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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
4                                  Because DNA methylators constitute an important class of chemotherap
5  repair-mediated iterative processing of DNA methylator damage, an effect that may be relevant to dam
6  activation or cell death in response to DNA methylator damage.
7   The response of mammalian cells to Sn1 DNA methylators depends on functional MutSalpha and MutLalph
8                       Because killing by Sn1 methylators has been attributed to O6-methylguanine (MeG
9                     The most prevalent known methylators included Desulfobulbus propionicus, Desulfov
10 optotic gene expression and attenuates S(N)1-methylator-induced cytotoxicity.
11 d demonstrate that p50 is required for S(N)1-methylator-induced cytotoxicity.
12  treatment of human cells with the S(N)1 DNA methylators N-methyl-N-nitrosourea or N-methyl-N'-nitro-
13      Identification of these organisms as Hg methylators now links methylation to discrete gene marke
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
22 icrosatellite instability and the CpG island methylator phenotype (CIMP) in colon cancer.
23                                   CpG island methylator phenotype (CIMP) in colorectal cancers is cha
24  described a novel pathway termed CpG island methylator phenotype (CIMP) in CRC, which is characteriz
25                               The CpG island methylator phenotype (CIMP) is a newly described mechani
26                               The CpG island methylator phenotype (CIMP) is a recently described mech
27         In colorectal cancer, the CpG island methylator phenotype (CIMP) is defined as widespread and
28                               The CpG island methylator phenotype (CIMP) is one of the mechanisms inv
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
31 ith microsatellite instability or CpG island methylator phenotype (CIMP) positivity.
32                      Although the CpG island methylator phenotype (CIMP) was first identified and has
33                                 A CpG island methylator phenotype (CIMP) was observed in a distinct s
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
37                  The concept of a CpG island methylator phenotype (CIMP), especially in microsatellit
38 ancer risk according to status of CpG island methylator phenotype (CIMP), microsatellite instability,
39                               The CpG island methylator phenotype (CIMP), thoroughly described in col
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
42 olon cancers characterized by the CpG island methylator phenotype (CIMP).
43 tations in BRAF and KRAS, and the CpG island methylator phenotype (CIMP).
44  subset of cases that display the CpG island methylator phenotype (CIMP).
45 ancers, which appear to display a CpG island methylator phenotype (CIMP).
46 osatellite instability (MSI); the CpG island methylator phenotype (CIMP); 18q loss of heterozygosity;
47        Most such cancers have the CpG island methylator phenotype (CIMP+) with methylation and transc
48                               The CpG island methylator phenotype (CIMP-high, CIMP1) is a distinct ph
49 DH mutant gliomas thus manifest a CpG island methylator phenotype (G-CIMP), although the functional i
50  by DNA methylation due to the presence of a methylator phenotype (MET+).
51 ces, in a small set of non-glioma CpG island methylator phenotype (non-G-CIMP) primary tumors.
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 [
60 o the expected subgroups based on CpG island methylator phenotype classification.
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
66 , microsatellite instability, and CpG island methylator phenotype pathways.
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
69 , microsatellite instability, and CpG island methylator phenotype were also evaluated.
70  a distinct trait referred to as 'CpG island methylator phenotype', or 'CIMP'.
71  with the less aggressive G-CIMP (Glioma CpG Methylator Phenotype) subset of GBM.
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
75 , BRAF wildtype, have no or a low CpG island methylator phenotype, and microsatellite stability.
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
80                      These glioma CpG island methylator phenotype, or G-CIMP tumors, have distinct ge
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
84                                   CpG island methylator phenotype-positive hindbrain ependymomas are
85      Two AD subtypes manifested a CpG island methylator phenotype.
86 s hindbrain ependymomas exhibit a CpG island methylator phenotype.
87 g some features consistent with a CpG island methylator phenotype.
88 romoter methylation termed as the CpG island methylator phenotype.
89 ion with long-range silencing and CpG island methylator phenotype.
90 , which occurs in tumors with the CpG island methylator phenotype.
91 astomas may be characterized by a CpG island methylator phenotype.
92 a distinct group of tumors with a CpG island methylator phenotype.
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
95             CRC tumors displaying CpG island methylator phenotypes (CIMPs), defined as DNA hypermethy
96                                            A methylator-resistant human glioblastoma multiforme xenog
97 f iron-reducing bacteria (IRB), potential Hg methylators, were active in SR sediments.
98  bacterium Nitrospina as a potential mercury methylator within sea ice.

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