ライフサイエンスコーパス: TP53 gene

1 6 patients (affecting TET2, ASXL1, IDH2, and TP53 genes).

2 lts primarily from germline mutations in the TP53 gene.

3 lation involving alternative splicing of the TP53 gene.

4 DNA oligomers spanning codons 270-276 of the TP53 gene.

5 orphisms (SNPs) of the Arg249Ser unit in the TP53 gene.

6 ancers through missense mutations within the Tp53 gene.

7 53 DNA sequences in both copies of the mouse TP53 gene.

8 ge T-antigen or because of a mutation in the TP53 gene.

9 sing an endogenous and transcribed gene, the TP53 gene.

10 lin gene and in one or both alleles of their TP53 gene.

11 y associated with inherited mutations in the TP53 gene.

12 a functionally inactivating mutation in the TP53 gene.

13 h corresponded to various regions within the TP53 gene.

14 is associated with germline mutation of the TP53 gene.

15 rt arm of chromosome 17 in the region of the TP53 gene.

16 were inactivated compared with those with WT TP53 genes.

17 et DNA sequence on the p53 tumor suppressor (TP53) gene.

18 Mutations in the TP53 gene, altering p53 functionality, are associated wi

19 Mutation of the TP53 gene alters its response pathway, and is central to

20 ) patients harbor germ line mutations in the TP53 gene and are at increased risk of hormone receptor-

21 Mutations of the TP53 gene and dysregulation of the TP53 pathway are impo

22 istically, E2F-4 binds constitutively to the TP53 gene and induces transcription.

23 A comprehensive analysis of the TP53 gene and its protein status was carried out on a pa

24 gnized class I HDAC-dependent control of the TP53 gene and provide evidence for a contribution of MYC

25 at HDAC1, HDAC2 and MYC directly bind to the TP53 gene and that MYC recruitment drops upon HDAC inhib

26 In contrast, CN alterations of the TP53 gene and the MYC family members were predominantly

27 ive type frequently contain mutations of the TP53 gene, and that 9p loss and CDKN2A deletions are ass

28 CLLs, 11 with mutations in either the ATM or TP53 genes, and compared with that induced by ionizing r

29 tudies that use probes to the SMS, RARA, and TP53 genes are an effective way to determine the true HE

30 y common to all classes of specimen, whereas TP53 gene C742T and G818C mutations were significantly m

31 The number of TP53 gene copies was investigated in gastric diseases by

32 ection limits for analyzing the Smallpox and TP53 genes correspond to 0.1 nM.

33 er cell invasion and reciprocally why mutant TP53 gene does not systematically induce cancer progress

34 To determine whether TP53 gene dosage affects the transcriptional regulation

35 demonstrate that many genes are affected by TP53 gene dosage for their expression.

36 the miR-15a/miR-16-1 cluster, miR-34 family, TP53 gene, downstream effectors cyclin-dependent kinase

37 tic point mutations (R267W and E258D) in the TP53 gene during the initiation of astrocytoma in a pati

38 The TP53 gene encodes 12 distinct isoforms, some of which ca

39 Human TP53 gene encodes the tumor suppressor p53 and, via alte

40 The TP53 gene, encoding tumour suppressor protein p53, is lo

41 Reduced TP53 gene expression and amplification/overexpression of

42 GSOC correlated with enrichment of a mutated TP53 gene expression signature and of EGFR pathway genes

43 ectly with the TP53 DNA sequence to regulate TP53 gene expression.

44 m 28 patients with germline mutations to the TP53 gene for loss of heterozygosity at TP53 using techn

45 In conclusion, deletion of the TP53 gene from MCF-10A cells eliminated p53 functions, a

46 Sequencing the entire TP53 gene from various types of cancer using next-genera

47 like other solid tumors, no mutations in the TP53 gene have been identified to date in random panels

48 However, allelic loss was observed at the TP53 gene in 25% of informative cases.

49 ences has offered a humanized replica of the TP53 gene in a murine genetic environment.

