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 identified in 10 of 20 (50%) metastatic melanoma

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

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

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

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

10 11p15 LOH was identified in 19 (41%) of 46 evaluable VLRWTs an

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

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

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

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

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

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

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

18 18q LOH has been reported to predict shorter survival in pat

19 nts with non-MSI-high colorectal cancer, 18q LOH or allelic imbalance was not associated with patient

20 did not show prognostic significance of 18q LOH.

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

22 However, it is unclear whether 18q LOH in colorectal cancer has any prognostic implication

23 positive tumors and 68% among those with 18q LOH-negative tumors (log-rank P = .54).

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

25 all survival was 70% among patients with 18q LOH-positive tumors and 68% among those with 18q LOH-neg

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 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

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

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

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

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

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

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

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

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

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

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

58 completely eliminated any selection for Arf LOH.

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

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

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

62 ASP5 and RBBP8 to identify gene deletions by LOH.

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

64 In paired sample cases, LOH detection for informative single nucleotide polymorp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 To examine LOH associated with DSB-induced interhomolog recombinati

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

97 entified five additional patients exhibiting LOH.

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

99 We find extensive LOH to arise from a new break-induced mechanism of isoch

100 double-strand break (DSB)-induced extensive LOH, and its suppression, using a non-essential minichro

101 ever, the mechanisms by which such extensive LOH arises, and how it is suppressed in normal cells is

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

103 romosome loss, thereby suppressing extensive LOH.

104 These events lead to extensive LOH because one arm of chromosome III is deleted.

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 n chromosomal aberrations (copy number gain, LOH, and somatic UPDs) during carcinogenesis may be depe

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

114 2, we assessed the ability of tumour genomic LOH, quantified with a next-generation sequencing assay,

115 75H mutation in TP53, whereas TOSE cells had LOH at the TP53 locus with a new R273H mutation at the p

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

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

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

119 nts characterized by loss of heterozygosity (LOH) and a normal copy number (two) but which are not au

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

121 bution of long-range loss of heterozygosity (LOH) and chromosome rearrangement events across the geno

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

123 ated with an 11p15.5 loss of heterozygosity (LOH) and may be confused with nonmyogenic, non-RMS soft

124 ported that frequent loss of heterozygosity (LOH) as well as allelic imbalances in chromosomes in eso

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

126 Loss of heterozygosity (LOH) at chromosome 18q frequently occurs late during col

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

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

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

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

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

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

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

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

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

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

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

138 conversion limiting loss of heterozygosity (LOH) for markers downstream of the site of repair and re

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

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

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

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

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

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

145 Loss of heterozygosity (LOH) is one of the most important mechanisms in the tumo

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

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

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

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

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

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

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

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

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

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

156 advanced melanomas, loss of heterozygosity (LOH) was assessed using microsatellite markers encompass

157 wild-type allele has loss of heterozygosity (LOH) within the cancer.

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

159 Loss of heterozygosity (LOH), a causal event in cancer and human genetic disease

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

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

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

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

164 (ESCC), we examined loss of heterozygosity (LOH), copy number (CN) loss, CN gain, and gene expressio

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

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

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

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

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

170 terations leading to loss of heterozygosity (LOH).

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

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

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

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

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

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

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

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

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

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 o platinum-based chemotherapy, we identified LOH of a 13q region to predict prolonged progression-fre

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

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

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

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

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

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

205 Inferred LOH rates are quite concordant across platforms/laborato

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

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

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

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

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

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

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

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

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

217 In contrast, nonreciprocal LOH events with increased chromosome loss largely result

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

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

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

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

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

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

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

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

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

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

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

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

230 One mechanism of LOH is mitotic crossover recombination between homologou

231 In general, there were a larger number of LOH events identified in the cell lines compared with th

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

233 hat gene expression profiles and patterns of LOH of ARMS cases lacking P-F translocations are indisti

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

235 of stroma contributes to under-reporting of LOH and copy number loss.

236 or contributing factor in underestimation of LOH and copy number loss events.

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

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

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

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

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

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

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

244 wth environments, while rates of short-range LOH were comparable for in vivo and in vitro populations

245 Recurrent LOH regions often harbor genes important for tumor suppr

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

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

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

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

250 ygous at these 16 loci, we found a mean (SD) LOH frequency of 58% (4.2%) compared with 50% (7.5%) at

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

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

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

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

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

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

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

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

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

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

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

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

263 is, and showed that MCP performs better than LOH analysis for allelic-imbalanced chromosome regions a

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

265 Our analysis shows that LOH was identified significantly more often in derived c

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

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

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

269 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

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

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

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

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

274 2-0.90, p=0.011) subgroups compared with the LOH low subgroup.

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

276 These LOH were also tested in 30 GBC specimens.

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

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

279 break-induced replication [BIR]), leading to LOH for all markers downstream of the site of strand inv

280 homologous chromosomes as template leads to LOH.

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

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

283 MCP extends tumor LOH analysis to allelic imbalance analysis and supplies

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

285 Twenty-two LOH regions were identified: four on 9p, seven on 9q, fo

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

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

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

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

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 array datasets to compare MCP analysis with LOH and copy number analysis, and showed that MCP perfor

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

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

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

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

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

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