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   1 cing bacteria (SRB) and methanogens were key methylators.                                            
     2 regimes involving alkylating agents, such as methylators and crosslinking nitrogen mustards, represen
     3 mes, gene orthologs are present in confirmed methylators but absent in nonmethylators, suggesting a c
  
     5  repair-mediated iterative processing of DNA methylator damage, an effect that may be relevant to dam
  
     7   The response of mammalian cells to Sn1 DNA methylators depends on functional MutSalpha and MutLalph
  
  
  
  
    12  treatment of human cells with the S(N)1 DNA methylators N-methyl-N-nitrosourea or N-methyl-N'-nitro-
  
    14  clusters, including a clear cell CpG island methylator phenotype (C-CIMP) subgroup associated with p
    15 pair) system, the presence of the CpG island methylator phenotype (CIMP or CIMP-High) and for the V60
    16 likely to be characterized by the CpG island methylator phenotype (CIMP) (multivariate odds ratio, 2.
    17 hydrogenase 1/2 (IDH1/2) have the CpG island methylator phenotype (CIMP) and significantly longer pat
    18  colorectal cancers (CRCs) have a CpG island methylator phenotype (CIMP) characterized by aberrant DN
    19 tivated BRAF (BRAF[V600E]) have a CpG island methylator phenotype (CIMP) characterized by aberrant hy
    20 stomas and other cancers with the CpG island methylator phenotype (CIMP) constitute a subset of tumou
    21 lation of multiple CpG islands as CpG island methylator phenotype (CIMP) has been described in tumors
  
  
    24  described a novel pathway termed CpG island methylator phenotype (CIMP) in CRC, which is characteriz
  
  
  
  
    29 recapitulated the hypermethylated CpG island methylator phenotype (CIMP) observed in EBV-associated c
    30 olorectal cancers (CRCs) with the CpG island methylator phenotype (CIMP) often associate with epigene
  
  
  
    34 ancers was postulated to have the CpG island methylator phenotype (CIMP), a higher propensity for CpG
    35 microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and mutations in BRAF and K
    36 mutation, MLH1 methylation, and a CpG island methylator phenotype (CIMP), but precursors are poorly e
  
    38 ancer risk according to status of CpG island methylator phenotype (CIMP), microsatellite instability,
  
    40 ermed cytosine phosphoguanosine (CpG) island methylator phenotype (CIMP), which appears to be a defin
    41  hypermethylator phenotype termed CpG island methylator phenotype (CIMP), which includes methylation 
  
  
  
  
    46 osatellite instability (MSI); the CpG island methylator phenotype (CIMP); 18q loss of heterozygosity;
  
  
    49 DH mutant gliomas thus manifest a CpG island methylator phenotype (G-CIMP), although the functional i
  
  
    52  enriched for those harboring the CpG island methylator phenotype (p = 0.036, Chi square test), and r
    53 sociated with the presence of the CpG island methylator phenotype (P<0.01), inversely related to p53 
    54 satellite instability [MSI]-high, CpG island methylator phenotype [CIMP] -positive, positive for BRAF
    55 ar cell tumours, coincides with a CpG island methylator phenotype affecting numerous other promoters 
    56 sporadic CRC characterized by the CpG island methylator phenotype and BRAF(V600E) mutation due to pro
    57 suggests that this viral oncogene may induce methylator phenotype and that JCV may be involved in CRC
    58 ever, the molecular processes underlying the methylator phenotype and the contribution of hepatitis v
    59 nt difference in the incidence of CpG island methylator phenotype between UC-Cs and S-CRCs (8 of 48 [
  
    61  genes, such as APC and TP53; (3) CpG island methylator phenotype CRCs in approximately 20% that over
    62 ted CpGs, a characteristic of the CpG island methylator phenotype in cancer, a novel filter statistic
    63 nvolved in angiogenesis is a hallmark of the methylator phenotype in ccRCC, implying a convergence to
    64 rch Network showed evidence for a CpG island methylator phenotype in glioblastomas that was associate
    65 or whether there is evidence of a CpG island methylator phenotype or associations of CpG island methy
  
    67  favor high expression and by the CpG island methylator phenotype that favors silencing in a subset o
    68 udy was to determine the contribution of the methylator phenotype to HCC and its relationship to geno
  
  
  
    72  (p53), PTGS2 (cyclooxygenase-2), CpG island methylator phenotype, and KRAS, BRAF, PIK3CA, and LINE-1
    73 BRAF, microsatellite instability, CpG island methylator phenotype, and methylation of long interspers
    74 BRAF [BRAF wildtype], no or a low CpG island methylator phenotype, and microsatellite stability), alt
  
    76 uding microsatellite instability, CpG island methylator phenotype, KRAS, BRAF, and PIK3CA mutations, 
    77 uding microsatellite instability, CpG island methylator phenotype, level of long interspersed nucleot
    78  BRAF, PIK3CA, beta-catenin, p53, CpG island methylator phenotype, LINE-1 methylation, and John Cunni
    79  tumor molecular characteristics (CpG island methylator phenotype, microsatellite instability, and th
  
    81 icant differences by KRAS2, TP53, CpG island methylator phenotype, or microsatellite instability stat
    82 th PTGS2 expression (P = 0.0035), CpG island methylator phenotype-high (P = 0.013), and LINE-1 hypome
    83 ylation of 3 or more CpG islands (CpG island methylator phenotype-high) was more common in duodenal c
  
  
  
  
  
  
  
  
  
    93 r microsatellite instability; the CpG island methylator phenotype; LINE-1 methylation; and KRAS, BRAF
    94 of pancreatic adenocarcinomas as "CpG island-methylator-phenotype positive (CIMP+)." Two of four carc
  
  
  
  
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