ライフサイエンスコーパス: ras oncogene

1 tive in mouse keratinocytes transformed by a ras oncogene.

2 thelial hyperplastic phenotype induced by Ha-ras oncogene.

3 t transformation by an introduced H-ras or K-ras oncogene.

4 lammation, and activating mutations of the K-Ras oncogene.

5 r similar to that caused by the activated Ha-ras oncogene.

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

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

8 esistant to a subsequent transformation by H-ras oncogene.

9 inal epithelial cells harboring an inducible ras oncogene.

10 er, specifically G to A transitions in the K-ras oncogene.

11 d kinases (MAPK/ERKs) when compared to the H-Ras oncogene.

12 SW480.7 cells contain an activated Ki-ras oncogene.

13 ma cell lines PA-1 that contain an activated ras oncogene.

14 growth advantage to cells transformed by the ras oncogene.

15 fied by virtue of its down-regulation by the ras oncogene.

16 o 30% of adenocarcinomas show mutations in K-RAS oncogene.

17 ined for the presence of mutations in the Ha-Ras oncogene.

18 rative transformation with the activated T24 ras oncogene.

19 s a necessary component in the action of the ras oncogene.

20 , is an antioncogene that down-regulates the RAS oncogene.

21 primer-labeled (109 bp) PCR product of the H-ras oncogene.

22 mids and plasmids expressing the Erb-B2 or v-ras oncogene.

23 -kDa gelatinase B expression by an activated ras oncogene.

24 previously correlated with the presence of a ras oncogene.

25 NIH-3T3 cells transformed by an activated Ha-ras oncogene.

26 tients for codon 12 point mutations of the K-ras oncogene.

27 formation of primary cells with an activated ras oncogene.

28 and abolish procancer pathways initiated by Ras oncogene.

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

30 controlled by Hsp72 was associated with the Ras oncogene.

31 targets in tumors expressing the activated K-Ras oncogene.

32 malignant transformation by an endogenous K-ras oncogene.

33 otch mammary cancer cells which also express ras oncogene.

34 igned to target tumors with mutations of the ras oncogene.

35 n both p53 alleles and harbor an activated H-ras oncogene.

36 ant to breast cancers induced by the neu and ras oncogenes.

37 ive autocrine loop coordinately activated by ras oncogenes.

38 associated with frequent activations of the Ras oncogenes.

39 5' G of the GG doublet in codon 12 of human ras oncogenes.

40 signaling pathway such as the Her-2/neu and ras oncogenes.

41 cotransformed with HPV-16 E6 and E7 and c-Ha-ras oncogenes.

42 roblasts (MEFs) expressing the E1A and T24 H-ras oncogenes.

43 la homologue of mammalian H-ras, K-ras and N-ras oncogenes.

44 tions in rat sarcoma viral oncogene homolog (RAS) oncogenes.

45 ity of cotransfected, malignantly activated, ras oncogenes (5-7-fold).

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

47 thioate oligonucleotides, which target the K-ras oncogene (a gene that is mutated in 85 to 95% of pan

48 Because the ras oncogene, a gene activated in many human cancers tre

49 papillary thyroid carcinoma was positive for ras oncogene abnormalities.

50 Our results imply that targeting NRAS or RAS oncogene-activated pathways is a good therapeutic st

51 Among the pivotal genetic alterations are Ki-RAS oncogene activation and p53 tumor suppressor gene in

52 is of many human malignancies, .OH-induced K-ras oncogene activation could be an important mechanism

53 Given the high frequency of ras oncogene activation in several common human cancers,

54 have compared the proliferative response to ras oncogene activation in two normal cell types--fibrob

55 ibitory effect on primary mesenchymal cells, RAS oncogene activation induces a proliferative phenotyp

56 e-derived .OH-induced DNA damage can cause K-ras oncogene activation, and suggests that there may be

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

58 y mechanisms that bypass the requirement for Ras oncogene activity and drive leukemia relapse.

