss

221 d mitotic recombination (MR) as the cause of LOH in 14 out of 72 (19%) total evaluable tumours.

222 ctives included prospective determination of LOH as a prognostic marker in OPLs.

223 The presence and clonal expansion of LOH mutations was formulated into mutational load (ML) f

224 lead to vastly overestimated frequencies of LOH without accompanying loss of DNA copies, so-called c

225 The low frequency of LOH during interhomolog recombination suggests that cros

226 The frequency of LOH events is higher in the chromosomes with shorter int

227 omosomal arms, with the highest frequency of LOH on 9p (33% of informative single nucleotide polymorp

228 These results support incorporation of LOH testing as a prognostic tool in routine clinical pra

229 ame sample, which was found independently of LOH for hDMP1.

230 This study shows that MR is a mechanism of LOH in NF2 and SMARCB1-negative schwannomatosis-related

231 One mechanism of LOH is mitotic crossover recombination between homologou

232 ssment of mutational load using our panel of LOH mutational markers may be a useful adjunct to micros

233 R-based assay, we determined the position of LOH in multiple independent recombination events to a re

234 ozygous mutations, the strong stimulation of LOHs in the rad27/FEN1 and tsa1/PRDX1 backgrounds leads

235 ups: BRCA mutant (n=40), LOH high (n=82), or LOH low (n=70).

236 ereas loss of chromosome 19p region by HD or LOH at the LKB1 region occured in 90% of NSCLC.

237 nactivation of the LKB1 gene by either HD or LOH with somatic mutation in 39% of tested samples, wher

238 No preneoplastic lesion or LOH was found in normal gallbladders.

239 hem by somatic status (germline, somatic, or LOH); while a comparison of normalized read depth deline

240 eatic organoids lacking p53 mutation and p53 LOH are insensitive to SOAT1 loss, indicating a potentia

241 In contrast, RNase H1 acts to prevent LOH within a small region of chromosome III where the in

242 itional clones selected for carrying primary LOH tracts revealed that they too contained unselected s

243 exome data to also be used for quantitative LOH/CNV analysis for tracking tumour progression and evo

244 Recurrent LOH regions often harbor genes important for tumor suppr

245 n LOH, P < 0.05), with significant recurrent LOH on chromosomes 1p, 9, 10, 14, 17p, 18, and 22.

246 N = 379); they were classified as high-risk (LOH-positive) or low-risk (LOH-negative) patients based

247 ied as high-risk (LOH-positive) or low-risk (LOH-negative) patients based on their LOH profiles and o

248 In the majority of AT/RT, LOH occurs at the genetic locus SNF5 (Ini1/BAF47/Smarcb1

249 We examined both selected LOH events on chromosome V and unselected events through

250 g LOH by microsatellite analysis also showed LOH by methylation analysis.

251 ere found to be deleted, and 16 genes showed LOH exclusively in disomy 3 metastasizing UM, suggesting

252 Familial intestinal GC (FIGC) tumors showed LOH in 9.4% and hypermethylation in 17.0%.

253 asizing UMs that were not deleted or showing LOH in the nonmetastatic tumors.

254 All evaluable tumors showing LOH by microsatellite analysis also showed LOH by methyl

255 r than expected if the two underlying single LOH events occurred independently of each other.

256 ling failures with the necessity for somatic LOH in a developmentally regulated cell type.

257 er than scores in tumors with locus-specific LOH (ovarian, P = 0.0004; breast P < 0.0001, two-tailed

258 Absence of locus-specific LOH is associated with decreased overall survival in ova

259 Locus-specific LOH may be a clinically useful biomarker to predict prim

260 ic combination of single-base substitutions, LOH, or large-scale genome instability signatures charac

261 We apply a statistical test for such LOH-influenced disruptions, and derive a maximum-likelih

262 We conclude that LOH of essential genes represents a rich class of non-dr

263 sing three different metrics, we report that LOH selectively occurs in early replicating regions; thi

264 Our results suggest that LOH can be a successful strategy for adaptation of hybri

265 The LOH events are significantly clustered near RNA polII-bo

266 erive a maximum-likelihood estimator for the LOH rate based on the observed number of heterozygotes.

267 s of Cre-mediated chromosome deletion in the LOH assay for HEB function in T cell development.

268 mutant subgroup, 5.7 months (5.3-7.6) in the LOH high subgroup, and 5.2 months (3.6-5.5) in the LOH l

269 the BRCA mutant subgroup, 56 patients in the LOH high subgroup, and 59 patients in the LOH low subgro

270 he LOH high subgroup, and 59 patients in the LOH low subgroup had disease progression or died.

271 gh subgroup, and 5.2 months (3.6-5.5) in the LOH low subgroup.

272 ocalize tumor-suppressor gene targets of the LOH events.

273 2-0.90, p=0.011) subgroups compared with the LOH low subgroup.

274 -risk (LOH-negative) patients based on their LOH profiles and oral cancer history.

275 These LOH were also tested in 30 GBC specimens.

276 Fine mapping of these LOH regions revealed three non-overlapping regions, one

277 gous for the Trp53 and Nf1 genes and through LOH develops lymphomas, sarcomas, or carcinomas with 100

278 homologous chromosomes as template leads to LOH.

279 A, along with allelic imbalances pointing to LOH, in ~ 24% of tumors.

280 In this trial, LOH was validated as a marker of oral cancer risk and fo

281 Tumor LOH at 1p and 16q was determined by microsatellite analy

282 ur results suggest that assessment of tumour LOH can be used to identify patients with BRCA wild-type

283 longer than in patients with BRCA wild-type LOH low carcinomas.

284 longer than in patients with BRCA wild-type LOH low carcinomas.

285 utant cohort, HRD cohort, and BRCA wild-type/LOH low patient subgroup, respectively.

286 ariants in 1278 essential genes that undergo LOH in cancer and evaluated the potential for each to be

287 enrolled in the protocol, and each underwent LOH profiling (N = 379); they were classified as high-ri

288 r a single region of one chromosome at which LOH events can be selected.

289 s, revealed a large number of loci for which LOH is beneficial.

290 The underlying mechanisms, of why LOH rates increase with age, are not well understood.

291 ghput DNA sequencing) to examine genome-wide LOH in a diploid yeast strain at a resolution averaging

292 th the highest ploidy had little genome-wide LOH, yet one of these had a homozygous somatic frame-shi

293 end into diploidy accompanied by genome-wide LOH.

294 tal of 395 participants were classified with LOH profiles, and 254 were classified LOH positive.

295 icantly lower for LOH-positive compared with LOH-negative groups (74% vs 87%, HR, 2.19; 95% CI, 1.25-

296 reased EGFR gene copy number correlated with LOH-positive status (P < .001) and lower CFS (P = .01).

297 ations were rarely observed in patients with LOH in 6q16.

298 ever, improve CFS in high-risk patients with LOH-positive or high-EGFR-gene-copy-number OPLs.

299 brid yeast recapitulates these results, with LOH occurring in just a few hundred generations of propa

300 A total of 62 of 124 samples with LOH at one or both markers immediately flanking the LKB1