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1 egions of copy number gain and 55 regions of copy number loss.
2 ma contributes to under-reporting of LOH and copy number loss.
3              None of the PKC genes exhibited copy number loss.
4 pression was also detected in the absence of copy number loss.
5 nome pairs to identify snoRNAs with frequent copy number loss.
6 3A-mediated epigenetic repression and/or DNA copy-number loss.
7                                          The copy number loss (0-copy/1-copy) of nsv823469 significan
8 evalent in copy-number gains (17.7%) than in copy-number losses (2.3%); an observation that supports
9  skin samples from patients with MF/SS, MTAP copy number loss (34%) was more frequent than CDKN2A (12
10                                      Genomic copy number loss and epigenetic silencing, respectively,
11 l clones also showed a higher degree of gene copy number loss and loss of heterozygosity in SNP array
12 l and ovarian cancers exhibit k-h expression/copy number loss and may have severe mutator phenotypes
13 ificantly associated with both chromosome 10 copy number loss and poorer survival.
14  within each tumor stage and with 1p and 16q copy number loss and/or loss of heterozygosity.
15 f the CNVRs analysed showed evidence of both copy number losses and gains at the same site.
16 nocarcinoma, we identify DOK2 as a target of copy-number loss and mRNA downregulation and find that D
17                              Conventionally, copy number losses are identified using metaphase cytoge
18 nsity microarrays, we found a common genomic copy number loss at 6q16.1-16.2, containing the FBXL4 ge
19 ctral karyotype analysis reveal that genomic copy number loss at the miR-24 locus is concordant with
20 nguish a simple interstitial deletion from a copy-number loss at an inversion junction, and detect a
21         Novel association between CDKN2A/p16 copy number loss, CDK2 activation, replication stress, a
22  both deletion and mutation in cancers, with copy number loss comprising the primary mode of inactiva
23 al deletions consistent with MTAP and CDKN2A copy number loss detected with quantitative reverse tran
24 ibuting factor in underestimation of LOH and copy number loss events.
25 concordant expression patterns with PTEN and copy number loss in cancers.
26  chromosome 18q that are subject to frequent copy number loss in CIN(+) CRC.
27 nervous system development that also sustain copy number loss in GBM through antineoplastic assay and
28 n mutations, homozygous deletion, as well as copy-number losses in multiple epithelial cancers, inclu
29                                        Focal copy number losses included 1p36.33-p36-22 in ACC, 9p13.
30                Cells harboring partial PSMC2 copy number loss lack this complex and die after PSMC2 s
31 ber neutral (NAFLD: 53.8%, controls: 68.6%), copy number losses (NAFLD: 13.3%, controls: 12.9%), copy
32                                  We detected copy number loss of ARID1A in 16% of patients with ccRCC
33                             Furthermore, the copy number loss of nsv823469 in normal pulmonary tissue
34                    The loss allele, inducing copy number loss of nsv823469, has a tendency to transmi
35                                              Copy number loss of PGR, the gene coding for PR, is a co
36          Four of the tumors also exhibited a copy number loss of proximal chromosome 11 (11A-B), a re
37 the proliferation of cells harboring partial copy number loss of that gene.
38  c-Myc gene, and six of the tumors exhibited copy number loss of whole or partial chromosome 14, incl
39  analyses, including measuring relative gene copy number, loss of heterozygosity, and comparative gen
40  genetic element(s) within a small CNV whose copy number loss or gain underlies a specific phenotype
41 evelopment when reduced in dosage by genomic copy number loss or other mechanisms.
42  adenomas in the Pirc rat have no detectable copy number losses or gains in genomic material and that
43 ity of NLRC5 caused by promoter methylation, copy number loss, or somatic mutations is associated wit
44 ed MTAP mRNA expression correlated with MTAP copy number loss (P < 0.01) but reduced MTAP expression
45 y >10%), we observed a distinct bias against copy-number losses, suggesting that deletions are subjec
46                                              Copy number losses tend to occur away from genes in non/
47 ole in USC, with 13 copy-number gains and 12 copy-number losses that occurred more often than expecte
48 cific vulnerabilities that are the result of copy number losses, we performed integrated analyses of

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