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1 thout evidence of other somatic mutations or loss of heterozygosity.
2  8p23.1, where human cancers frequently show loss of heterozygosity.
3                    We also assessed APC gene loss of heterozygosity.
4 rossover-promoting repair pathways, prevents loss of heterozygosity.
5 enes by determining homozygous deletions and loss of heterozygosity.
6 ied mutations with limited branching through loss of heterozygosity.
7 plasmic bacteria and results in an immediate loss of heterozygosity.
8 hromosomal defects and acquired copy-neutral loss of heterozygosity.
9 d as excessive sister chromatid exchange and loss of heterozygosity.
10 lances in chromosome number (aneuploidy) and loss of heterozygosity.
11 l lesion, indicating uniparental disomy with loss of heterozygosity.
12 s borderline tumor shared similar regions of loss of heterozygosity.
13 letion of wild-type alleles of both genes by loss of heterozygosity.
14 d with homozygous mutations in the region of loss of heterozygosity.
15 es demonstrated a high level of copy-neutral loss of heterozygosity.
16 at the mating locus through whole-chromosome loss of heterozygosity.
17 , arm-level copy number alterations, and HLA loss of heterozygosity.
18 A mutation or high percentage of genome-wide loss of heterozygosity.
19 potential for chromosomal rearrangements and loss of heterozygosity.
20 ion can expose deleterious mutations through loss of heterozygosity.
21  and with 1p and 16q copy number loss and/or loss of heterozygosity.
22 ed tumor and cell-free DNA samples revealing loss of heterozygosity.
23 tus was associated relapse (20% relapse with loss of heterozygosity, 25% with loss of imprinting, and
24 genotyping enables diagnosis of copy-neutral loss of heterozygosity, a lesion that cannot be detected
25 dromic and common form of fibroids; however, loss of heterozygosity across FH appeared as a significa
26                                              Loss of heterozygosity affecting chromosome 7q is common
27 ter excluding cases with clonal copy-neutral loss-of-heterozygosity affecting class I HLA genes (8.6%
28 ng for mutation hot spots and microsatellite loss of heterozygosity analysis.
29        We show that age-induced increases in loss of heterozygosity and chromosome loss events are co
30                                              Loss of heterozygosity and decreased copy number delimit
31 tal cancers and cell lines, we find frequent loss of heterozygosity and mutations in BCL9L in aneuplo
32 of genetic stability in all species, with no loss of heterozygosity and no shifts in allele frequenci
33 reconstruction of MF phylogeny demonstrating loss of heterozygosity and parallel evolution as recurre
34 in both families exhibited 9p deletion, with loss of heterozygosity and retention of the mutant PAX5
35 evel of global gene copy number alterations, loss of heterozygosity and single nucleotide variation (
36 segregation while limiting the potential for loss of heterozygosity and sister-chromatid exchanges.
37 was activation of the hedgehog pathway, with loss of heterozygosity and somatic mutation of the gene
38                 Finally, we demonstrate that loss of heterozygosity and temporal dissection of mutati
39 we show how TGCTs gain additional reciprocal loss of heterozygosity and that this is associated with
40 hances de novo tumor formation and precludes loss of heterozygosity and the PTEN locus.
41 o, and further characterize the link between loss of heterozygosity and the typical CALMs that appear
42 TEN) or have reduced PTEN expression through loss of heterozygosity and/or epigenetic silencing mecha
43         In this study, the loss of TIMP-3 by loss of heterozygosity and/or promoter hypermethylation
44 ele was homozygous after copy number-neutral loss-of-heterozygosity and amplified through a chromosom
45 velop lymphomas at higher incidence with p53 loss-of-heterozygosity and severe genome aneuploidy, sug
46 cies (BRCA mutant or BRCA wild-type and high loss of heterozygosity), and the intention-to-treat popu
47 e basis of evidence of activating mutations, loss of heterozygosity, and a mass forming proliferation
48 dy might be protective against TALEN-induced loss of heterozygosity, and indeed Apc gene editing was
49 ifferent in each tumor (frameshift mutation, loss of heterozygosity, and methylation).
