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1 ks from progressing beyond the normal 100-kb amplified region.
2 ing to false-positive results in copy number-amplified regions.
3 hybridization (array CGH) to map the minimal amplified regions.
4 sequence tag were located in the two common amplified regions.
5 ngth polymorphism (RFLP) patterns within the amplified regions.
7 ts were transitions occurring throughout the amplified region, although frameshifts and transversions
8 ization (array CGH) to define minimum common amplified regions and then used expression analysis to i
9 for driver genes within large deletions and amplified regions, and identifies therapeutic targets.
10 906 and D11S937, at the telomeric end of the amplified region at 11q13, and found that it was amplifi
11 Positional cloning efforts directed at the amplified region at 3q26-q27 identified three highly ove
12 of CKS1B, a gene mapping within a minimally amplified region between 153 to 154 Mb of chromosome 1q2
14 More importantly, by honing in on minimally amplified regions containing three or fewer genes, we id
15 (ddPCR) of mouse p-TGCs, we identified five amplified regions, each containing a gene family known t
17 sess the performance of HATS using simulated amplified regions generated from varying copy number and
18 n cancers compared to other genes within the amplified region, implicating RAB25 as a driving event i
19 hybridization analysis to identify possible amplified regions (implying amplified/overexpressed gene
20 d CpG islands and the characterization of an amplified region in a breast tumor that spanned <230 kb
24 -24, which is one of the three most commonly amplified regions in head and neck squamous cell carcino
25 eakpoints that coincide with the four highly amplified regions in MCF-7 detected by array CGH located
32 l gains and losses were not observed, a 1-Mb amplified region of 7q34 was detected in multiple patien
33 elanoma model to test genes in a recurrently amplified region of chromosome 1 for the ability to coop
35 number and expression of all genes within an amplified region of the genome have not been performed.
38 nd erd pedigrees were sought by digestion of amplified regions of the CFRDSP gene with different rest
39 were deduced from polymerase chain reaction-amplified regions of the corresponding genes and subsequ
40 ly, ERDS accommodates both unique and highly amplified regions of the genome and does so without requ
45 A method based on Sequence-Characterized Amplified Regions (SCARs) was developed to detect the pr
46 om all 44 isolates, while eight primer pairs amplified regions that were polymorphic between isolates
49 tative measurement of DNA copy number across amplified regions using array comparative genomic hybrid
50 normal metaphase spreads, confirmed that the amplified region was derived from sequences from 9q34.
53 itate the identification of genes mapping to amplified regions, we have used a technique based on the
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