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1 pression was also detected in the absence of copy number loss.
2 nome pairs to identify snoRNAs with frequent copy number loss.
3 egions of copy number gain and 55 regions of copy number loss.
4 ma contributes to under-reporting of LOH and copy number loss.
5              None of the PKC genes exhibited copy number loss.
6  elevated in RCC with vhl point mutations or copy number loss.
7 3A-mediated epigenetic repression and/or DNA copy-number loss.
8 y mutated genes, 18 copy number gains, and 8 copy number losses.
9                                          The copy number loss (0-copy/1-copy) of nsv823469 significan
10 evalent in copy-number gains (17.7%) than in copy-number losses (2.3%); an observation that supports
11  skin samples from patients with MF/SS, MTAP copy number loss (34%) was more frequent than CDKN2A (12
12                                      Genomic copy number loss and epigenetic silencing, respectively,
13 l clones also showed a higher degree of gene copy number loss and loss of heterozygosity in SNP array
14 l and ovarian cancers exhibit k-h expression/copy number loss and may have severe mutator phenotypes
15 ificantly associated with both chromosome 10 copy number loss and poorer survival.
16  within each tumor stage and with 1p and 16q copy number loss and/or loss of heterozygosity.
17 f the CNVRs analysed showed evidence of both copy number losses and gains at the same site.
18 nocarcinoma, we identify DOK2 as a target of copy-number loss and mRNA downregulation and find that D
19                              Conventionally, copy number losses are identified using metaphase cytoge
20 ARCB1 deficiency, defined as genomic SMARCB1 copy number loss associated with reduced mRNA, drives di
21 nsity microarrays, we found a common genomic copy number loss at 6q16.1-16.2, containing the FBXL4 ge
22 ctral karyotype analysis reveal that genomic copy number loss at the miR-24 locus is concordant with
23 nguish a simple interstitial deletion from a copy-number loss at an inversion junction, and detect a
24         Novel association between CDKN2A/p16 copy number loss, CDK2 activation, replication stress, a
25 levels of C > A substitutions correlate with copy number loss (CNL) of OGG1 or MUTYH Both genes encod
26  both deletion and mutation in cancers, with copy number loss comprising the primary mode of inactiva
27 in HGSOC, these findings suggest that ZC3H18 copy number losses could contribute to HR defects in HGS
28 al deletions consistent with MTAP and CDKN2A copy number loss detected with quantitative reverse tran
29  A, c.1601C > G; p.S534* and an heterozygous copy number loss encompassing exons 15 to 17).
30 ibuting factor in underestimation of LOH and copy number loss events.
31 enomic instability, tumor mutational burden, copy-number loss events, and clonal diversity.
32 inocytes and that human tumors without ITGA9 copy number loss have increased promoter methylation.
33 inocytes and that human tumors without ITGA9 copy number loss have increased promoter methylation.
34 concordant expression patterns with PTEN and copy number loss in cancers.
35  chromosome 18q that are subject to frequent copy number loss in CIN(+) CRC.
36 nervous system development that also sustain copy number loss in GBM through antineoplastic assay and
37  lies within 16q24.2, a region with frequent copy number loss in HGSOC, these findings suggest that Z
38                                 Furthermore, copy number loss in HLA class I/II and antigen-presentin
39 ough at least two mechanisms: (i) ITGA9 gene copy number loss in human tumors and (ii) epigenetic sil
40 ough at least two mechanisms: (i) ITGA9 gene copy number loss in human tumors and (ii) epigenetic sil
41 her-order chromatin structure that undergoes copy number loss in over half of all breast cancers, but
42   Mutational analysis demonstrated focal NF1 copy number loss in PN and MPNST patient plasma but not
43 ARH77 contain large deletions, while IM9 has copy number losses in multiple EBV loci.
44 romosome arms 1q, 7p, 8q, 9q, and 17q; focal copy number losses in SUZ12, SMARCA2, CDKN2A/B, and chro
45          Although the majority of NRs showed copy-number losses in cancer, both recurrent focal gains
46 n mutations, homozygous deletion, as well as copy-number losses in multiple epithelial cancers, inclu
