ライフサイエンスコーパス: RAS

1 RAS also regulates cell motility and tumour invasiveness

2 RAS association domain family 4 (RASSF4) is involved in

3 RAS component dysregulation was recently found in some m

4 RAS genes are mutated in 20% of human tumors, but these

5 RAS hotspots in NS5A were found at amino acids 28, 30, 3

6 RAS lesions in test group were exposed to ozone in air f

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

8 RAS proteins are binary switches, cycling between ON and

9 RAS signalling is involved in the control of several met

10 RAS-like protein expressed in many tissues 1 (RIT1) is a

11 RASs in NS3 associated with simeprevir or paritaprevir f

12 RASs in NS5A were heterogeneous among patients with HCV

13 0.62; without infiltrates, 4.5 (BOS), 0.00 (RAS), 4.56 (control), P = 0.74).

14 nchiole: with infiltrates, 5.00 (BOS), 9.00 (RAS), 4.00 (control), P = 0.62; without infiltrates, 4.5

15 ategory (hazard ratio [HR] 2.12; P = 0.021), RAS mutation (HR 1.74; P = 0.015), and double mutation (

16 Only 2 RAS mutated samples (6.5%) were identified.

17 ber of LVs per bronchiole: 4.75 (BOS), 6.47 (RAS), 4.25 (control), P = 0.97).

18 = 0.15 [BOS]; 60.5 vs 69.5 months, P = 0.80 [RAS]).

19 A RAS-binding domain pulldown assay indicated that RIT1 A5

20 gosertib, a styryl-benzyl sulfone, acts as a RAS-mimetic and interacts with the RBDs of RAF kinases,

21 We establish a RAS mutant cancer cell model where the autophagy gene AT

22 -, N-, or HRAS genes that encode an abnormal RAS protein locked in a constitutively activated state t

23 These reports of direct-acting RAS inhibitors provide valuable insight for further disc

24 ell-validated role of mutationally activated RAS genes in driving cancer development and growth has s

25 utations in RAS genes or otherwise activated RAS proteins.

26 Similarly, in Burkitt lymphoma, activating RAS mutations may propagate immunoglobulin-crippled tumo

27 The high incidence of activating RAS mutations and hyperactivated ERK1/2 signaling observ

28 expression of ERAS, a constitutively active RAS protein normally expressed only in embryonic stem ce

29 gnalling downstream of constitutively active RAS with which it interacts in a BH4-dependent manner.

30 ved drugs that are broadly effective against RAS-driven cancers.

31 All RAS biology occurs in membranes: a precise understanding

32 Although RAS proteins are often said to be "undruggable," there i

33 e immunological processes leading to BOS and RAS.

34 tients with NOTCH1/FBXW7 (N/F) mutations and RAS/PTEN (R/P) germ line (GL) were classified as oncogen

35 f two RASGAP genes, neurofibromin1 (Nf1) and RAS p21 protein activator (Rasa1).

36 in factors involved in cytokine receptor and RAS signaling (62.2%), hematopoietic development (29.7%)

37 f research effort, clinically effective anti-RAS therapies have remained elusive, prompting a percept

38 se feedback inhibition of GTP-bound RAS, are RAS-independent and signal either as active monomers (cl

39 oduction and/or oncogene activation, such as RAS, MYC, and c-SRC.

40 any tissues 1 (RIT1) is a disease-associated RAS subfamily small guanosine triphosphatase (GTPase).

41 rapeutics need to be engineered to arrive at RAS-driven precision medicine.

42 Targeting mevalonate activity attenuated RAS-ERK-dependent BTIC growth and self-renewal.

43 well as the co-operativity observed between RAS activity and RAF kinase inhibitors in driving RAF ac

44 linical study has been shown to inhibit both RAS and BRAF mutant cell proliferation in vitro and xeno

45 tants cause feedback inhibition of GTP-bound RAS, are RAS-independent and signal either as active mon

46 By reducing BP, RAS inhibitors limit secondary immune activation respond

47 sms to control BP and RMR and that the brain RAS functions as a major integrator for RMR control thro

48 therapy and are molecularly characterized by RAS pathway activation.

49 TRAF3 autophagy is driven by RAS and results in activation of the NF-kappaB family me

50 ions that influence tumor spectra induced by RAS oncoproteins.

51 criptional repressor negatively regulated by RAS/MAPK signaling.

52 or axis as counter-regulatory to the classic RAS Ang II/Ang II Type 1 (AT1) receptor axis.