50  level, including promoter hypermethylation, loss of heterozygosity, and proteosomal degradation by n
51            p.Gly374Glu-DLST tumors exhibited loss of heterozygosity, and their methylation and expres
52 tates; (ii) it can identify the copy-neutral loss of heterozygosity; and (iii) it is efficient in ter
53 ypermethylation of genes that also displayed loss of heterozygosity, as well as of genes that show co
54 t frequent somatic chromosome alteration was loss of heterozygosity at 16p (in 8 of 33 patients for w
55 The most frequent recurrent aberrations were loss of heterozygosity at 3p and 9p, observed in 39 (65%
56  be associated with favorable prognosis, and loss of heterozygosity at chromosome 6q (LOH6q) was repo
57 y, and volume; response to chemotherapy; and loss of heterozygosity at chromosomes 1p and 16q.
58         Molecular tumor profiling revealed a loss of heterozygosity at GPR161 in all affected MB(SHH)
59 supertype (including HLA-B*15:01) or somatic loss of heterozygosity at HLA-I was associated with poor
60 ll set of chromosomes from each parent, with loss of heterozygosity at some loci, and uniparental ret
61                                    Of these, loss of heterozygosity at specific chromosomal sites sta
62                                 Furthermore, loss of heterozygosity at the Chr.16q24.3 locus in breas
63  to germline genotype misclassification from loss of heterozygosity at the CYP2D6 locus.
64 py number loss of chromosome 22q, leading to loss of heterozygosity at the DGCR8 locus, was found in
65 ute lymphoblastic lymphoma, we reported that loss of heterozygosity at the Fbxw7 locus occurs frequen
66                                  We found no loss of heterozygosity at the genomic level for the PTEN
67 ound of germline haploinsufficiency to cause loss of heterozygosity at the GNAS locus and lead to the
68 oteins were tested for the ability to induce loss of heterozygosity at the golden locus in zebrafish
69                                     However, loss of heterozygosity at the human leukocyte antigen (H
70 ting mutations of PIK3CA (13.6%, n = 22) and loss of heterozygosity at the PTEN locus (25%, n = 8).
71                                 Preferential loss of heterozygosity at the rs1042522 locus of the tum
72 ry breast tumors revealed that 23% displayed loss of heterozygosity at the SPEN locus and that 3% to
73 well as adenocarcinoma of the colon, without loss of heterozygosity at the Tgfbr1 locus.
74 fected tissue for genotyping; in such cases, loss of heterozygosity at the TP53 locus could lead to d
75 ional selective advantage resulting from the loss of heterozygosity at the TP53 locus.
76              Using microsatellite PCR to map loss-of-heterozygosity breakpoints within individual col
77 e lost their WT copy of the Apc gene through loss of heterozygosity by homologous somatic recombinati
78 ntributes to genomic instability, leading to loss of heterozygosity, chromosome rearrangements and ce
79 ng recurrent microdeletions and copy-neutral loss of heterozygosity (CN-LOH) in patients with diverse
80 urdens had evidence of acquired copy-neutral loss of heterozygosity (CN-LOH) of chromosome 1p in gran
81              In addition, three copy-neutral loss of heterozygosity (CN-LOH) regions greater than 1 M
82 cs, and their associated copy number neutral loss of heterozygosity (CN-LOH) were identified by STR a
83 ns (deletions, duplications and copy-neutral loss of heterozygosity (CN-LOH)) on all chromosomes(1,2,
84 usly hidden chromosomal defect, copy neutral loss of heterozygosity (CN-LOH).
85 ns (e.g., monosomy 7) or copy number neutral loss of heterozygosity (CN-LOH).
86 y-number aberrations (CNAs) and copy-neutral loss of heterozygosity (cnLOH) identified by chromosome
87 an stimulate IHR and associated copy-neutral loss of heterozygosity (cnLOH) in human cells.
88           Subchromosomal copy number neutral loss of heterozygosity (CNN-LOH) can also be detected us
89  including TNFRSF14, but copy-number neutral loss of heterozygosity (CNN-LOH) of this locus was more
90              Remarkably, copy number-neutral loss of heterozygosity (CNN-LOH) on either 7q or 9p incl
91 t of p53 mutations, or p53 mutations and 17p-loss of heterozygosity combined on survival in AML.
