ライフサイエンスコーパス: K-ras gene

1 e preferential DNA damage at codon 12 of the K-ras gene.

2 is of single nucleotide polymorphisms in the k-ras gene.

3 ight reflect an unusual vulnerability of the K-ras gene.

4 Tumors were typed for mutations in the K-ras gene.

5 pression via targeted knockout of the mutant K-ras gene.

6 U and analysed for mutations in the lacI and K-ras genes.

7 carcinomas, and in combination with mutated K-ras genes.

8 lasmid pMIKcys, which encodes a mini human c-K-ras gene (15 kb) containing a cysteine mutation at cod

9 e codons and their surrounding codons in the K-ras gene, (2) the chromatin structure, and/or (3) epig

10 1 ras (Ad.K-ras scAb), (2) an antisense (AS) K-ras gene (Ad.K-ras AS) or (3) both mda-7/IL-24 and a K

11 ines with oncogenic mutations in their H- or K-ras genes after treatment with prenyltransferase inhib

12 number of mutations, including those in the K-ras gene and CTNNB1, that codes for beta-catenin.

13 d by PCR amplification and sequencing of the K-ras gene and microsatellite PCR analysis of proliferat

14 pecific allele-specific transcription of the K-ras gene and provide further support to the thesis tha

15 subset of PILs that contain mutations of the K-ras gene and that these mutations might identify high-

16 ated mutations of the APC, beta-catenin, and K-ras genes, and microsatellite instability (MSI) status

17 Nine (69%) of these had wild-type K-ras genes, and one had microsatellite instability (MSI

18 Mutations in the K-ras gene are frequent in human cancer.

19 Mutations of the K-ras gene are known to occur in PILs, but their high pr

20 rmore, DNA adducts formed at codon 12 of the K-ras gene are poorly repaired compared with those at ot

21 Using the K- ras gene as a model system, multiplex PCR/LDR followe

22 examined the mutational status of the N- and K-ras genes at codons 12, 13, and 61 in 160 newly diagno

23 d in the promoter sequences of the BCL-2 and k-RAS genes, both of which are dis-regulated in many hum

24 r a mutation in either codon 12 or 13 of the K-ras gene by direct sequencing.

25 Clones which also expressed the activated c-K-ras gene displayed a transformed morphology, decreased

26 ons in Nf1(+/-) mast cells is decreased in a K-ras gene dose-dependent fashion in cells containing mu

27 ally form adducts at codons 12 and 14 in the K-ras gene exon 1 in intact as well as in fragmented gen

28 tro synthesized DNA fragments containing the K-ras gene exon 1 sequence with or without methylation o

29 n PCR-amplified DNA fragments containing the K-ras gene exon 1 sequence.

30 al isogenic counterparts in which the mutant K-Ras gene had been disrupted (DKS-8).

31 d high mutation frequency at codon 12 of the K-ras gene in human cancers.

32 discriminate single base differences in the K-ras gene in less than 5 min at a frequency of 1 mutant

33 nd G to A point mutations in codon 12 of the K-ras gene in many tumors.

34 adducts at codons 12 and 14 (-CGTAG-) in the K-ras gene in normal human bronchial epithelial (NHBE) c

35 nalysis of the 3' untranslated region of the K-ras gene in normal lung, spleen, liver and kidney from

36 To investigate the role of an activated K-Ras gene in the initiation and maintenance of lung ade

37 n mutations occurring throughout the p53 and K-ras genes in sputum of lung cancer patients.

38 Sequence analysis of the K-ras gene indicated that the mutations had occurred at

39 ysis of 16 cancer cell lines carrying mutant K-ras genes indicated that 50% of cancer cells harbor no

40 gene superfamily, codon 12 (-TGGTG-) of the K-ras gene is the most frequently mutated codon in human

41 mice heterozygous for a null mutation of the K-ras gene (K-ras+/-) show normal hippocampal mitogen-ac

42 METHODS AND We used H- and K-Ras gene knockout mice and subjected them to pressure

43 All of them had the K-ras gene mutated.

44 Among the 16 cases with a K-ras gene mutation in the tumor, the same mutation was

45 K-ras gene mutations have been reported as early events

46 ding is consistent with an important role of K-ras gene mutations in the transformation from normal e

47 repair capacity, and increased incidence of K-ras gene mutations in women.

48 eased p53 and beta-catenin immunoreactivity, K-ras gene mutations, microsatellite instability, and lo

49 nt mutations in codons 12, 13, and 61 of the K-ras gene occur early in the development of colorectal

50 Activating mutations in the c-K-ras gene occur in about 40% of human colorectal carcin

51 Oncogenic mutations in the K-ras gene occur in approximately 50% of human colorecta

52 cancers, irrespective of the status of their K-ras gene, only when tumor cells simultaneously express

53 se and one focal), and no alterations in the K-ras gene or p53 expression were detected.

54 Tumor cell lines bearing mutant K-ras genes required higher concentrations for inhibitio

55 pe in MM cell lines harboring a mutant N- or K-ras gene requires EZH 2 activity.

56 d type) for unknown mutations in the p53 and K-ras genes, respectively, opening prospects as an early

57 using either the nonspecific sequence or the K-ras gene sequence containing a single dG-N2-TAM at the

58 arcinomas of the pancreas and that wild-type K-ras gene status and a medullary phenotype characterize

59 e nucleotide polymorphism in codon 12 of the K-ras gene that are frequently occurring in early stages

60 Inducible expression of a mutated K-ras gene under the control of the K5 promoter led to t

61 R-spFRET detection of point mutations in the K-ras gene was accomplished in PMMA microfluidic devices

62 The K-ras gene was amplified by polymerase chain reaction an

63 istribution of carcinogen-DNA adducts in the K-ras gene was mapped at the nucleotide sequence level u

64 The K-ras gene was sequenced at codon 12 and 13 to confirm t

65 with either a constitutively activated N- or K-ras gene was used.

66 at G to A point mutations in codon 12 of the K-ras gene would occur.

67 s of the pancreas typically contain a mutant K-ras gene, yet all three RER+ carcinomas had wild-type