ライフサイエンスコーパス: p16 gene

1 difier when cosegregating with a deleterious p16 gene.

2 nd 4 of 15 (26.7%) showed methylation of the p16 gene.

3 condary to homozygous deletion of the CDKN2A/p16 gene.

4 ne, that contains homozygous deletion of the p16 gene.

5 ion, thus suggesting a novel function of the p16 gene.

6 8%) studied, all through inactivation of the p16 gene.

7 t unique rearrangement involving the p15 and p16 genes.

8 ce lacking p53, p21, retinoblastoma (Rb), or p16 genes.

9 primarily due to codeletion of the MTAP and p16 genes.

10 EAC has thus far been limited to the CDKN2A (p16) gene.

11 stitutes a common mechanism in silencing the p16 gene, 3) p16 inactivation may play an important role

12 high as, if not greater than, those for the p16 gene (80% at diagnosis and 74% at relapse).

13 ranscription factor binding proteins and the p16 gene, a key regulator of the cell cycle.

14 ties and abnormal P16 expression in 59% with P16 gene abnormalities.

15 Here we show that p16 gene activity inversely modulates p53 status and fun

16 duced by an adenoviral vector containing the p16 gene (AdRSVp16) produced a p16 protein that suppress

17 It is suggested that alterations of the p16 gene affect a subset of PILs that contain mutations

18 papillomavirus detected, only one also had a p16 gene alteration.

19 In addition, the association of p16 gene alterations and abnormalities of p53, PRAD-1 (c

20 Since then, a high frequency of p16 gene alterations were observed in many primary tumor

21 nctionally damaging mutations of the CDKN2A (p16) gene: an Arg 24 Pro substitution in exon 1 in one f

22 y tumor as the origin for dysfunction of the p16 gene and implicate CpG island methylation as the maj

23 We examined the CDKN2A/p16 gene and p16 protein in NFs and MPNSTs from patients

24 3.0; P = 0.03), and with methylation of the p16 gene and the MINT31 locus [odds ratio, 12.2 (P = 0.0

25 A methyltransferase activity, methylated the p16 gene, and suppressed the expression of p16.

26 at aberrant promoter hypermethylation of the p16 gene, and to a lesser extent, DAP kinase, occurs fre

27 the expression and genetic integrity of the p16 gene appear in intermediate lesions, and the inactiv

28 shown that the preproenkephalin (ppENK) and p16 genes are aberrantly methylated in pancreatic adenoc

29 y suggests that abnormalities of the P15 and P16 genes are common in both early and advanced stages o

30 hoblastic leukemia (T-ALL), both the p15 and p16 genes are deleted at a high frequency, with p16 gene

31 The P15 and P16 genes are intricately linked on 9p21 and can be inac

32 an cell lines, J82 and LD419, expressing the p16 gene at 25-fold different levels showed that the two

33 promoter methylation of RASSF1A gene but not p16 gene (both frequently inactivated by promoter methyl

34 ial contribution of somatic silencing of the p16 gene by DNA methylation in 30 cases of sporadic cuta

35 etic alteration, aberrant methylation of the p16 gene, can be an early event in lung cancer and may c

36 genes are deleted at a high frequency, with p16 gene deletion occurring slightly more frequently tha

37 Homozygous p16(INK4A) (p16) gene deletion is frequent in primary tumor cells fr

38 Recent studies have reported frequent p16 gene deletions in cell lines from squamous cell carc

39 To restore the missing wild-type p16 gene efficiently in glioma cells an adenovirus vecto

40 esent study we investigated the frequency of p16 gene exon 2 mutations in 35 malignant gliomas, using

41 ebularine to T24 cells induces and maintains p16 gene expression and sustains demethylation of the 5'

42 se activity of CDK4 and CDK6, members of the p16 gene family play different roles in controlling cell

43 cts that may contribute to the impairment of p16 gene function.

44 cancer cell line in which a hypermethylated p16 gene had been reactivated by transient treatment wit

45 ence of point mutations and deletions of the p16 gene in 33 SCCHN.

46 lthough this study revealed deletions of the p16 gene in a significant number of sporadic primary and

47 Transcriptional silencing of the p16 gene in association with methylation of its 5'-CpG i

48 ate the expression of the densely methylated p16 gene in cancer cells.

49 in expression correlated with methylation of p16 gene in carcinoid tumors (p = 0.006).

50 ndicate a potentially important role for the p16 gene in head and neck tumorigenesis.

51 ion of the CpG island in the promoter of the p16 gene in human bladder cancer cells did not stop the

52 These results suggest that deletion of p16 gene in JKB human ALL cells is associated with dysre

53 (iii) Overexpression of P16 gene in the hepatoma cell lines Hep G2 and Hep 3B en

54 fine the methylation status of the ppENK and p16 genes in various grades of PanINs.