92 d its functionality for testing tumors using loss of heterozygosity data or copy number arrays.
93 ing a missense mutation in one allele and a 'loss of heterozygosity' deletion encompassing the other.
94 nly observed in tumor phylogenies due to the loss of heterozygosity, deletions, and convergent evolut
95               In contrast, TP53 deletion and loss of heterozygosity did not confer worse survival.
96             Msh3/p53 tumors showed increased loss of heterozygosity, elevated genome-wide copy-number
97 ovide additional results for copy number and loss-of-heterozygosity estimation and assessing tumour p
98 ulent to Sr50 contained a 2.5 mega-base pair loss-of-heterozygosity event.
99 wed mutually exclusive endoreduplication and loss of heterozygosity events in clones present at diffe
100       Cancer chemotherapy targeting frequent loss of heterozygosity events is an attractive concept,
101 ral abnormalities, defined as copy number or loss of heterozygosity events that are large and present
102 cinoma tumor sample; two of which are likely loss-of-heterozygosity events.
103 n Markov model to identify copy-neutral LOH (loss of heterozygosity) events as short as 11 Mb in mixt
104 ent with these observations, cells with TSC2 loss of heterozygosity expressed the OPG receptors, rece
105 e derived from a single parent, resulting in loss of heterozygosity for all single-nucleotide polymor
106 duals in family UW-AP exhibited copy-neutral loss of heterozygosity for large portions of the long ar
107                                    Moreover, loss of heterozygosity for the ATR locus was noted in or
108 alysis revealed no change in copy number but loss of heterozygosity for the entire length of chromoso
109  tumors collected from BALB/c-Trp53+/- mice, loss of heterozygosity for Trp53 was detected in more th
110                                              Loss of heterozygosity for TSC1 or TSC2 was found in 22%
111 ced migration of LAM cells identified by the loss of heterozygosity for TSC2.
112  was due to promoter hypermethylation and/or loss of heterozygosity, found in the majority of thyroid
113 anisms, has the potential to cause extensive loss of heterozygosity, genetic disease, or cell death.
114               This study therefore shows how loss of heterozygosity, hallmarked by VHL deletion in cc
115 ded as a nonneoplastic proliferation, albeit loss of heterozygosity has long been reported in a part
116                       WT1 mutation and 11p15 loss of heterozygosity have been associated with relapse
117 rs (mean homologous recombination deficiency-loss of heterozygosity/homologous recombination deficien
118 ous recombination deficiency was assessed by loss of heterozygosity (HRD-LOH) in pretreatment core br
119 tation of the remaining wild-type allele (or loss of heterozygosity), illustrating the strict correla
120 ressor gene that has been shown to undergo a loss of heterozygosity in 40-75% of human breast, ovaria
121 of Leu misincorporation resulted in complete loss of heterozygosity in a large region of chromosome V
122 hromosomal region frequently associated with loss of heterozygosity in a number of malignancies inclu
123 zed to chromosome 18q21, a frequent site for loss of heterozygosity in advanced stage colon cancers.
124 with NLS-RecA-Gal4 protein are able to cause loss of heterozygosity in approximately 3% of the inject
125 n reported to be associated with significant loss of heterozygosity in breast cancer.
126 coded in 16q24.3, a region in which there is loss of heterozygosity in breast, ovarian, hepatocellula
127  on 13q, and this region frequently displays loss of heterozygosity in human cancers.
128                             Here, we present loss of heterozygosity in human leukocyte antigen (LOHHL
129 exhibited ongoing immunoediting, with either loss of heterozygosity in human leukocyte antigens or de
130 es from two patients but identified possible loss of heterozygosity in iPS cell lines from one patien
131                         We observe an excess loss of heterozygosity in lung tumors among ATM L2307F a
132                      We found mutations with loss of heterozygosity in LZTR1, encoding an adaptor of
133  this behavior is recapitulated by recurrent loss of heterozygosity in multiple metabolic genes adjac
134 es and may explain the high incidence of p53 loss of heterozygosity in mutant tumors.