53 We compared RASs in NS3, NS5A, and NS5B among patients failed by DAA

54 Here, we report that concurrent RAS pathway and TP53 mutations are identified in a subse

55 We considered RASs to be relevant if they were associated with DAA fai

56 ut T/Y93H and daclatasvir, or that contained RAS previously reported from patients.

57 icate that within the same cellular context, RAS can exert different, even antagonistic, effects, dep

58 tumour invasiveness, but the role of direct RAS binding to PI3-Kinase in this remains uncertain.

59 y leads to aberrant activation of downstream RAS signaling and thus contributes importantly to MPNST

60 During RAS activation, infiltration of immune cells into the ki

61 ge accumulation in the injured kidney during RAS activation by constraining the proinflammatory actio

62 The development of effective RAS inhibitors has been challenging, necessitating new a

63 Elevation of the EGFR, RAS and TGFbeta pathways was observed in one subtype whe

64 ance by preferentially substituting for EGFR/RAS/ERK signaling rather than ERBB3/PI3K/AKT signaling.

65 Here we report that EGFR/RAS/MAPK signalling is required and sufficient to drive

66 treat malignancies characterized by elevated RAS-ERK1/2 signaling.

67 ibromas, which are characterized by elevated RAS-mitogen-activated protein kinase (MAPK) signaling.

68 V600E dimerization directly or by elevating RAS-GTP.

69 in a negative feedback loop that encompasses RAS and RAF, MEK, and ERK that inhibits SOS via phosphor

70 ral ureteral obstruction model of endogenous RAS activation, CCL5 KO mice similarly developed more se

71 irming a colitogenic role for the endogenous RAS.

72 RAF inhibitors also enhance RAS-RAF association.

73 uppresses MRN complex expression to escalate RAS-induced DNA damage and thereby reinforce oncogene-in

74 gnaling in normal and tumor cells exhibiting RAS activity.

75 Variants with the pre-existing RAS T/Y93H acquired additional NS5A changes during escap

76 have mutations detected after such extended RAS testing.

77 were tested retrospectively for NOTCH1/FBXW7/RAS and PTEN alterations.

78 ate dehydrogenase level and the NOTCH1/FBXW7/RAS/PTEN oncogene (a four-gene oncogenetic classifier) s

79 lving NPM1 or signaling molecules (eg, FLT3, RAS) typically are secondary events that occur later dur

80 y and development of clinical candidates for RAS-driven cancers involving mutations in RAS genes or o

81 al assays indicate that this is critical for RAS-induced expression of stemness regulators and mainte

82 RBD-mediated interactions are essential for RAS signaling, blocking RBD association with small molec

83 PSCs provide an essential platform for RAS-induced phosphorylation and activation of the prosen

84 ity to eradicate nuclear FOXO4 proteins from RAS-mutant cancer cells.

85 at up-regulate (GEF) and down-regulate (GAP) RAS activity.

86 Accordingly, treatment with global RAS antagonists attenuates cardiovascular risk and slows

87 erative (borderline) Brenner tumors both had RAS mutations.

88 th these class 3 BRAF mutations also harbour RAS mutations or NF1 deletions.

89 f) animals were more invasive and had higher RAS/MAPK pathway activation.

90 However, RAS activation in hematopoietic cells has immunologic ef

91 delta and mTORC2, whereas in activated HSCs, RAS signaling shifts to RAF-MEK-ERK.

92 enocopied the histological features of human RAS-driven, poorly differentiated thyroid cancers.

93 leukemogenesis is linked to a hyperactivated RAS pathway, with driver mutations in the KRAS, NRAS, NF

94 ranulocyte macrophage-CSF due to hyperactive RAS/ERK signaling.

95 Importance: RAS wild-type (wt) status is necessary but not sufficien

96 ches are normally tightly controlled, but in RAS-related diseases, such as cancer, RASopathies, and m

97 d FOLFIRI plus bevacizumab); in contrast, in RAS wt patients with poor-prognosis right-sided tumors,

98 hat CK1alpha similarly destabilizes FOXO4 in RAS-mutant cells by phosphorylation at serines 265/268.

99 to understand RAS action and to intervene in RAS-driven diseases.

100 or RAS-driven cancers involving mutations in RAS genes or otherwise activated RAS proteins.

101 patients with tumors harboring mutations in RAS or RAF genes.