59 ascades play the critical role in regulating Ras oncogene activity by phosphorylation-dependent mecha

60 eport LDR-SERS multiplex SNP genotyping of K-Ras oncogene alleles at 10 pM detection levels, optimiza

61 including the ability to be transformed by a ras oncogene alone.

62 The Ras oncogene also activates signaling via the related Rh

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

64 ny of these effects are cell autonomous, the ras oncogene also regulates the expression of genes that

65 However, there is increasing evidence that RAS oncogenes also alter the mechanical properties of bo

66 Signaling through the K-ras oncogene, also frequently mutated in benign colonic

67 Uncovering how RAS oncogenes alter cell mechanics will lead to a better

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

69 as potential anticancer agents targeting the ras oncogene and are currently in clinical trials.

70 e, which undergo somatic activation of the K-ras oncogene and display morphologic changes in alveolar

71 feration and tumorigenicity activated by the ras oncogene and highlight an alternative functional rol

72 We studied the interaction between the ras oncogene and hypoxia in up-regulating glut1 mRNA lev

73 errelationship between activation of the c-K-ras oncogene and increased expression of cyclin D1 and R

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

75 latency and in transgene expression among N-ras oncogene and N-ras proto-oncogene transgenics.

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

77 denocarcinomas, including mutations in the K-ras oncogene and p53 and DPC4 tumor suppressor genes, us

78 have established that splicing of both the K-ras oncogene and proto-oncogene is altered in CRC in fav

79 y, we show that DiRas3 associates with the H-Ras oncogene and that activation of H-Ras enforces this

80 diated by the cooperation of the activated H-ras oncogene and the inactivated p53 tumor suppressor ge

81 pes is in agreement with the idea that the N-ras oncogene and the N-ras proto-oncogene act through th

82 We compared the tumorigenic effects of the N-ras oncogene and the N-ras proto-oncogene in lymphoid an

83 ocarcinomas for genetic alterations in the K-ras oncogene and the p16, p53, and DPC4 tumor suppressor

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

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

86 UPase expression is affected by the c-H-ras oncogene and various cytokines through unknown mecha

87 Our experiments are the first to show that ras oncogenes and oncogenic transcription factors can in

88 d from p21 knockout mice, transformed with a ras oncogene, and injected subcutaneously into nude mice

89 ng the epidermal growth factor receptor, the ras oncogene, and the immune system.

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

91 Activating mutations in the RAS oncogene are common in cancer but are difficult to t

92 Mutations in the Ras oncogene are one of the most frequent events in huma

93 nknown, activating mutations in the N- and K-ras oncogenes are common.

94 Although activating mutations in RAS oncogenes are known to result in aberrant signaling

95 ras oncogenes are mutated in at variety of human tumors,

96 30% of all human cancers; however, different RAS oncogenes are preferentially associated with differe

97 Furthermore, unlike the Ras oncogene, ARHI inhibits cell growth, and loss of its

98 Human tumor cell lines with or without a ras oncogene as well as a pair of isogenic cell lines wi

99 f ribozymes targeted against the activated H-ras oncogene as well as against the nuclear proto-oncoge

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

101 t were examined had the mutation of the c-Ki-ras oncogene at codon 12 and all tumors expressed blood

102 kemogenesis driven by Bcr-Abl or activated N-Ras oncogenes but enhancing the selection for and leukem

103 t an activating hot spot, codon 12, of the K-ras oncogene, but none in their adjacent normal tissues.

104 Y294002 radiosensitized cells bearing mutant ras oncogenes, but the survival of cells with wild-type

105 volved in the pattern of activation of human ras oncogenes, by causing GC-->AT transitions preferenti

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

107 RAS oncogenes (collectively NRAS, HRAS and especially KR

108 ion of primary murine fibroblasts by the E1A/ras oncogene combination and dramatically accelerated my

109 This may occur by the ras oncogene compromising an S-phase checkpoint.

110 2-145%), thus demonstrating efficacy against ras oncogene-containing tumors in vivo.