135 mors were screened for somatic mutations and loss of heterozygosity in mutL homolog 1 (MLH1) and mutS
136  the left kidney, one from the right) showed loss of heterozygosity in one tumor, and four different
137                            Deepening somatic loss of heterozygosity in serial tumor samples is observ
138 a higher degree of gene copy number loss and loss of heterozygosity in SNP array analyses.
139 ur results indicate that de novo mutation or loss of heterozygosity in stromal APC is sufficient to i
140 on carriers with dominant inheritance due to loss of heterozygosity in susceptible cells.
141 ans simultaneously deletes one copy of BAP1, loss of heterozygosity in the corresponding Vhl region i
142 , pancreatic, and parathyroid tumors showing loss of heterozygosity in the putative tumor suppressor
143 indicate that tumorigenesis necessitates NF1 loss of heterozygosity in the Schwann cell.
144                   Despite this requisite NF1 loss of heterozygosity in the tumor cell of origin, nont
145        In particular, somatic mutations with loss of heterozygosity in TP53 were strongly associated
146 ressor encoded in 16q24.3 for which there is loss of heterozygosity in various solid tumors, is respo
147 r somatic, inherited, or de novo--as well as loss-of-heterozygosity in cancer cells.
148 s identified somatic mutations combined with loss-of-heterozygosity in the splicing factor SUGP1 in f
149 ts with a germ line FAS mutation and somatic loss of heterozygosity, in whom biallelic mutant cells c
150 chment for WGD in tumor types with extensive loss of heterozygosity, including lung squamous cell car
151 umor suppressor, and its inactivation due to loss of heterozygosity is associated with cancers of dif
152 deficiency, providing an explanation for why loss of heterozygosity is not required for the developme
153  CpG island methylator phenotype (CIMP); 18q loss of heterozygosity; KRAS, BRAF, and PIK3CA mutations
154     Thus, the oncological concept of somatic loss of heterozygosity leading to selected cell expansio
155 0.26, P = 0.002), and increased frequency of loss of heterozygosity (LOH) across the genome (median 9
156                      For two of these genes, loss of heterozygosity (LOH) analysis of tSNPs in 314 ov
157 ssection followed by KRAS pyrosequencing and loss of heterozygosity (LOH) analysis on chromosomes 6q
158 se are chromosomal segments characterized by loss of heterozygosity (LOH) and a normal copy number (t
159 BIR results in greatly increased spontaneous loss of heterozygosity (LOH) and chromosome mis-segregat
160 nterestingly, the distribution of long-range loss of heterozygosity (LOH) and chromosome rearrangemen
161 ons (indels), copy-number variations (CNVs), loss of heterozygosity (LOH) and complex rearrangements,
162 current areas of somatic copy number-neutral loss of heterozygosity (LOH) and deletions of chromosome
163           ERMS is associated with an 11p15.5 loss of heterozygosity (LOH) and may be confused with no
164 resulting in copy number variation (CNV) and loss of heterozygosity (LOH) are frequently observed dur
165   Recent studies have reported that frequent loss of heterozygosity (LOH) as well as allelic imbalanc
166  the wild-type allele in their tumors due to loss of heterozygosity (LOH) at 8p22.
167  chromosome (chr) 8p with a common region of loss of heterozygosity (LOH) at chr8p22 locus.
168                                              Loss of heterozygosity (LOH) at chromosome 18q frequentl
169 atients with stage III FHWT without combined loss of heterozygosity (LOH) at chromosomes 1p and 16q t
170 ies to detect deletions, amplifications, and loss of heterozygosity (LOH) at high resolution.
171 ostic challenge by comparing the presence of loss of heterozygosity (LOH) at selected genetic locatio
172 dly accelerate retinoblastoma, with frequent loss of heterozygosity (LOH) at the Arf locus.
