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1 ergent from those in well-studied, confirmed methylators.
2 cing bacteria (SRB) and methanogens were key methylators.
3 ose, only the aerobic species were efficient methylators.
4                                           Hg-methylator abundance was also determined by quantitative
5  as biomarkers in PCR-based estimators of Hg-methylator abundance.
6 eria in the Geobacteraceae were important Hg methylators across all wetlands and seasons examined, as
7 regimes involving alkylating agents, such as methylators and crosslinking nitrogen mustards, represen
8                                  To identify methylators and demethylators and evaluate their occurre
9 d on two general factors: the activity of Hg methylators and their uptake of IHg.
10 mes, gene orthologs are present in confirmed methylators but absent in nonmethylators, suggesting a c
11                                  Because DNA methylators constitute an important class of chemotherap
12  repair-mediated iterative processing of DNA methylator damage, an effect that may be relevant to dam
13  activation or cell death in response to DNA methylator damage.
14   The response of mammalian cells to Sn1 DNA methylators depends on functional MutSalpha and MutLalph
15 enomic and hgcAB results were similar for Hg-methylator diversity and clade-specific qPCR-based appro
16                       Because killing by Sn1 methylators has been attributed to O6-methylguanine (MeG
17 r, our understanding of the ecophysiology of methylators in natural ecosystems is still limited.
18 ghlighted the versatility of putative Hg(II) methylators in the water column of the Baltic Sea.
19                     The most prevalent known methylators included Desulfobulbus propionicus, Desulfov
20 optotic gene expression and attenuates S(N)1-methylator-induced cytotoxicity.
21 d demonstrate that p50 is required for S(N)1-methylator-induced cytotoxicity.
22 esulfovibrio desulfuricans ND132 (a known Hg methylator), more Hg was methylated from the coprecipita
23  treatment of human cells with the S(N)1 DNA methylators N-methyl-N-nitrosourea or N-methyl-N'-nitro-
24      Identification of these organisms as Hg methylators now links methylation to discrete gene marke
25  clusters, including a clear cell CpG island methylator phenotype (C-CIMP) subgroup associated with p
26 pair) system, the presence of the CpG island methylator phenotype (CIMP or CIMP-High) and for the V60
27 likely to be characterized by the CpG island methylator phenotype (CIMP) (multivariate odds ratio, 2.
28 their microsatellite instability, CpG Island Methylator Phenotype (CIMP) and chromosomal instability,
29 hydrogenase 1/2 (IDH1/2) have the CpG island methylator phenotype (CIMP) and significantly longer pat
30  colorectal cancers (CRCs) have a CpG island methylator phenotype (CIMP) characterized by aberrant DN
31 tivated BRAF (BRAF[V600E]) have a CpG island methylator phenotype (CIMP) characterized by aberrant hy
32 stomas and other cancers with the CpG island methylator phenotype (CIMP) constitute a subset of tumou
33 lation of multiple CpG islands as CpG island methylator phenotype (CIMP) has been described in tumors
34 icrosatellite instability and the CpG island methylator phenotype (CIMP) in colon cancer.
35                                   CpG island methylator phenotype (CIMP) in colorectal cancers is cha
36  described a novel pathway termed CpG island methylator phenotype (CIMP) in CRC, which is characteriz
37                               The CpG island methylator phenotype (CIMP) is a newly described mechani
38                               The CpG island methylator phenotype (CIMP) is a recently described mech
39         In colorectal cancer, the CpG island methylator phenotype (CIMP) is defined as widespread and
40                               The CpG island methylator phenotype (CIMP) is one of the mechanisms inv
41      Colorectal cancer (CRC) with CpG island methylator phenotype (CIMP) is recognized as a subgroup
42 recapitulated the hypermethylated CpG island methylator phenotype (CIMP) observed in EBV-associated c
43 olorectal cancers (CRCs) with the CpG island methylator phenotype (CIMP) often associate with epigene
44 ith microsatellite instability or CpG island methylator phenotype (CIMP) positivity.
45 stic relevance of DNA methylation CpG island methylator phenotype (CIMP) risk stratification in 2 ped
46                      Although the CpG island methylator phenotype (CIMP) was first identified and has
47                                 A CpG island methylator phenotype (CIMP) was observed in a distinct s
48 ancers was postulated to have the CpG island methylator phenotype (CIMP), a higher propensity for CpG
49 ability (MSI), genetic mutations, CpG island methylator phenotype (CIMP), and immunostaining includin
50 microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and mutations in BRAF and K
51 microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and mutations in KRAS and B
52 microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and somatic mutations in BR
53 microsatellite instability (MSI), CpG island methylator phenotype (CIMP), B-Raf proto-oncogene serine
54 mutation, MLH1 methylation, and a CpG island methylator phenotype (CIMP), but precursors are poorly e
55                  The concept of a CpG island methylator phenotype (CIMP), especially in microsatellit
56 ancer risk according to status of CpG island methylator phenotype (CIMP), microsatellite instability,
57                               The CpG island methylator phenotype (CIMP), thoroughly described in col
58 ermed cytosine phosphoguanosine (CpG) island methylator phenotype (CIMP), which appears to be a defin
59  hypermethylator phenotype termed CpG island methylator phenotype (CIMP), which includes methylation
60 ancers, which appear to display a CpG island methylator phenotype (CIMP).
61 tion of CpG islands, known as the CpG island methylator phenotype (CIMP).
62  elements including CGIs, underpinning a CGI methylator phenotype (CIMP).
63 gene-promoter CpG-island methylation, or the methylator phenotype (CIMP).
64 olon cancers characterized by the CpG island methylator phenotype (CIMP).
65 tations in BRAF and KRAS, and the CpG island methylator phenotype (CIMP).