111 n that enforced expression of an activated H-ras oncogene converted non-tumorigenic, TNF-resistant C3

112 Human tumor cells containing ras oncogenes display enhanced sensitivity to 1-beta-D-a

113 However, because introduction of ras oncogenes does not increase radiation survival in al

114 mation of NIH-3T3 cells with an activated Ha-ras oncogene down-modulated RAR expression and abolished

115 ogether, these experimental results define a RAS oncogene-driven function that is critical for leukem

116 show that Fancd2-deficient mice are prone to Ras-oncogene-driven skin carcinogenesis, while Usp1-defi

117 In particular, malignant transformation by Ras oncogenes exploits mitochondrial STAT3 functions.

118 rmation and extracellular matrix invasion of ras oncogene expressing NIH 3T3 fibroblasts by expressin

119 n(TAM67) had no effect on the ability of the ras oncogene-expressing cells to grow in soft agar or in

120 nsformed cells was dependent on the level of ras oncogene expression.

121 ogenic cell lines with and without activated Ras oncogene expression.

122 c flux, a process that required RAB24 member RAS oncogene family (RAB24), a small GTPase that facilit

123 n the small GTPases RAS and RAP1A, member of RAS oncogene family (RAP1) in human Kit 225 lymphoid cel

124 d RUNX3; association of SVZ involvement with Ras oncogene family members, such as RAP2A, and the meta

125 ssociated athanogene 5, Rab7L1 (RAB7, member RAS oncogene family-like 1), and Cyclin-G-associated kin

126 ine truncating mutation in the member of the RAS oncogene family-like 3 (RABL3) gene.

127 ras-bound GTP to GDP, thereby converting the ras oncogene from its active to inactive form.

128 ouse line (Tg.AC) carrying an activated v-Ha-ras oncogene fused to the embryonic zeta-globin promoter

129 op lung cancer from activation of a latent K-ras oncogene had high intratumoral JNK activity and low

130 s in the p53 tumor suppressor gene and the K-ras oncogene have been frequently found in sputum and br

131 RAS oncogenes have been implicated in >30% of human canc

132 Mutations in the ras oncogenes have been linked to many different cancers

133 nown, although adhesion or transformation by ras oncogenes have been shown to protect epithelial cell

134 p53-normal MEFs expressing the E1A and T24 H-ras oncogenes have suffered compensatory alterations tha

135 We found that all three RAS oncogenes have the ability to induce myeloid leukemi

136 of patients with neuroblastoma RAS viral (v-ras) oncogene homolog (NRAS)-mutant melanoma is currentl

137 titutively active neuroblastoma RAS viral (v-ras) oncogene homolog with Gly12Val substitution (NRAS(G

138 h wild-type BRAF, neuroblastoma RAS viral (v-ras) oncogene homolog, and phosphatase and tensin homolo

139 mutation in NRAS [neuroblastoma RAS viral (v-ras) oncogene homolog].

140 and FGFR3, tyrosine phosphatase PTPN11, and RAS oncogene homologs HRAS and KRAS) from 16 of 22 tubul

141 erature-sensitive activating mutation in the Ras oncogene homologue let-60.

142 Unlike the Ras oncogene, however, ARHI inhibits tumor cell growth.

143 Ras oncogenes (Hras, Kras and Nras) are important driver

144 ults strongly support the involvement of the ras oncogene in both the initiation and regression of ke

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

146 tivation of expression of a single copy of K-ras oncogene in cultured murine embryonic cells induced

147 When coexpressed with the activated Ha-ras oncogene in double transgenic mice, EGFr had no appa

148 to inhibit the transforming activity of the ras oncogene in NIH 3T3 fibroblasts and was hence named

149 Prolonged expression of a ras oncogene in primary cells accelerates the natural pr

150 th Tg.AC transgenic mice, which express v-Ha-ras oncogene in the skin, and compared the susceptibilit

151 monstrated through the detection of a mutant ras oncogene in the stool of patients with colorectal ca

152 t the constitutive expression of an active H-Ras oncogene in these cells further attenuates the check