173 umor phenotype is attenuated and altered and loss of heterozygosity (LOH) at the Trp53 wild-type locu
174                            TOSE cells showed loss of heterozygosity (LOH) at TP53, increased nuclear
175 mmary epithelial cell model and show that 8p loss of heterozygosity (LOH) attenuates the action of se
176 H1 mutations, promoter hypermethylation, and loss of heterozygosity (LOH) by polymerase chain reactio
177 cordance between tumor and cell line for raw loss of heterozygosity (LOH) calls was 96% (range, 91-99
178 eds to thousands of non-driver genes undergo loss of heterozygosity (LOH) events per tumor, generatin
179                                Nevertheless, loss of heterozygosity (LOH) for either Pdcd10 or Ccm2 r
180 formative sporadic cases of cHL, we detected loss of heterozygosity (LOH) for KLHDC8B in RS cells, bu
181 air events occur by gene conversion limiting loss of heterozygosity (LOH) for markers downstream of t
182 from ewsa(m/m);tp53(w/m) zebrafish displayed loss of heterozygosity (LOH) for the wildtype tp53 locus
183 ty to detect copy-number variation (CNV) and loss of heterozygosity (LOH) from exome sequencing data
184         By a genome-wide analysis of CNV and loss of heterozygosity (LOH) in 25 primary seminomas, we
185 s, we observed point mutations, deletions or loss of heterozygosity (LOH) in beta-2-microglobulin (B2
186 lele-specific mutations-such as copy-neutral loss of heterozygosity (LOH) in cancer-are missed.
187 hoid system, we developed a method to induce loss of heterozygosity (LOH) in developing lymphocytes t
188 Men1(+/-); Cdk4(-/-) mice showed no signs of loss of heterozygosity (LOH) in the Men1 locus, whereas
189                                              Loss of heterozygosity (LOH) is one of the most importan
190 I, 5.93 to 9.53 months]); and BRCA wild-type/loss of heterozygosity (LOH) low patient subgroup (107 r
191  VLRWTs with low WT1 expression and/or 11p15 loss of heterozygosity (LOH) may have increased risk of
192 ith BRCA1 and BRCA2 (BRCA) mutations genomic loss of heterozygosity (LOH) might also represent homolo
193                        Most cases (91%) show loss of heterozygosity (LOH) of chromosome 11p, with uni
194 he earliest events, followed by deletions or loss of heterozygosity (LOH) of chromosomes carrying TP5
195      Such recombination events often lead to loss of heterozygosity (LOH) of SNPs that are centromere
196                                              Loss of heterozygosity (LOH) of the hDMP1 locus was foun
197  revealed 95 deleted genes and 16 genes with loss of heterozygosity (LOH) on chromosome 3 in the diso
198  from p53+/- and p53-/- mice showed frequent loss of heterozygosity (LOH) on chromosome 6.
199  diploid DNA index, chromosome arm 1p or 11q loss of heterozygosity (LOH) status, and symptoms.
200  We examined DNA copy number alterations and loss of heterozygosity (LOH) to define the spectrum of m
201 from microdissected targets and analyzed for loss of heterozygosity (LOH) using a panel of 16 LOH mut
202 FABP7 expression loss in advanced melanomas, loss of heterozygosity (LOH) was assessed using microsat
203  cause cancers when the wild-type allele has loss of heterozygosity (LOH) within the cancer.
204 1 or BRCA2 allele (absence of locus-specific loss of heterozygosity (LOH)) is observed in 7% of BRCA1
205                                              Loss of heterozygosity (LOH), a causal event in cancer a
206  detailed information of copy number status, loss of heterozygosity (LOH), and event break points, wh
207 mal inversions, subtelomeric hypervariation, loss of heterozygosity (LOH), and whole or partial chrom
208 eled the chimeric tissue genotype of somatic loss of heterozygosity (LOH), by conditionally inactivat
209  determine copy number variations (CNVs) and loss of heterozygosity (LOH), comparing 138 cfDNA sample
210  squamous cell carcinoma (ESCC), we examined loss of heterozygosity (LOH), copy number (CN) loss, CN
211 use chromosomal rearrangements and extensive loss of heterozygosity (LOH), hallmarks of cancer cells.
212  oncocytoma, and clear cell with concomitant loss of heterozygosity (LOH), supporting a tumor suppres
213 his syndrome detected four shared regions of loss of heterozygosity (LOH).
214 ks by homologous recombination (HR) leads to loss of heterozygosity (LOH).
