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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.
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
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
16 nocarcinoma, we identify DOK2 as a target of copy-number loss and mRNA downregulation and find that D
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
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
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
31 ber neutral (NAFLD: 53.8%, controls: 68.6%), copy number losses (NAFLD: 13.3%, controls: 12.9%), copy
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
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
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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