102 onan syndrome (NS) is caused by mutations in RAS/ERK pathway genes, and is characterized by craniofac

103 al inhibition of the EGFR-MEK-ERK pathway in RAS mutant organoids induced a transient cell-cycle arre

104 /mitogen-activated protein kinase pathway in RAS-mutant cancers are particularly promising approaches

105 We engineered HCV variants that included RAS identified in escape experiments, using recombinants

106 KIT knockdown also increased RAS/MAPK pathway activation in a BRAF(V600E)-mutant huma

107 Notably, increased RAS activity and downstream MAPK signaling was observed

108 A positive feedback loop involving RAS and SOS, which leads to bistability and allows for s

109 d genes and pathways, particularly involving RAS and MYC, may point to molecular drivers of a diverge

110 edback and their activation of signalling is RAS-dependent.

111 etastatic colon cancers and that oncogenic K-RAS activates TGF-beta signaling to promote tumor invasi

112 f CRC in which the expression of oncogenic K-RAS is regulated by doxycycline.

113 ate that continued expression of oncogenic K-RAS is required for the survival of primary and metastat

114 e model of lung cancer driven by oncogenic K-RAS.

115 oinformatics analysis detected a prominent K-RAS signature and predicted activation of several import

116 We identified 575 patients with known RAS mutation status who underwent hepatic resection for

117 However, the exact mechanism of local RAS activation in tumors is still unclear.

118 quires coexistent mechanisms for maintaining RAS activation despite ERK-dependent feedback.

119 was analyzed for HDAC, PI3K, HER2, and MAPK/RAS/RAF gene alterations from sarcoma TCGA.

120 CGA data revealed HDAC, PI3K, HER2, and MAPK/RAS/RAF gene alterations in 112/243 (46%) of patients pr

121 PLX8394 resistance occurs via EGFR-mediated RAS-mTOR signaling and is prevented by upfront combinati

122 We found that these interactions modulate RAS signaling, and that a single e1a molecule must bind

123 rgistically inhibited the growth of multiple RAS-mutant human cancer cell lines of diverse tissue ori

124 Mutant RAS-driven cancers are infamously resistant to chemother

125 In addition, mutant RAS coordinately elevates proteasome subunit expression

126 ronous CCLM (HR 1.45, P = 0.012), and mutant RAS (HR 1.43, P = 0.0040).

127 velop therapeutic strategies to block mutant RAS function for cancer treatment.

128 rganoids carrying either wild-type or mutant RAS, as well as normal organoids and tumor organoids wit

129 ation in malignancy and suggests that mutant RAS can control endothelial cell proliferation in neo-va

130 This is the first time that mutant RAS has been shown to stimulate non-cell autonomous prol

131 experiencing renewed excitement that mutant RAS may finally be conquered.

132 olorectal cancers with class 3 BRAF mutants, RAS is typically activated by receptor tyrosine kinase s

133 es prominently in PSC and that neuroblastoma RAS viral oncogene homolog (NRAS) is activated in PSC ch

134 iated with resistance to daclatasvir, but no RASs were associated with ledipasvir failure, pointing t

135 es a significantly worse prognosis than NPM1-RAS combinations.

136 F1AX and in NF1, USP9X, KRAS, BRAF, and NRAS RAS pathway mutations were mutually exclusive; however,

137 of 13 patients with detectable baseline NS5A RASs and in 98 (100%) of 98 without.

138 ith shorter survival than was the absence of RAS pathway mutations (P=0.004), owing to a high risk of

139 of relapse, as compared with the absence of RAS pathway mutations, was evident only with reduced-int

140 Oncogenic activation of RAS genes via point mutations occurs in 20%-30% of human

141 ptor tyrosine kinase-dependent activation of RAS more potently in colorectal cancer than in melanoma

142 Aberrant activation of RAS/MAPK signaling is a driver of over one third of all

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

144 However, specific combinations of RAS and deletion of amino acid 32 led to significant res

145 n HCV variants with specific combinations of RAS, showing high fitness and high resistance.

146 greater appreciation of the complexities of RAS that thwarted past efforts, and armed with new techn

147 intensive research aimed at the discovery of RAS-directed therapeutics, there are no FDA-approved dru

148 MEK signaling downstream of RAS leads to phosphorylation and inhibition of TTP by th

149 on of gene expression programs downstream of RAS/MAPK signaling.

150 By contrast, the adverse effect of RAS pathway mutations on the risk of relapse, as compare

151 strate discrepant tissue-specific effects of RAS stimulation on cisplatin nephrotoxicity and raise th

152 orectal liver metastases (CLM) in the era of RAS mutation analysis.

