ライフサイエンスコーパス: CpG island methylator phenotype

1 Two AD subtypes manifested a CpG island methylator phenotype.

2 or-prognosis hindbrain ependymomas exhibit a CpG island methylator phenotype.

3 roup showing some features consistent with a CpG island methylator phenotype.

4 idence of promoter methylation termed as the CpG island methylator phenotype.

5 d its relation with long-range silencing and CpG island methylator phenotype.

6 e MLH1 gene, which occurs in tumors with the CpG island methylator phenotype.

7 of neuroblastomas may be characterized by a CpG island methylator phenotype.

8 idence for a distinct group of tumors with a CpG island methylator phenotype.

9 sent in clear cell tumours, coincides with a CpG island methylator phenotype affecting numerous other

10 subset of sporadic CRC characterized by the CpG island methylator phenotype and BRAF(V600E) mutation

11 ility, TP53 (p53), PTGS2 (cyclooxygenase-2), CpG island methylator phenotype, and KRAS, BRAF, PIK3CA,

12 AKT, KRAS, BRAF, microsatellite instability, CpG island methylator phenotype, and methylation of long

13 AS wildtype, BRAF wildtype, have no or a low CpG island methylator phenotype, and microsatellite stab

14 ldtype] or BRAF [BRAF wildtype], no or a low CpG island methylator phenotype, and microsatellite stab

15 a significant difference in the incidence of CpG island methylator phenotype between UC-Cs and S-CRCs

16 epigenetic clusters, including a clear cell CpG island methylator phenotype (C-CIMP) subgroup associ

17 mismatch repair) system, the presence of the CpG island methylator phenotype (CIMP or CIMP-High) and

18 were more likely to be characterized by the CpG island methylator phenotype (CIMP) (multivariate odd

19 ocitrate dehydrogenase 1/2 (IDH1/2) have the CpG island methylator phenotype (CIMP) and significantly

20 ntaining activated BRAF (BRAF[V600E]) have a CpG island methylator phenotype (CIMP) characterized by

21 AS-positive colorectal cancers (CRCs) have a CpG island methylator phenotype (CIMP) characterized by

22 Glioblastomas and other cancers with the CpG island methylator phenotype (CIMP) constitute a subs

23 rdant methylation of multiple CpG islands as CpG island methylator phenotype (CIMP) has been describe

24 ated with microsatellite instability and the CpG island methylator phenotype (CIMP) in colon cancer.

25 CpG island methylator phenotype (CIMP) in colorectal can

26 ve recently described a novel pathway termed CpG island methylator phenotype (CIMP) in CRC, which is

27 The CpG island methylator phenotype (CIMP) is a newly descri

28 The CpG island methylator phenotype (CIMP) is a recently des

29 In colorectal cancer, the CpG island methylator phenotype (CIMP) is defined as wid

30 The CpG island methylator phenotype (CIMP) is one of the mec

31 dification recapitulated the hypermethylated CpG island methylator phenotype (CIMP) observed in EBV-a

32 Colorectal cancers (CRCs) with the CpG island methylator phenotype (CIMP) often associate w

33 ) but not with microsatellite instability or CpG island methylator phenotype (CIMP) positivity.

34 Although the CpG island methylator phenotype (CIMP) was first identif

35 A CpG island methylator phenotype (CIMP) was observed in a

36 olorectal cancers was postulated to have the CpG island methylator phenotype (CIMP), a higher propens

37 nations of microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and mutations in

38 hibit BRAF mutation, MLH1 methylation, and a CpG island methylator phenotype (CIMP), but precursors a

39 The concept of a CpG island methylator phenotype (CIMP), especially in mi

40 olorectal cancer risk according to status of CpG island methylator phenotype (CIMP), microsatellite i

41 The CpG island methylator phenotype (CIMP), thoroughly descr

42 erized by a hypermethylator phenotype termed CpG island methylator phenotype (CIMP), which includes m

43 somatic mutations in BRAF and KRAS, and the CpG island methylator phenotype (CIMP).

44 occurs in a subset of cases that display the CpG island methylator phenotype (CIMP).

45 olorectal cancers, which appear to display a CpG island methylator phenotype (CIMP).

46 regulated colon cancers characterized by the CpG island methylator phenotype (CIMP).

47 WRN); microsatellite instability (MSI); the CpG island methylator phenotype (CIMP); 18q loss of hete

48 Most such cancers have the CpG island methylator phenotype (CIMP+) with methylation

49 The CpG island methylator phenotype (CIMP-high, CIMP1) is a

50 phenotype termed cytosine phosphoguanosine (CpG) island methylator phenotype (CIMP), which appears t

51 pe 1 (microsatellite instability [MSI]-high, CpG island methylator phenotype [CIMP] -positive, positi

52 CRC tumors displaying CpG island methylator phenotypes (CIMPs), defined as DNA

53 tumors into the expected subgroups based on CpG island methylator phenotype classification.

54 suppressor genes, such as APC and TP53; (3) CpG island methylator phenotype CRCs in approximately 20

55 IDH mutant gliomas thus manifest a CpG island methylator phenotype (G-CIMP), although the f

56 sociated with PTGS2 expression (P = 0.0035), CpG island methylator phenotype-high (P = 0.013), and LI

57 aneous methylation of 3 or more CpG islands (CpG island methylator phenotype-high) was more common in

58 y unmethylated CpGs, a characteristic of the CpG island methylator phenotype in cancer, a novel filte

59 Atlas Research Network showed evidence for a CpG island methylator phenotype in glioblastomas that wa

60 stics (including microsatellite instability, CpG island methylator phenotype, KRAS, BRAF, and PIK3CA

61 tures, including microsatellite instability, CpG island methylator phenotype, level of long intersper

62 uding KRAS, BRAF, PIK3CA, beta-catenin, p53, CpG island methylator phenotype, LINE-1 methylation, and

63 adjusted for microsatellite instability; the CpG island methylator phenotype; LINE-1 methylation; and

64 correlated tumor molecular characteristics (CpG island methylator phenotype, microsatellite instabil

65 er differences, in a small set of non-glioma CpG island methylator phenotype (non-G-CIMP) primary tum

66 this data for whether there is evidence of a CpG island methylator phenotype or associations of CpG i

67 ggestion of a distinct trait referred to as 'CpG island methylator phenotype', or 'CIMP'.

68 These glioma CpG island methylator phenotype, or G-CIMP tumors, have

69 any significant differences by KRAS2, TP53, CpG island methylator phenotype, or microsatellite insta

70 gnificantly enriched for those harboring the CpG island methylator phenotype (p = 0.036, Chi square t

71 strongly associated with the presence of the CpG island methylator phenotype (P<0.01), inversely rela

72 ility (CIN), microsatellite instability, and CpG island methylator phenotype pathways.

73 s subgroup of pancreatic adenocarcinomas as "CpG island-methylator-phenotype positive (CIMP+)." Two o

74 CpG island methylator phenotype-positive hindbrain epend

75 actors that favor high expression and by the CpG island methylator phenotype that favors silencing in

76 tion status, microsatellite instability, and CpG island methylator phenotype were also evaluated.