47                                        Focal copy number losses included 1p36.33-p36-22 in ACC, 9p13.
48                Cells harboring partial PSMC2 copy number loss lack this complex and die after PSMC2 s
49 ber neutral (NAFLD: 53.8%, controls: 68.6%), copy number losses (NAFLD: 13.3%, controls: 12.9%), copy
50 ypermethylation is nearly universal and PTEN copy number loss occurs in ~25% of fusion-negative rhabd
51 chanism of oncogene activation whereby focal copy number loss of an intronic element within the FTO g
52                                  We detected copy number loss of ARID1A in 16% of patients with ccRCC
53                                     Acquired copy number loss of CD274, PDCD1LG2, and JAK2 were assoc
54                                    Recurrent copy number loss of chromosome 16 was observed.
55                                              Copy number loss of chromosome 22q, leading to loss of h
56 ocation between Ewsr1 and Atf1, resulting in copy number loss of chromosome 6 and chromosome 15 insta
57                                 Furthermore, copy number loss of IFN-y pathway genes is frequently ob
58                             Furthermore, the copy number loss of nsv823469 in normal pulmonary tissue
59                    The loss allele, inducing copy number loss of nsv823469, has a tendency to transmi
60                                              Copy number loss of PGR, the gene coding for PR, is a co
61                                              Copy number loss of PIK3R1 (p85alpha) most commonly occu
62        Furthermore, ~50% of CRPC tumors have copy number loss of pre-RC complex genes, particularly C
63          Four of the tumors also exhibited a copy number loss of proximal chromosome 11 (11A-B), a re
64 RNA variations among subtypes correlate with copy number loss of RP genes.
65 the proliferation of cells harboring partial copy number loss of that gene.
66 st frequent genomic alteration was biallelic copy number loss of the FOX1A gene.
67  c-Myc gene, and six of the tumors exhibited copy number loss of whole or partial chromosome 14, incl
68  analyses, including measuring relative gene copy number, loss of heterozygosity, and comparative gen
69  indicative of historical immune editing, or copy-number loss of previously clonal neoantigens.
70 llular fitness by dictating gene-independent copy number loss-of-fitness effects and antiproliferativ
71 nivolumab treatment exhibited 9p21.3 somatic copy-number loss on pretreatment biopsy, while only 4 of
72  genetic element(s) within a small CNV whose copy number loss or gain underlies a specific phenotype
73               NF1(low) status, identified by copy number loss or low mRNA/protein expression, is asso
74 evelopment when reduced in dosage by genomic copy number loss or other mechanisms.
75  and in female subjects de novo heterozygous copy number loss or truncating mutations cause haploinsu
76  adenomas in the Pirc rat have no detectable copy number losses or gains in genomic material and that
77 fic GATA2 expression was observed, either by copy-number loss or by an unexplained allelic imbalance.
78 ity of NLRC5 caused by promoter methylation, copy number loss, or somatic mutations is associated wit
79 ed MTAP mRNA expression correlated with MTAP copy number loss (P < 0.01) but reduced MTAP expression
80  meningiomas revealed that MRMs have greater copy number losses (P = 0.0313) and increased DNA methyl
81 e African-European-restricted subtype GMS-C (copy-number losses) predicts poor clinical outcomes.
82 y >10%), we observed a distinct bias against copy-number losses, suggesting that deletions are subjec
83                                              Copy number losses tend to occur away from genes in non/
84 A copy number, counteracting the spontaneous copy number loss that occurs during aging.
85 ranged chromosomes lacking the extensive DNA copy-number losses that are characteristic of canonical
86 ole in USC, with 13 copy-number gains and 12 copy-number losses that occurred more often than expecte
87                                Emerging CCR4 copy number loss was detected in 2 patients with CCR4 mu
88 cantly greater in invasive ADC, whereas more copy number loss was observed in AIS and MIA.
89 cific vulnerabilities that are the result of copy number losses, we performed integrated analyses of
90 alysis revealed an association between TRAF3 copy number loss with accumulation of NIK, the central n