55 In addition, p16 gene inactivation was determined by DNA sequence ana

56 and relatively simple method for evaluating p16 gene inactivation.

57 Thus, inactivation of the p16 gene is a common event in all non-small cell lung ca

58 Our data confirm that the p16 gene is frequently inactivated in NSCLC.

59 The p16 gene is resilenced with kinetics similar to 5-aza-Cd

60 lation-related inactivation of the ppENK and p16 genes is an intermediate or late event during pancre

61 However, homozygous deletion of the p16 gene locus and point mutation of p16 gene were only

62 timing and kinetics of remethylation of the p16 gene locus under conditions of either G(0)-G(1) grow

63 ene in 3 of 25 tumors, suggesting homozygous p16 gene loss.

64 Methylation of the p16 gene may contribute to the malignant transformation

65 The biological and clinical implications of p16 gene methylation in multiple myeloma (MM) are still

66 r goal was to determine whether the aberrant p16 gene methylation seen in human tumors is a conserved

67 demonstrate that human glioma cells contain p16 gene microdeletions and rearrangements that contribu

68 ently seen in malignancy, alterations in the p16 gene, microsatellite instability and loss of heteroz

69 JKB cells were transfected either with a p16 gene mutated at position 119 (E119G) to confer tempe

70 The presence of p16 gene mutations only in glioblastomas suggests that t

71 s to active GAs, whereas that encoded by the P16 gene of pumpkin endosperm leads to biosynthesis of i

72 eviously shown to contain alterations in the p16 gene or its promoter.

73 genetic evidence recently suggested that the p16 gene plays a role in the progression of these "duct

74 histochemical analysis for expression of the p16 gene product is an accurate and relatively simple me

75 We conclude that altered expression of the p16 gene product occurs at a high frequency in human pit

76 By Western blot analysis, the p16 gene product was undetectable in 25 human pituitary

77 P15 and P16 gene promoter methylation was found in 45% and 29% o

78 idyl)-1-butanone were hypermethylated at the p16 gene promoter; most important, this methylation chan

79 Furthermore, we found that the p15 or p16 gene promoters were frequently methylated in the leu

80 ere also positive for LOH on 9p21 (where the p16 gene resides), implying that both p16 alleles were i

81 experiment using a probe from exon 1 of the p16 gene, signal was detected from MCA products of a col

82 (HNSC) cell lines and 46 primary tumors for p16 gene status by protein, mRNA, and DNA genetic/epigen

83 ence of a chromatin boundary upstream of the p16 gene that is lost when this gene is aberrantly silen

84 On the other hand, methylation of the p16 gene was a rare event, occurring in 4% (2 of 49) of

85 The rat p16 gene was cloned and sequenced, and the predicted ami

86 on was recapitulated in human SCCs where the p16 gene was coordinately methylated in 75% of carcinoma

87 Methylation of the p16 gene was detected in sputum from 23 of 66 controls.

88 Homozygous deletion of the p16 gene was detected in the 4 remaining cases by micros

89 Aberrant methylation of the p16 gene was found in 12% of PanIN-1A, 2.6% of PanIN-1B,

90 Hypermethylation of the p16 gene was found in 60% of MI+ cancers, compared to on

91 No deletion in the p16 gene was found in any of the tumor cell lines examin

92 We reported previously that the p16 gene was genetically inactivated in 82% of pancreati

93 observed in tumors from smokers, whereas the p16 gene was inactivated in tumors from nonsmokers only

94 The p16 gene was methylated in 27% (19 of 71) of adenomas.

95 A comprehensive genetic analysis of the p16 gene was performed in 33 primary sporadic ciliochoro

96 Sequence analysis of the p16 gene was performed on those tumors with 9p21 loss of

97 Furthermore, a dormant p16 gene was reactivated in T24 cells growing in nu/nu r

98 Alternative alteration of K-ras and p16 genes was an independent prognostic factor in human

99 ll ALL (T-ALL) patients have deletion in the p16 gene, we examined the status of the MTAP gene in T-A

100 iplex PCR, homozygous deletions of the CDKN2/p16 gene were detected in 24 GBMs (57%) and in 2 anaplas

101 to methylate the CpG island in exon 2 of the p16 gene were observed after transient demethylation by

102 of the p16 gene locus and point mutation of p16 gene were only observed in tumors from smokers, wher

103 , and higher basal levels of CDK2, CDK4, and p16 genes were constitutively expressed in PC-3 cells.

104 e phenotype, mutations at both the K-ras and p16 genes were sought within PILs of 10 pancreata resect

105 tion of methylation in the CpG island of the p16 gene will require methylation analysis of the three

106 The P16 gene with specific multi-methylated sites, a well-st