50 Using DNA-based sequencing, we evaluated the TP53 gene in all 44 patients.

51 c cell gene targeting was used to delete the TP53 gene in the non-tumorigenic epithelial cell line, M

52 Inactivation of the ATM or TP53 gene is frequent in B-cell lymphocytic leukemia (B-

53 Although the TP53 gene is frequently mutated in human cancers, the TP

54 However, the TP53 gene is frequently mutated in tumors, and the role

55 Although the TP53 gene is mutated in many PIPs, it is unclear whether

56 Thus, beyond miR-125b and miR-504, the human TP53 gene is negatively regulated by two more miRNAs: mi

57 ave obtained show that loss of the wild-type TP53 gene is observed in under half (44%) of all tumours

58 icted to be effective in tumors in which the TP53 gene is wild type, by preventing TP53 protein degra

59 The tumor suppressor p53, encoded by the TP53 gene, is recognized as the guardian of the human ge

60 transfected with a BAC containing the human TP53 gene locus expressed p53, showing native promoter e

61 t finding of P14ARF loss in conjunction with TP53 gene loss in some tumors suggests the protein may h

62 Only one of the 14 cases with 17p LOH/TP53 gene mutation also had LOH for 1p and 19q, and sign

63 least a 50% risk of being a BRCA1, BRCA2, or TP53 gene mutation carrier were recruited from August 19

64 TP53 gene mutation is associated with poor prognosis in

65 we searched for allele loss for 5q loci and TP53 gene mutations in the same leukemic samples.

66 f this study is to correlate the presence of TP53 gene mutations with the clinical outcome of a cohor

67 ging drugs such as cisplatin, rarely exhibit TP53 gene mutations, express normal p53 protein, and und

68 bset of such tumors, resistance is linked to TP53 gene mutations.

69 Mutations in the TP53 gene not only inactivate its tumor suppressor funct

70 Tumor-driving mutations in the TP53 gene occur frequently in human cancers.

71 LOH for 17p and/or mutations of the TP53 gene occurred in 14 of these 55 tumors.

72 frequencies of all types of mutations in the TP53 gene of nonsmokers' lung tumors and in the cII tran

73 rs, whereas tumors that retain the wild-type TP53 gene often use alternative mechanisms to repress th

74 to harbor a tumor suppressor gene(1) and the TP53 gene on 17p.

75 er group of seven cell lines had a wild-type TP53 gene or a mutation in exons 1-4 of TP53 and concomi

76 nearly all cancer types by mutations in the TP53 gene or by overexpression of its negative regulator

77 We investigated whether mutations in the TP53 gene or the degree of expression of p53 protein in

78 Compared with patients with wild-type ATM/TP53 genes, patients with ATM mutations had statisticall

79 Although we confirmed a TP53 gene-PML NB association, immuno-TRAP allowed us to

80 lines characteristically retain a wild-type TP53 gene, providing an opportunity to test the relevanc

81 Hupki mouse with the homologous normal human TP53 gene sequences has offered a humanized replica of t

82 Here, we present the results of TP53 gene sequencing and fluorescence in situ hybridizat

83 Accurate assessment of TP53 gene status in sporadic tumors and in the germline

84 lyzed tumor samples independently of ATM and TP53 gene status, whereas 6 of 26 B-CLLs, mostly ATM mut

85 cell senescence independent of TAp63 and/or TP53 gene status.

86 cell lines that carried six mutations in the TP53 gene that encodes the tumour suppressor P53.

87 The TP53 gene underwent ultra-deep-next generation sequencin

88 Only the TP53 gene was mutated at significant frequency across al

89 Germline sequencing of the TP53 gene was performed.

90 Strikingly, for the famous 'TP53' gene, we not only accurately identified the apopto

91 Mutations and polymorphisms in the TP53 gene were confirmed by traditional sequencing.

92 ing the G(2)/M transition in the cells whose TP53 genes were inactivated compared with those with WT

93 ith p53 and that mutations in the ARID1A and TP53 genes were mutually exclusive in tumor specimens ex

94 progression of early stages of MDS, and the TP53 gene when mutated, causes transformation to AML.

95 usively in glioblastomas harboring wild-type TP53 genes, which raises the alternative hypotheses that

96 d tumors carry inactivating mutations in the TP53 gene, while in the remaining cases, TP53 activity i

97 tations in the KRAS, NRAS, BRAF, PIK3CA, and TP53 genes, with discordant results between paired sampl