215 s by homologous recombination often leads to loss of heterozygosity (LOH).
216 llustrated by genetic alterations leading to loss of heterozygosity (LOH).
217  revealed an overall rate of 65% (80 of 124) loss of heterozygosity (LOH).
218 s are made of equal parental copy number and loss of heterozygosity (LOH).
219 ction with either a second point mutation or loss of heterozygosity (LOH).
220 53 mutant PDAC cells that have undergone p53 loss of heterozygosity (LOH).
221 f one parental genome, a phenomenon known as loss of heterozygosity (LOH).
222 nd imbalanced losses and gains, copy-neutral loss-of-heterozygosity (LOH) and tetraploidy.
223 es, we studied the frequency and location of loss-of-heterozygosity (LOH) events on chromosome III in
224                Many cancers are initiated by loss-of-heterozygosity (LOH) events that lead to the rep
225 morphisms (SNPs), copy-number variations and loss-of-heterozygosity (LOH) events.
226                       Identifying regions of loss-of-heterozygosity (LOH) in a tumor sample is a chal
227 ized the occurrence of bursts of genome-wide loss-of-heterozygosity (LOH) in Saccharomyces cerevisiae
228 neck lineages revealed a diverse spectrum of loss-of-heterozygosity (LOH) signatures characterized by
229  brain-tissue-specific, large copy-number or loss-of-heterozygosity (LOH) variants involving multiple
230        The allelic shift signal measures the loss-of-heterozygosity (LOH) which is valuable for CNV i
231 ozygous/heterozygous deletions, copy-neutral loss-of-heterozygosity (LOH), allele-specific gains/ampl
232 mutations in one TP53 allele are followed by loss-of-heterozygosity (LOH), so tumors express only mut
233 any strains exhibit large genomic regions of loss-of-heterozygosity (LOH), suggesting that mitotic re
234 Completion of HR in G1 cells can lead to the loss-of-heterozygosity (LOH), which is potentially carci
235  different number of copies and copy-neutral loss-of-heterozygosity (LOH).
236 atus, and tumor location), molecular (1p/19q loss of heterozygosity [LOH], IDH1 mutation, and MGMT me
237 ice, intestinal adenomas showed copy-neutral loss of heterozygosity, making them homozygous for the m
238 both corrected for CN in aneuploid regions), loss of heterozygosity, megabase-scale phased haplotypes
239 l gains and losses, and several copy neutral loss-of-heterozygosity mutations at a genome-wide level,
240 et of OSCC patient samples in the absence of loss of heterozygosity, mutations, and promoter methylat
241 s of which, due to chromosomal deletions and loss of heterozygosity, necessitate the development of i
242 ed that a high percentage of genomic loss or loss of heterozygosity occurs at this locus in breast ca
243                 Significant, tumour-specific loss of heterozygosity occurs in nine genes (ATM, BAP1,
244                                WTs that show loss of heterozygosity of 11p15 or loss of imprinting of
245 d high-density SNP-A karyotyping to identify loss of heterozygosity of 11q in 442 patients with MDS,
246 17q11, 14q32 amplification, and copy-neutral loss of heterozygosity of 9p were gained in the B-LBL ce
247 sitional cell carcinomas of the bladder show loss of heterozygosity of a region spanning the TSC1 loc
248 e broadly applied to induce sporadic in vivo loss of heterozygosity of any conditional alleles in pro
249                                              Loss of heterozygosity of Apc and expression of cytokine
250        Apcmin/+/Sigirr-/- mice had increased loss of heterozygosity of Apc and microadenoma formation
251 MB(SHH) tumors revealed somatic copy-neutral loss of heterozygosity of chromosome 1q as the hallmark
252 or Study 5 (NWTS-5), tumor-specific combined loss of heterozygosity of chromosomes 1p and 16q (LOH1p/
253                                   Subsequent loss of heterozygosity of Dpc4 restores metastatic compe
254 tem, we examined our hypothesis by mimicking loss of heterozygosity of GNAS expression using dominant
255 bromas are a hallmark of NF1 and result from loss of heterozygosity of NF1 in Schwann cells, leading
256                                     However, loss of heterozygosity of Plk4 in mouse embryonic fibrob
257                      The tumors did not show loss of heterozygosity of Ptc1, despite high levels of G
258                     Among those with SHH-MB, loss of heterozygosity of PTCH1 was associated with prol
259 egard to whether osteochondroma results from loss of heterozygosity of the Ext genes.