153 n cells partially dependent on expression of RAS proteins.

154 e have identified here that the incidence of RAS, BRAF, and EGFR mutations is low in cSCC.

155 This effect appears to be independent of RAS mutation status.

156 -terminal regulatory region independently of RAS activity.

157 molecular basis to explain the induction of RAS-RAF association by RAF inhibitors, as well as the co

158 e tumours are sensitive to the inhibition of RAS activation by inhibitors of receptor tyrosine kinase

159 ated in heart failure (HF) and inhibition of RAS is a mainstay therapy for HF.

160 tress, results in JNK-mediated inhibition of RAS-MAPK pathway components SOS and RAF.

161 Pharmacological inhibition of RAS/MAPK reduced ETS1 and CDKN2A protein expression and

162 be feasible to develop direct inhibitors of RAS proteins.

163 o clinically used multi-kinase inhibitors of RAS/RAF/MEK/ERK signaling, including regorafenib and sor

164 n interactions, including the interaction of RAS proteins and their effectors, may provide chemical p

165 nds capable of inhibiting the interaction of RAS proteins with their effectors that transduce the sig

166 s in hypertensive and normotensive models of RAS stimulation.

167 ive selection driven by BCL-XL modulation of RAS-induced self-renewal, and during which apoptotic res

168 Mutations of RAS, PTEN, and TSC1, which cause mTORC1 hyperactivation,

169 se the innately immunoresistant phenotype of RAS mutant cancers.

170 f statins is independent from prenylation of RAS family proteins and is associated with a cancer cell

171 did not have TP53 mutations, the presence of RAS pathway mutations was associated with shorter surviv

172 ay due to the loss of negative regulators of RAS may be a common event in basal breast cancer.

173 reduces expression of negative regulators of RAS/MAPK signaling.

174 heir effectors that transduce the signals of RAS and that drive and sustain malignant transformation

175 munologic effects that diverge from those of RAS stimulation in the kidney and vasculature.

176 ly no effective therapy for the treatment of RAS mutant cancers.

177 urs in membranes: a precise understanding of RAS' interaction with membranes is essential to understa

178 Oncogenic RAS mutations are present in 15-30% of thyroid carcinoma

179 in Kinase 1 alpha (CK1alpha) in an oncogenic RAS-specific manner, but whether this mode of regulation

180 the difference between normal and oncogenic RAS pathway signaling, this study shows that oncogenic R

181 istics that distinguish normal and oncogenic RAS signaling remain obscure.

182 text of cancer and illustrates how oncogenic RAS-mediated degradation of FOXOs, via post-translationa

183 OX2, which is broadly expressed in oncogenic RAS-associated cancers, we show that despite widespread

184 ow impaired immuno-surveillance of oncogenic RAS and reduced tissue inflammation upon ionizing radiat

185 , by the PI3K/AKT effector axis of oncogenic RAS signalling.

186 ing organ-specific contribution of oncogenic RAS to LCH pathogenesis.

187 a more comprehensive inhibition of oncogenic RAS-driven transcription programs in lung cancers with N

188 formation is a critical feature of oncogenic RAS/BRAF signaling in cancer cells that controls signal

189 nces cell migration, and overrides oncogenic RAS-induced senescence independently of its interaction

190 ng cancer cell lines by supporting oncogenic RAS transcriptional responses.

191 Here, we show that oncogenic RAS and BRAF induce perinuclear relocalization of severa

192 typing of the tumors revealed that oncogenic RAS mutations were found in 58% of the evaluable tumor s

193 We report that oncogenic RAS signaling can upregulate tumor cell PD-L1 expression

194 y signaling, this study shows that oncogenic RAS specifically triggers constitutive endocytosis-depen

195 n of ATXN7 mutants cooperated with oncogenic RAS to induce thyroid cell proliferation, pointing to AT

196 All patients continued optimised RAS blockade treatment throughout the trial.

197 TRF-budesonide 16 mg/day, added to optimised RAS blockade, reduced proteinuria in patients with IgA n

198 not impact the time to development of BOS or RAS in lung transplantation (low vs high LVD: 38.5 vs 86

199 iving a lung retransplantation due to BOS or RAS were collected.

