ライフサイエンスコーパス: melanoma cell line

1 ased after expressing Maspin in a metastatic melanoma cell line.

2 way activation in a BRAF(V600E)-mutant human melanoma cell line.

3 ghly expressing alphavbeta3 human metastatic melanoma cell line.

4 ted cell response to UV radiations also in a melanoma cell line.

5 II, which reduced the viability of the DB-1 melanoma cell line.

6 ptibilities from a series of patient-derived melanoma cell lines.

7 he C-terminus of the endogenous NME1 gene in melanoma cell lines.

8 drogenase (high) cells (a marker of MICs) in melanoma cell lines.

9 R inhibitor was effective in BRAFi-resistant melanoma cell lines.

10 ition transcriptional profiles in a panel of melanoma cell lines.

11 hibition reduced invasion in mouse and human melanoma cell lines.

12 tides on cell adhesion was examined in A2058 melanoma cell lines.

13 sion of a large subset of lysosomal genes in melanoma cell lines.

14 to induce CD82 expression in highly invasive melanoma cell lines.

15 enotype is common among mutant BRAF and NRAS melanoma cell lines.

16 that exhibit excellent in vitro efficacy in melanoma cell lines.

17 ell lines with particular selectivity toward melanoma cell lines.

18 ee pairs of matched primary/metastatic human melanoma cell lines.

19 tors and promotes survival in V600E-positive melanoma cell lines.

20 sive potential of approximately 20% of human melanoma cell lines.

21 ufficient embryos and in Magoh siRNA treated melanoma cell lines.

22 ere highly cytotoxic to a panel of different melanoma cell lines.

23 xamine their effect on survival signaling in melanoma cell lines.

24 ctivated reporter and increases apoptosis in melanoma cell lines.

25 a cell bank of immunologically characterized melanoma cell lines.

26 ements, are hypomethylated in advanced stage melanoma cell lines.

27 ic stimuli and was found to be cytostatic in melanoma cell lines.

28 3 is expressed at varying levels in numerous melanoma cell lines.

29 ing also directly decreases proliferation in melanoma cell lines.

30 in a high percentage of human melanomas and melanoma cell lines.

31 olony formation in soft agar across multiple melanoma cell lines.

32 hemical efflux capacity, is present in human melanoma cell lines.

33 y of normal melanocytes and a broad panel of melanoma cell lines.

34 -mediated cytolytic activity against various melanoma cell lines.

35 ubset of benign nevi (33%) and in some human melanoma cell lines.

36 easured using qPCR and Western blot in uveal melanoma cell lines.

37 cation in samples from colorectal cancer and melanoma cell lines.

38 after PLX4032/4720 treatment in mutant B-RAF melanoma cell lines.

39 lanocytes and Nox4 in a subset of metastatic melanoma cell lines.

40 rentiation, and higher rates of apoptosis in melanoma cell lines.

41 correlated inversely with that of miR-205 in melanoma cell lines.

42 wn CN, including tonsil, placentae, and FFPE melanoma cell lines.

43 oth RMi-sensitive (RMS) and -resistant (RMR) melanoma cell lines.

44 Braf-mutant and 3 wild-type human cutaneous melanoma cell lines.

45 al expression was suppressed in all analyzed melanoma cell lines.

46 ir in both normal melanocytes and a panel of melanoma cell lines.

47 ssion of Maspin in PAR-1-silenced metastatic melanoma cell lines.

48 uced expression of NME1 (NME1(LOW)) in human melanoma cell lines.

49 a cell bank of immunologically characterised melanoma cell lines.

50 mily members in a comprehensive set of human melanoma cell lines.

51 relates with gene copy number in a subset of melanoma cell lines.

52 ecreased after PAR-1 silencing in metastatic melanoma cell lines.

53 lted in premature senescence of a variety of melanoma cell lines.

54 d in a series of patient-derived BRAF mutant melanoma cell lines.

55 f base loaders were further characterized in melanoma cell lines.

56 rize resistance mechanisms in two BRAF V600E melanoma cell lines.

57 ible pairs among 108 cancer drugs applied to melanoma cell lines.

58 nisms of BRAFi resistance in two independent melanoma cell lines.

59 -dependent, but not KIT-independent GIST and melanoma cell lines.

60 the SREBP1 transcription factor in multiple melanoma cell lines.

61 panel of patient-derived BRAF(V600) -mutant melanoma cell lines.

62 analysis of 216 melanoma tumors and 13 human melanoma cell lines.

63 25W was enriched to MAF = 0.65 in the NCI-60 melanoma cell lines.

64 d resistance to BRAFi and in BRAFi-resistant melanoma cell lines.