260  antigen presentation caused by mutations or loss of heterozygosity of the major histocompatibility c
261                                              Loss of heterozygosity of the TRIM3 locus in approximate
262 urthermore, all tumors displayed concomitant loss of heterozygosity of Trp53 and Pten along with freq
263 cancer cells, which were identified by their loss of heterozygosity of Trp53 gene.
264                      These data suggest that loss of heterozygosity of TSC1 or TSC2 may play an impor
265 nduced selective migration of cells, showing loss of heterozygosity of TSC2 from a heterogeneous popu
266 tivation of KRAS and PIK3CA and mutation and loss of heterozygosity of tumor suppressor genes, such a
267  that further affect oncogenic signaling and loss of heterozygosity of tumor-suppressor genes.
268 rmalities, either aneuploidy or copy-neutral loss of heterozygosity, of >2 Mb in size in autosomes of
269 ertant clones of normal skin that arise from loss of heterozygosity on chromosome 17q via mitotic rec
270                      Oligodendrogliomas with loss of heterozygosity on chromosomes 1p and 19q have a
271 reated oligodendroglioma, WHO grade II, with loss of heterozygosity on chromosomes 1p and 19q, which
272 ster templates has the potential to generate loss of heterozygosity or genome rearrangements.
273  including inactivating mutations in WT1 and loss of heterozygosity or loss of imprinting at 11p15, w
274 els (corrected for aneuploidy), regions with loss of heterozygosity, phased haplotypes extending to e
275 justed for performance status score, age, 1p loss of heterozygosity, presence of oligodendroglial ele
276 l carcinoma (OSCC) samples in the absence of loss-of-heterozygosity, promoter methylation, and mutati
277 ariations, mapped copy-number variations and loss of heterozygosity regions, and phased variants acro
278     Using SNP-A, we identified chromosome 7q loss of heterozygosity segments in 161 of 1458 patients
279 constrained by the inbreeding-like effect of loss of heterozygosity that accrues as gene conversion a
280 omatic mutation in a MMR gene, with possible loss of heterozygosity that could lead to MMR deficiency
281 detecting abnormalities such as copy-neutral loss of heterozygosity that elude other approaches.
282 c expression or loss, somatic mutagenesis or loss-of-heterozygosity (the first three also in a tumor-
283 st to the cell, as BIR promotes mutagenesis, loss of heterozygosity, translocations, and copy number
284  clonal abnormalities including copy-neutral loss of heterozygosity (UPD, 7%).
285 for acquired genomic copy number changes and loss of heterozygosity using Affymetrix SNP 6.0 arrays,
286 Dict also detects differences in somatic and loss of heterozygosity variants between paired samples.
287 cations and reciprocal deletions (reciprocal loss of heterozygosity), variations that are significant
288                                              Loss of heterozygosity was associated with the onset of
289                                 Evidence for loss of heterozygosity was found in 100 and 76% of cases
290                                  The rate of loss of heterozygosity was higher (6%) for those with po
291                     Genome-wide detection of loss of heterozygosity was performed using the Affymetri
292                                 Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patient
293 c recombination events resulting in extended loss of heterozygosity were not observed in DS iPSCs.
294            Recurrent regions of copy-neutral loss-of-heterozygosity were identified at 1p (1%), 4q (0
295 of chromosomes 13q and 13q, and copy-neutral loss of heterozygosity) were between two and six times l
296 otype AD) such aneuploidies have resulted in loss of heterozygosity, where a chromosomal region is re
297 el in any organism and show large regions of loss of heterozygosity, which we hypothesise to be a sho
298 ation or a germline FAS mutation and somatic loss-of-heterozygosity, which allows comparing the fate
299                                              Loss of heterozygosity with retention of an LZTR1 mutati
300 ormation-somatic copy number alterations and loss of heterozygosity-within a unified probabilistic fr

 
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