200 markers, including a signature outperforming RAS/RAF mutations in predicting sensitivity to the EGFR

201 and testing of potential small-molecule pan-RAS ligands, which were designed to interact with adjace

202 These findings suggest that pan-RAS inhibition may be an effective therapeutic strategy

203 athway, protein kinase B (AKT)/PI3K pathway, RAS, etc.

204 Placental RAS is increased in pre-eclampsia (PE), characterised by

205 n mouse primary cortical neurons via a Rac1 (RAS-related C3 botulinum toxin substrate 1)-dependent me

206 lt of inhibitor-induced formation of the RAF/RAS-GTP complex.

207 l mutations affecting growth factor receptor-RAS signaling, highlight its prevalence in older men, an

208 in the RAS genes or their regulators render RAS proteins persistently active.

209 induce perinuclear relocalization of several RAS pathway proteins, including the kinases CK2 and p-ER

210 lassic effector molecule of the RAS, several RAS enzymes affect immune homeostasis independently of c

211 In addition, several RASs were specifically associated with failure of simepr

212 xisting resistance-associated substitutions (RAS) on HCV escape from treatment.

213 sis for resistance-associated substitutions (RASs) in HCV genes (nonstructural protein [NS]3, NS5A, N

214 and NS3 resistance-associated substitutions (RASs) on response to the combination of ledipasvir and s

215 mergent resistance-associated substitutions (RASs).

216 Our findings suggest RAS blockade is associated with better patient and graft

217 ome (BOS) or restrictive allograft syndrome (RAS) is the major limiting factor of long-term survival

218 The renin-angiotensin (Ang) system (RAS) has been reported as an important modulator of infl

219 The renin-angiotensin system (RAS) and angiotensin AT1 receptors within the brain are

220 ctioning placental renin-angiotensin system (RAS) appears necessary for uncomplicated pregnancy and i

221 despite optimised renin-angiotensin system (RAS) blockade.

222 activation of the renin-angiotensin system (RAS) contributes to many CKDs.

223 activation of the renin-angiotensin system (RAS) exacerbates renal and vascular injury.

224 Renin angiotensin system (RAS) is a key hormonal system which regulates the cardio

225 The renin-angiotensin system (RAS) is a principal determinant of arterial blood pressu

226 The renin-angiotensin system (RAS) is activated in heart failure (HF) and inhibition o

227 m dysfunction, and renin-angiotensin system (RAS) over-activity in thoracic aortas, resulting in redu

228 pies targeting the renin-angiotensin system (RAS) to improve beta-cell function in type 2 diabetes.

229 For the remaining NS5A inhibitors tested, RAS at amino acids 28 and 93 led to high levels of resis

230 In this issue, Chen et al. demonstrate that RAS association domain family 4 (RASSF4) positively infl

231 We demonstrate that RAS can drive cell-intrinsic PD-L1 expression, thus pres

232 of the switch and many of the pathways that RAS controls are well known, but the precise mechanisms

233 emained elusive, prompting a perception that RAS may be undruggable.

234 The RAS association domain family protein 1a (RASSF1A), a tu

235 The RAS blockade was associated with an adjusted-hazard rati

236 e evidence that these mutations activate the RAS/mitogen-activated protein kinase pathway in melanoma

237 inase activity of EGFRvIII and activates the RAS/RAF/MEK/ERK and STAT3 pathways.

238 RB, LYN, NTRK3, PDGFRA, PTK2B, TYK2, and the RAS signaling pathway.

239 ein kinase (MAPK) cascade, also known as the RAS-MEK-extracellular signal-related kinase (ERK1/2) pat

240 with known functional annotation (e.g., the RAS-RAF-MEK-ERK cascade).

241 nd excessive KIT activity hyperactivates the RAS/MAPK pathway and can drive formation of melanomas, m

242 many psychiatric disorders, mutations in the RAS genes or their regulators render RAS proteins persis

243 In the RAS wt populations of CRYSTAL and FIRE-3, patients with

244 In the RAS wt populations of the CRYSTAL and FIRE-3 trials, pat

245 ses associated with somatic mutations in the RAS-MEK-ERK pathway such as BRAF(V600E), suggests a poss

246 ell as human T-ALL carrying mutations in the RAS/MAPK pathway display a genetic signature indicative

247 d the expression changes and activity of the RAS family GTPases and thereby investigated the signalin

248 Targeting of the RAS pathway has long been a critical therapeutic challen

249 on of 12 genes, ten of which are part of the RAS pathway.