65 y knocking down of NLRP1 in human metastatic melanoma cell lines 1205Lu and HS294T, indicating that N

66 Motivated by experimental observations on melanoma cells lines (1205Lu and SBcl2) migrating on fib

67 mTOR gene in 12 thyroid cancer cell lines, 3 melanoma cell lines, 20 anaplastic thyroid cancer (ATC)

68 s were tested in the highly aggressive human melanoma cell lines A2058 and A375.

69 ry in a cell-based assay for invasion by the melanoma cell line A375.

70 From these results, a metastatic melanoma cell line (A375) and two inhibitors that inhibi

71 Treatment of human melanoma cell lines (A375, Hs294t, SK-Mel28 and SK-Mel11

72 ere found to be expressed in three different melanoma cell lines - A375, MeWo, and HS695T - and inclu

73 vemurafenib resistance in two V600E BRAF+ve melanoma cell lines, A375 and DM443, by serial in vitro

74 ith the in vitro invasive potential of the 5 melanoma cell lines (A375P, A375M, A375P10, A375P5, and

75 ference observed between a highly metastatic melanoma cell line (A375SM) or its parental line (A375P)

76 silenced MUC18 expression in two metastatic melanoma cell lines, A375SM and C8161, and conducted cDN

77 is study, we demonstrate that in BRAF(V600E) melanoma cell lines, activating MEK mutations drive resi

78 In our analysis of melanoma cell lines, all produced MIF constitutively.

79 cell cycle arrest and senescence in several melanoma cell lines along with apoptosis.

80 Analysis of a male melanoma cell line and normal skin cells from the same i

81 rrelates strongly with that of MITF in human melanoma cell lines and biopsy specimens.

82 tion of p63 mRNA and protein was observed in melanoma cell lines and clinical samples, providing the

83 in human primary melanoma tissue samples and melanoma cell lines and correlates with MITF-M mRNA leve

84 anti-proliferative activity against various melanoma cell lines and could induce G2/M phase arrest a

85 ctions of a cDNA library, derived from human melanoma cell lines and expressed using the highly immun

86 2's role in melanoma, we analyzed a panel of melanoma cell lines and found that EphA2 levels are elev

87 In this study, we developed BRAFi-resistant melanoma cell lines and found that metastasis-related ep

88 of comparing CDK4 activity between different melanoma cell lines and further responds to CDK4 downreg

89 be significantly reduced in human metastatic melanoma cell lines and human tissue from metastatic les

90 or, GPR56, inhibits VEGF production from the melanoma cell lines and impedes melanoma angiogenesis an

91 In multiple human melanoma cell lines and in melanoma patient-derived xeno

92 stance to RAF pathway inhibitors in cultured melanoma cell lines and in mouse xenograft models.

93 studied in the conditioned medium of 9 uveal melanoma cell lines and in the blood serum samples of 24

94 reduced viability and clonogenic capacity of melanoma cell lines and increased cellular levels of 5-c

95 mGlu1h mRNA was observed in two different melanoma cell lines and is overexpressed, compared with

96 amoeboid compared with elongated-mesenchymal melanoma cell lines and its levels are controlled by ROC

97 Analysis of melanoma cell lines and matched patient samples indicate

98 way component expression in a panel of human melanoma cell lines and melanocytic lesions, and charact

99 in melanoma, the PHIP locus was preserved in melanoma cell lines and patient samples, and its overexp

100 recurrent melanoma and was conserved across melanoma cell lines and patients' tumor specimens.

101 The conditioned medium of uveal melanoma cell lines and the blood serum samples of mice

102 melanoma, is commonly up-regulated in human melanoma cell lines and tissue samples; this up-regulati

103 is with higher expression seen in metastatic melanoma cell lines and tissue specimens.

104 NK), CYLD was decreased in a majority of the melanoma cell lines and tissues examined.

105 the related inhibitor cystatin E/M occur in melanoma cell lines and to evaluate to what extent the u

106 rs or a specific inhibitor of BRAF(V600E) in melanoma cell lines and tumor digests results in increas

107 hat GAB2 is co-expressed with mutant NRAS in melanoma cell lines and tumor samples and its expression

108 tor-1 (PAR-1) is overexpressed in metastatic melanoma cell lines and tumor specimens.

109 NFAT1 expression and metastatic potential in melanoma cell lines and tumor specimens.

110 In BRAFi-resistant melanoma cell lines and tumors, activation of RhoA is co

111 XN was almost universally hypermethylated in melanoma cell lines and tumors, and treatment of the cel

112 P-Rex1 is elevated in the majority of human melanoma cell lines and tumour tissue.

113 ificially derived from B-RAF(V600E)-positive melanoma cell lines and validated key findings in PLX403

114 we introduced Plexin C1 into a primary human melanoma cell line, and phenotypes including migration,

115 ression was analyzed in primary melanocytes, melanoma cell lines, and 83 melanocytic tumors, and its

116 as verified at transcript level in different melanoma cell lines, and at protein level in A2058 cells

117 primary melanocytes and B-RafV600E-positive melanoma cell lines, and between melanoma cells treated

118 RNA expression was detectable in 90.1% of 65 melanoma cell lines, and increased copy number of the Ep

119 h in a subset of cancer cell lines, and some melanoma cell lines are quite susceptible.

