ライフサイエンスコーパス: K-ras oncogene

1 nflammation, and activating mutations of the K-Ras oncogene.

2 a mouse model of lung cancer induced by the K-Ras oncogene.

3 r targets in tumors expressing the activated K-Ras oncogene.

4 to malignant transformation by an endogenous K-ras oncogene.

5 ant transformation by an introduced H-ras or K-ras oncogene.

6 that have been transfected with an activated K-ras oncogene.

7 ncer, specifically G to A transitions in the K-ras oncogene.

8 to 30% of adenocarcinomas show mutations in K-RAS oncogene.

9 patients for codon 12 point mutations of the K-ras oncogene.

10 he detection of point mutations in the human K-ras oncogene.

11 e in pancreatic cancer are activation of the K-ras oncogene (~90%) and inactivation of the p16 (~95%)

12 rothioate oligonucleotides, which target the K-ras oncogene (a gene that is mutated in 85 to 95% of p

13 esis of many human malignancies, .OH-induced K-ras oncogene activation could be an important mechanis

14 yte-derived .OH-induced DNA damage can cause K-ras oncogene activation, and suggests that there may b

15 y be a characteristic pattern of .OH-induced K-ras oncogene activation.

16 report LDR-SERS multiplex SNP genotyping of K-Ras oncogene alleles at 10 pM detection levels, optimi

17 In colon cancer, the frequently mutated K-ras oncogene also can regulate VEGF expression, but th

18 Signaling through the K-ras oncogene, also frequently mutated in benign coloni

19 Y80A can also detect the G13D mutation in K-ras oncogene, an A/C mismatch embedded in a G/C rich s

20 ice, which undergo somatic activation of the K-ras oncogene and display morphologic changes in alveol

21 nterrelationship between activation of the c-K-ras oncogene and increased expression of cyclin D1 and

22 Activating mutations in K-Ras oncogene and increased expression of FOXM1 protein

23 MCF10A cells that stably express the K-Ras oncogene and obscurin short hairpin RNA (shRNA), b

24 adenocarcinomas, including mutations in the K-ras oncogene and p53 and DPC4 tumor suppressor genes,

25 s have established that splicing of both the K-ras oncogene and proto-oncogene is altered in CRC in f

26 enocarcinomas for genetic alterations in the K-ras oncogene and the p16, p53, and DPC4 tumor suppress

27 l adenocarcinomas including mutations in the K-ras oncogene and the p53 and DPC4 tumor suppressor gen

28 In addition to mutations in the k-ras oncogene and the p53 gene, which are frequently se

29 Many patients have mutations of the K-ras oncogene, and various tumour-suppressor genes are

30 unknown, activating mutations in the N- and K-ras oncogenes are common.

31 ray was used to detect a point mutation in a K-ras oncogene at a level of 1 mutant DNA in 10,000 wild

32 at an activating hot spot, codon 12, of the K-ras oncogene, but none in their adjacent normal tissue

33 53 tumor suppressor gene (exons 5-8) and the K-ras oncogene (codons 12 and 13) by polymerase chain re

34 elop lung cancer from activation of a latent K-ras oncogene had high intratumoral JNK activity and lo

35 ons in the p53 tumor suppressor gene and the K-ras oncogene have been frequently found in sputum and

36 to the appearance of G to A mutations in the K-ras oncogene in colorectal tumors.

37 activation of expression of a single copy of K-ras oncogene in cultured murine embryonic cells induce

38 Whereas the effect of K-ras oncogenes in the intestine can been observed only

39 Since activation of the K-ras oncogene is believed to play a crucial role in the

40 Mutational activation of the K-Ras oncogene is well established as a key genetic step

41 expression, thereby activating the PLAU and K-Ras oncogenes is important for distinct aspects of cel

42 Chronic pancreatitis, K-ras oncogene mutations, and the subsequent generation

43 he similarity of the mutation spectra in the K-ras oncogene observed in tobacco smoke-induced tumors,

44 Mutations in the Kirsten-ras (K-ras) oncogene occur early and frequently (approximatel

45 imultaneously, via conditional activation of K-ras oncogene or deletion of Nf1 or Pten tumor suppress

46 However, the precise role that K-ras oncogenes play in tumor formation is still unclear

47 gnant stages of pancreatic adenocarcinoma is K-ras oncogene point mutation.

48 ctivating point mutations in codon 12 of the K-ras oncogene, suggesting that K-ras mutational status

49 ion with transforming growth factor-alpha or K-Ras oncogene, synergistically induced AR expression an

50 tify a single base mutation in codon 12 of a K-ras oncogene that has high diagnostic value for colore

51 Since mouse lung tumors present a mutated K-ras oncogene, we hypothesized that this special suscep

52 Whereas cells lacking the K-Ras oncogene were unable to efficiently form xenograft