ライフサイエンスコーパス: v-Ha-ras

1 deficient cell types could be transformed by v-Ha-Ras.

2 or example, mammary tumors initiated by neu, v-Ha-ras and c-myc have high levels of active Erk/MAP ki

3 m initiated by neu, heregulin/NDF, TGFalpha, v-Ha-ras and c-myc in transgenic mice.

4 s, a remarkable synergy occurred between the v-Ha-ras and HPV16 E6/E7 oncogenes in the development of

5 hey showed that activated forms of c-Ha-ras (v-Ha-ras) and c-src (v-src or srcY527F), two molecules t

6 ansferase inhibitor can induce regression of v-Ha-ras-bearing tumors by multiple mechanisms, includin

7 Finally, the previously described v-Ha-ras block of keratinocyte differentiation correlate

8 wnregulation by Myc and v-Src but not c-Fos, v-Ha-Ras, c-Src or c-Ski.

9 These unexpected observations indicate that v-Ha-ras can lead to both NE and non-NE hyperplasia/neop

10 rries a transgene consisting of an oncogenic v-Ha-ras coding region flanked 5' by a mouse zeta-globin

11 Consistent with this idea, expression of v-Ha-ras complemented these mutants in primary bone marr

12 hat carry the Tg.AC transgene (consisting of v-Ha-Ras driven by an embryonic zeta-globin promoter) wo

13 rine cell (PNEC) hyperplasia/neoplasia using v-Ha-ras driven by the neural/neuroendocrine (NE)-specif

14 belief that the zeta-globin promoter directs v-Ha-ras expression in erythroid progenitor cells, ultim

15 s in ODC activity and putrescine levels, but v-Ha-ras expression was not affected in the regressed tu

16 in Tg.AC mice, resulting from skin-specific v-Ha-ras expression, was completely abrogated in the ksr

17 FVB/n mice transgenic for v-Ha-ras gene (R+) were crossed with transgenic C57BL/6

18 evelop in bitransgenic mice bearing both the v-Ha-ras gene and a heterozygous mutant p53 allele tend

19 Transduction with an activated v-Ha-ras gene, which signals downstream of the EGF-R, in

20 v-Ha-ras has been demonstrated previously to induce neur

21 rategies can be selected to collaborate with v-Ha-ras in tumorigenesis.

22 B2/Her2) transgene but had no effect on MMTV-v-Ha-ras-induced cancer, although both oncogenes rely on

23 tiated tumor cell lines, but not in c-myc or v-Ha-ras initiated tumor cell lines.

24 Tumor v-Ha-ras levels were 3-fold higher with arsenic plus TPA

25 for LOH using the mouse mammary tumor virus/v-Ha-ras mammary carcinoma model in female (FVB/N x Mus

26 3'-kinase, appears KSR1 independent, whereas v-Ha-ras-mediated skin cancer, signaled through the Raf-

27 rs independent of KSR1, KSR1 is obligate for v-Ha-ras-mediated skin tumor formation.

28 and found that the tumor regression in MMTV-v-Ha-ras mice could be attributed entirely to elevation

29 cond study, tumor formation was monitored in v-Ha-ras mice expressing or lacking p27(Kip1).

30 r, the results show that tumor onset in MMTV/v-Ha-ras mice is p21-dependent with loss of p21 associat

31 MMTV-v-Ha-ras mice were also interbred with MMTV-c-myc mice t

32 sis and the resultant tumor regression, MMTV-v-Ha-ras mice were interbred with p53(-/-) mice.

33 Similar to its effects in v-Ha-ras mice, loss of p21(Cip1) accelerated tumor onset

34 hand, had no effect on tumor growth rate in v-Ha-ras mice.

35 nic mouse line (Tg.AC) carrying an activated v-Ha-ras oncogene fused to the embryonic zeta-globin pro

36 ce with Tg.AC transgenic mice, which express v-Ha-ras oncogene in the skin, and compared the suscepti

37 omas occurred in Tg.AC mice, which carry the v-Ha-ras oncogene, that received arsenic in the drinking

38 y tumor models to evaluate how the c-myc and v-Ha-ras oncogenes influence tumor growth characteristic

39 n of murine melanocytes by transfection with v-Ha-ras or Ela was accompanied by depigmentation and le

40 ow that heregulin but not her2/neu, c-Myc or v-Ha-ras plays a major role in constitutive NF-kappaB ac

41 mice harboring the mouse mammary tumor virus/v-Ha-ras (ras) transgene that induces breast tumors.

42 s study investigates whether HPV16 E6/E7 and v-Ha-ras synergize in vivo.

43 main of Ron (TK(-/-) mice) were crossed with v-Ha-ras (Tg.AC) transgenic mice; the resulting TK(-/-)

44 p50 with a retrovirus for the expression of v-Ha-Ras to determine whether individual NF-kappaB famil

45 This LOH provided a clue that linked v-Ha-ras to the inactivation of the Ink4a locus in 25 of

46 AC transgenic mouse, a line that harbors the v-Ha-ras transgene and spontaneously develops an array o

47 ion, we showed that mice expressing the MMTV/v-Ha-ras transgene developed tumors earlier and at highe

48 to skin carcinogenesis via activation of the v-Ha-ras transgene likely in KSCs.

49 e tumorigenesis by cooperating with either a v-Ha-ras transgene to induce benign skin papillomas or p

50 E2F1 transgene is found to cooperate with a v-Ha-ras transgene to induce skin tumors in double trans

51 DGKiota-deficient mice with mice carrying a v-Ha-Ras transgene, and then we assessed tumor formation

52 lyzed by in situ hybridization expressed the v-Ha-ras transgene.

53 gression in mouse mammary tumor virus (MMTV)-v-Ha-ras transgenic mice and tumor stasis in MMTV-N-ras

54 se (ODC) overexpression in the skin of TG.AC v-Ha-ras transgenic mice induces the formation of sponta

55 To test this hypothesis, we crossed MMTV/v-Ha-ras transgenic mice into a p21-deficient background

56 In v-Ha-ras transgenic mice, C/EBPbeta deficiency also led

57 arcinogenesis in genetically initiated Tg.AC v-Ha-ras transgenic mice.

58 rcinomas in mouse mammary tumor virus (MMTV)-v-Ha-ras transgenic mice.

59 The v-Ha-ras transgenic Tg.AC mouse line has proven to be a

60 ficiently to L-744,832 treatment as the MMTV-v-Ha-ras tumors, although no induction of apoptosis was

61 h L-744,832 regressed as efficiently as MMTV-v-Ha-ras tumors, although this response was found to be

62 in vivo has been investigated by expressing v-Ha-ras under control of the neural/neuroendocrine spec

63 CEF overexpressing other oncogenes including v-Ha-ras, v-Src, c-Fos, and Myc revealed that it's overe

64 er with arsenic plus TPA than TPA alone, and v-Ha-ras was overexpressed early on in arsenic-treated f