66  subset of cases that display the CpG island methylator phenotype (CIMP).
67 osatellite instability (MSI); the CpG island methylator phenotype (CIMP); 18q loss of heterozygosity;
68        Most such cancers have the CpG island methylator phenotype (CIMP+) with methylation and transc
69                               The CpG island methylator phenotype (CIMP-high, CIMP1) is a distinct ph
70 DH mutant gliomas thus manifest a CpG island methylator phenotype (G-CIMP), although the functional i
71  by DNA methylation due to the presence of a methylator phenotype (MET+).
72 ces, in a small set of non-glioma CpG island methylator phenotype (non-G-CIMP) primary tumors.
73  enriched for those harboring the CpG island methylator phenotype (p = 0.036, Chi square test), and r
74 sociated with the presence of the CpG island methylator phenotype (P<0.01), inversely related to p53
75 satellite instability [MSI]-high, CpG island methylator phenotype [CIMP] -positive, positive for BRAF
76 ar cell tumours, coincides with a CpG island methylator phenotype affecting numerous other promoters
77 sporadic CRC characterized by the CpG island methylator phenotype and BRAF(V600E) mutation due to pro
78 suggests that this viral oncogene may induce methylator phenotype and that JCV may be involved in CRC
79 ever, the molecular processes underlying the methylator phenotype and the contribution of hepatitis v
80 nt difference in the incidence of CpG island methylator phenotype between UC-Cs and S-CRCs (8 of 48 [
81 o the expected subgroups based on CpG island methylator phenotype classification.
82  genes, such as APC and TP53; (3) CpG island methylator phenotype CRCs in approximately 20% that over
83 ted CpGs, a characteristic of the CpG island methylator phenotype in cancer, a novel filter statistic
84 nvolved in angiogenesis is a hallmark of the methylator phenotype in ccRCC, implying a convergence to
85 rch Network showed evidence for a CpG island methylator phenotype in glioblastomas that was associate
86 or whether there is evidence of a CpG island methylator phenotype or associations of CpG island methy
87 , microsatellite instability, and CpG island methylator phenotype pathways.
88  favor high expression and by the CpG island methylator phenotype that favors silencing in a subset o
89 udy was to determine the contribution of the methylator phenotype to HCC and its relationship to geno
90 , microsatellite instability, and CpG island methylator phenotype were also evaluated.
91  a distinct trait referred to as 'CpG island methylator phenotype', or 'CIMP'.
92                             CIMP (CpG island methylator phenotype) is an epigenetic molecular subtype
93  with the less aggressive G-CIMP (Glioma CpG Methylator Phenotype) subset of GBM.
94  (p53), PTGS2 (cyclooxygenase-2), CpG island methylator phenotype, and KRAS, BRAF, PIK3CA, and LINE-1
95 BRAF, microsatellite instability, CpG island methylator phenotype, and methylation of long interspers
96 BRAF [BRAF wildtype], no or a low CpG island methylator phenotype, and microsatellite stability), alt
97 , BRAF wildtype, have no or a low CpG island methylator phenotype, and microsatellite stability.
98 uding microsatellite instability, CpG island methylator phenotype, KRAS, BRAF, and PIK3CA mutations,
99 uding microsatellite instability, CpG island methylator phenotype, level of long interspersed nucleot
100  BRAF, PIK3CA, beta-catenin, p53, CpG island methylator phenotype, LINE-1 methylation, and John Cunni
101  tumor molecular characteristics (CpG island methylator phenotype, microsatellite instability, and th
102                      These glioma CpG island methylator phenotype, or G-CIMP tumors, have distinct ge
103 icant differences by KRAS2, TP53, CpG island methylator phenotype, or microsatellite instability stat
104 ion patterns, the hypermethylated CpG island methylator phenotype-associated (CIMP) RCCs and metaboli
105 th PTGS2 expression (P = 0.0035), CpG island methylator phenotype-high (P = 0.013), and LINE-1 hypome
106 ylation of 3 or more CpG islands (CpG island methylator phenotype-high) was more common in duodenal c
107                                   CpG island methylator phenotype-positive hindbrain ependymomas are
108 astomas may be characterized by a CpG island methylator phenotype.
109 a distinct group of tumors with a CpG island methylator phenotype.
110 a subgroup of such leukemias with CpG Island Methylator Phenotype.
111 ntal factors, and 5'-C-phosphate-G-3' island methylator phenotype.
112      Two AD subtypes manifested a CpG island methylator phenotype.
113 s hindbrain ependymomas exhibit a CpG island methylator phenotype.
114 g some features consistent with a CpG island methylator phenotype.
115 romoter methylation termed as the CpG island methylator phenotype.
116 ion with long-range silencing and CpG island methylator phenotype.
117 , which occurs in tumors with the CpG island methylator phenotype.
118 r microsatellite instability; the CpG island methylator phenotype; LINE-1 methylation; and KRAS, BRAF
119 of pancreatic adenocarcinomas as "CpG island-methylator-phenotype positive (CIMP+)." Two of four carc
120             CRC tumors displaying CpG island methylator phenotypes (CIMPs), defined as DNA hypermethy
121 ogy, adaptive immune response and CpG island methylator profile.
122                                            A methylator-resistant human glioblastoma multiforme xenog
123  Microbial analysis indicated three putative methylators (two methanogens and one novel bacteria) as
124                                     Putative methylators were dominated by hgcA sequences divergent f
125 f iron-reducing bacteria (IRB), potential Hg methylators, were active in SR sediments.
126 the Deltaproteobacteria were the dominant Hg-methylators while Firmicutes and methanogenic Archaea we
127  bacterium Nitrospina as a potential mercury methylator within sea ice.

 
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