250 as reviewed here, multiple components of the RAS signaling cascade influence inflammatory cell phenot

251 ulating data indicate that activation of the RAS superfamily are poor biomarkers of statin sensitivit

252 topic expression of different members of the RAS superfamily did not uniformly sensitize cells to flu

253 ins can be uncoupled from prenylation of the RAS superfamily of oncoproteins.

254 enylation, including the oncoproteins of the RAS superfamily.

255 The dynamic range of the RAS was large, with equilibrium angiotensin levels being

256 as the incidence of somatic mutations of the RAS, BRAF, and EGFR genes and association of cetuximab e

257 n II is the classic effector molecule of the RAS, several RAS enzymes affect immune homeostasis indep

258 rapies to elicit long-term inhibition of the RAS-ERK1/2 signaling pathway add to the importance of di

259 leotide exchange factor and activator of the RAS-MAPK pathway following T cell antigen receptor (TCR)

260 Despite the importance of the RAS-RAF-MAPK pathway in normal physiology and disease of

261 ion of RAF activation, and inhibition of the RAS-RAF-MEK pathway.

262 variably harbored lesions in elements of the RAS-RAF-MEK-ERK pathway.

263 ]), are important negative regulators of the RAS.

264 tors in breast cancer, and inhibitors of the RAS/RAF/mitogen-activated protein kinase pathway in RAS-

265 ked with H3K36me2 and that contribute to the RAS transcription program.

266 Y93H in NS5A was the RAS most frequently associated with failure of daclatasv

267 C316N) or genotype 3 infection, whereas the RAS S282T was rarely observed.

268 ucleus in Deltaras2 RAS2 interacted with the RAS-binding domain of the adenylate cyclase in vitro, an

269 E-3: HR, 0.40; 95% CI, 0.23-0.70) within the RAS wt populations of both studies in multivariable mode

270 As a central element within the RAS/ERK pathway, the serine/threonine kinase BRAF plays

271 When these RASs do have effects, they could be largely overcome by

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

273 compound, termed 3144, was found to bind to RAS proteins using microscale thermophoresis, nuclear ma

274 ses, resulting in their inability to bind to RAS, disruption of RAF activation, and inhibition of the

275 nts bind more tightly than wild-type BRAF to RAS-GTP, and their binding to and activation of wild-typ

276 In human lung and colorectal tumors, RAS pathway activation is associated with elevated PD-L1

277 r size <3 cm (OR 1.97; P = 0.004), wild-type RAS (OR 2.00; P = 0.003), and absence of double mutation

278 We show that wild-type RAS amplification increases receptor tyrosine kinase-dep

279 ng was preserved through remaining wild-type RAS isoforms.

280 Genetic amplification of wild-type RAS was a recurrent mechanism of resistance in colorecta

281 , and mouse embryonic fibroblasts undergoing RAS-induced senescence.

282 on with membranes is essential to understand RAS action and to intervene in RAS-driven diseases.

283 nchorage-independent growth, and upregulated RAS/MAPK signaling with silencing of hypermethylated gen

284 tigate gastric adenocarcinoma subtypes where RAS/MAPK pathway activation and E-cadherin attenuation a

285 Whether RAS activation, mucosal ILCs and antibodies to V2 are al

286 l known, but the precise mechanisms by which RAS proteins function are less clear.

287 yperkalemia, especially when associated with RAS inhibitors.

288 d in nonresponding patients, consistent with RAS signaling contributing to primary therapeutic resist

289 ent resistance to pibrentasvir, and HCV with RAS at amino acid 93 had a low level of resistance to th

290 n cancers and significantly co-occurred with RAS or NF1 mutations.

291 had a striking pattern of co-occurrence with RAS mutations.

292 e of primary tumor location in patients with RAS wild-type (wt) mCRC treated with first-line fluorour

293 y for anti-EGFR therapy in all patients with RAS wt aCRC should be questioned.

294 Among CRYSTAL and FIRE-3 study patients with RAS wt left-sided tumors, FOLFIRI plus cetuximab signifi

295 In this retrospective analysis patients with RAS wt metastatic colorectal cancer from the CRYSTAL and

296 vir was more effective against variants with RAS at amino acid 30 and some variants with RAS at amino

297 RAS at amino acid 30 and some variants with RAS at amino acid 31 than the other agents.

298 l of efficacy against variants; viruses with RAS at amino acids 28, 30, or 31 had no apparent resista

299 g genotype 1-7 NS5A proteins with or without RAS.

300 ts with metastatic colorectal tumors without RAS mutations.