153 PRL also activated Ras oncogene in these cells.

154 This system uses expression of the Ras oncogene in which an 8OG replaces guanine in codon 6

155 Discoveries of the roles of RAS oncogenes in cancer development four decades ago ope

156 ven by the Akt1, c-MYC, HER2/neu, Wnt1, or H-Ras oncogenes in genetically engineered mice, correlatin

157 we show that genetic inactivation of K- or N-ras oncogenes in human tumor cells (DLD-1 and HT1080, re

158 The most frequently observed mutations in ras oncogenes in solid human tumors are GC-->AT transiti

159 s to the most frequent mode of activation of ras oncogenes in solid human tumors, the results of thes

160 activating point mutations in N-, Ki- and Ha-ras oncogenes in solid human tumors.

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

162 The introduction of the c-Myc and H-RAS oncogenes in the setting of loss of p53 function eff

163 Since the discovery of the role of ras oncogenes in tumorigenesis, we have witnessed an exp

164 ence pathways are activated in response to a ras oncogene, inactivation of TGFbeta1 secretion or resp

165 Our findings demonstrate that Ras oncogene-independent activation of RALB signaling is

166 Transforming fibroblasts with the Ras oncogene induced mitochondrial biogenesis, which fur

167 trate that the inhibitory effect of FOXO1 on Ras oncogene-induced colony formation in fibroblasts is

168 biting replicative senescence, Ndy1 inhibits Ras oncogene-induced senescence via a similar molecular

169 topic Runx-induced senescence contrasts with Ras oncogene-induced senescence, as it occurs directly a

170 tly, they are highly resistant to endogenous Ras oncogene-induced tumorigenesis.

171 An activated ras oncogene induces a program of differentiation in the

172 Among the mechanisms by which the Ras oncogene induces cellular transformation, Ras activa

173 or models to evaluate how the c-myc and v-Ha-ras oncogenes influence tumor growth characteristics in

174 lecular reasoning for repurposing statins as Ras oncogene inhibitors and the failure of using prenylt

175 Unlike previously reported Ras oncogene inhibitors, the proteins we designed not on

176 use model that the MYC oncogene, but not the RAS oncogene, initiates and maintains RCC.

177 any human tumor lines that lack an activated ras oncogene is also blocked by treatment with SCH 66336

178 The Ki-RAS oncogene is altered in pancreatic ductal neoplasms.

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

180 e used a recently described model in which a ras oncogene is expressed in cytokeratin 5 (K5)-expressi

181 n fibroblasts, an important effector for the Ras oncogene is Phosphatidylinositol 3-kinase (PtdIns 3-

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

183 xpression, thereby activating the PLAU and K-Ras oncogenes is important for distinct aspects of cellu

184 imary cells in cooperation with an activated ras oncogene, JunD antagonizes ras-mediated transformati

185 ically, by directly targeting errant kirsten ras oncogene (KRAS) signaling, miR-206 impeded the mitog

186 Transformation with Ela and ras oncogenes leads to the abrogation of this arrest and

187 The three RAS oncogenes make up the most frequently mutated gene f

188 in keratinocytes expressing the activated Ha-ras oncogene, making it a candidate tumor suppressor gen

189 These results suggest that the ras oncogene may play a determinant role in rendering tu

190 Organ-specific cancers with activated ras oncogenes most often are associated exclusively with

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

192 ss than 10% marrow monocytes, and absence of RAS oncogene mutations.

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

194 Mutations in the Kirsten-ras (K-ras) oncogene occur early and frequently (approximately

195 Activation of ras oncogenes occurs in a high percentage of tumors, mak

196 The influence of activated ras oncogenes on the sensitivity of human tumor cells to

197 mice from tumors induced by mutations of the RAS oncogene or a hot spot mutation in the tumor suppres

198 cells to escape OIS caused by the activated Ras oncogene or by reduced expression of the tumor suppr

199 ultaneously, via conditional activation of K-ras oncogene or deletion of Nf1 or Pten tumor suppressor

200 erated transgenic mice with high levels of N-ras oncogene or N-ras proto-oncogene expression, driven

201 ts) and transgenic mice with low levels of N-ras oncogene or N-ras proto-oncogene expression, driven

202 ine NIH3T3 and C127 cells transformed by the Ras oncogene overexpress the Met receptor, resulting in

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

204 The ras oncogene plays an important role in the multistep pr

205 ant stages of pancreatic adenocarcinoma is K-ras oncogene point mutation.

206 Cysteine farnesylation of the ras oncogene product Ras is required for its transformin

207 NORE1A has been shown to bind to the active Ras oncogene product.

208 The Ras oncogene products regulate the expression of genes i

209 ansforming activity than the closely related Ras oncogene products.

210 Activated ras oncogenes protect cells from this form of apoptosis.

211 Ras oncogene proteins are plasma membrane-associated sig

212 terest in their more celebrated cousins, the Ras oncogene proteins.

213 The Ras oncogene regulates cellular proliferation, different

214 er transformation to tumorigenicity with the ras oncogene resulted in loss of detectable LRAT express

215 Transformation with ras oncogenes results in increased radiation sur vival i

216 hown to inhibit the transforming activity of Ras oncogene signaling.

217 , a key function of Nf1 is repression of the Ras oncogene signalling cascade.

218 Thus, the ras oncogene specifically renders human cells more sensi

219 ivating point mutations in codon 12 of the K-ras oncogene, suggesting that K-ras mutational status ma

220 n with transforming growth factor-alpha or K-Ras oncogene, synergistically induced AR expression and

221 In this study, we provide evidence that the ras oncogene, targeted to a specifically sensitive cell

222 The mice carry in the germline a mutant ras oncogene that has an arginine at codon 12 instead of

223 fy a single base mutation in codon 12 of a K-ras oncogene that has high diagnostic value for colorect

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

225 n (col1a1) is markedly down-regulated by the ras oncogene through the mitogen-activated protein kinas

226 The ability of the Ras oncogene to transform normal cells has been well est

227 However, T24 c-Ha-ras oncogene-transfected MCF10A cells (MCF10AT) form sma

228 factors (RalGEFs) serve as key effectors for Ras oncogene transformation of immortalized human cells.

229 ly restores AP-2 transcriptional activity in ras oncogene-transformed cells suggesting that it might

230 ras oncogene-transformed PA-1 human teratocarcinoma cell

231 We found that human tumor cells containing ras oncogenes upon entry into the S phase of the cell cy

232 In both tumors, the N-ras oncogene was mutated.

233 The presence of a mutant ras oncogene was not a prerequisite for sensitivity.

234 For instance, the Ras oncogene was postulated to signal through cyclin D1,

235 G of GG doublets in codon 12 in the various ras oncogenes was affected by the base immediately upstr

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

237 Mutations of the ras oncogene were not identified.

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

239 cell lines with one containing an activated ras oncogene were used to study the basis for differenti

240 had been transfected with the c-myc or c-Ha-ras oncogene were X-irradiated, after which individual c

241 Ras-oncogenes were discovered over three decades ago, bu

242 ng to the leucine 61 oncogenic lesion of the ras oncogenes when introduced into R-ras3, activates its

243 A few cultures were transformed by ras oncogenes when transfected with DNA from neoplastic

244 us carcinomas (SCCs) induced by an activated Ras oncogene, whereas FVB/N mice are highly susceptible.

245 A549 and NCI-H460, each have a mutant active Ras oncogene, whereas the two melanoma lines G361 and M1

246 ancer is an activating point mutation in the Ras oncogene, which disrupts its GTPase activity and lea

247 cal for the function of the gene products of ras oncogenes, which are frequently mutated in cancer.

248 hat both, the N-ras proto-oncogene and the N-ras oncogene with a C:G-->A:T mutation at codon 61, lead

249 lay marked differences in the association of RAS oncogenes with tumor type.

250 anchorage-independent growth induced by the ras oncogene, with the use of a somatic cell mutant fibr