120 icant downregulation of IGFBP3 expression in melanoma cell lines as compared with a normal melanocyte

121 s an miRNA that is strongly downregulated in melanoma cell lines as compared with primary melanocytes

122 a high level of expression in multiple human melanoma cell lines as well as in a subset of human mela

123 CTLA4 is also highly expressed by most human melanoma cell lines, as well as in normal human melanocy

124 Using the melanoma cell line B16 as a murine model of pulmonary me

125 l vaccination against the poorly immunogenic melanoma cell line B16-F10.

126 th tumor cell aggressiveness in the isogenic melanoma cell lines (B16-F0, -F10, and -BL6).

127 The melanoma cell line B16BL6, although it is nonmyeloid lin

128 Two melanoma cell lines (B16F10 and A375M) that highly expre

129 Cells derived from the cutaneous B16 melanoma cell line (B16LS9) were transplanted either int

130 CSCs were isolated from the B16-F10 murine melanoma cell line based on expression of the putative C

131 short-term melanoma cultures and established melanoma cell lines blocked the production of the interl

132 In BRAF(V600E) melanoma cell lines, BRAFi or BRAF/MEK inhibition induce

133 gonist increased Ca(2+) in several different melanoma cell lines but not in melanocytes.

134 Restoration of 5-hmC, as assessed in a human melanoma cell line by introducing full-length TET2 and T

135 proliferating and senescent melanocytes and melanoma cell lines by RNA sequencing emphasizes the imp

136 Moreover, cultures of the human melanoma cell line C81-61 with sera from patients with t

137 nalling and induced G1 arrest selectively in melanoma cell lines carrying GNAQ or GNA11 mutations.

138 viability and caused cell death in multiple melanoma cells lines (carrying either BRAF or NRAS mutat

139 Here we show that TDG knockdown in melanoma cell lines causes cell cycle arrest, senescence

140 In cultured GRM1(+) melanoma cell lines, CB-839, a potent, selective, and or

141 nd show that p63 isoforms are upregulated in melanoma cell lines chronically exposed to BRAF and MEK

142 Most wild-type p53-expressing melanoma cell lines coexpress high levels of phosphoryla

143 orrespondingly, increased levels of c-Jun in melanoma cell lines coincide with up-regulation of PDK1

144 lymphoblastic leukemias (T-ALLs) and a human melanoma cell line, COLO-829, identified 160 somatic str

145 le genome sequencing of a matched metastatic melanoma cell line (COLO829) and normal across three lin

146 e found that CK2alpha protein is elevated in melanoma cell lines compared with normal human melanocyt

147 th higher SKI activity in seven out of eight melanoma cell lines compared with normal melanocytes.

148 n normal human melanocytes and proliferative melanoma cell lines, compared with other skin cells (ker

149 Expression of ERAS in human melanoma cell lines conferred resistance to PLX4720 and

150 oma-associated marker tyrosinase in adherent melanoma cell lines corresponding to different cancer pr

151 Recent evidence indicates that in melanoma cell lines, CQ induces apoptosis by preventing

152 TF transcriptional and oncogenic activity in melanoma cell lines, derived from human melanoma patient

153 first presented here in two human amelanotic melanoma cell lines, derived from vertical growth phase

154 ncy mice that the HAGE knockdown in a ABCB5+ melanoma cell line displayed a significant decrease in t

155 scovered that in WM1158, a highly aggressive melanoma cell line, down-regulation of ACTN4 by shRNA in

156 In melanoma cell lines, elevated baseline expression relied

157 ession and shRNA(S100B) knockdown studies in melanoma cell lines, elevated S100B was found to enhance

158 In summary, Nox1 was overexpressed in all melanoma cell lines examined, and enhanced cell invasion

159 o knock-down NIK, the resultant NIK-depleted melanoma cell lines exhibited decreased proliferation, i

160 By using RT-PCR we have shown that two human melanoma cell lines express both mGlu1a and mGlu1b recep

161 Pancreatic cancer and melanoma cell lines express PrP.

162 e, we show that the aggressive B16-BL6 mouse melanoma cell line expresses low basal levels of Cx26 an

163 Both in fibroblasts and in a murine melanoma cell line expressing mutant B-Raf, MKK6 activat

164 sing losartan or shRNA-mediated knockdown in melanoma cell lines expressing AGTR1 resulted in acquisi

165 on in a panel of tumor cell lines, including melanoma cell lines expressing BRAF(V600E) or other muta

166 Treatment of melanoma cell lines expressing endogenous AT2R with eith

167 Herein, the tumor growth of melanoma cell lines expressing major histocompatibility

168 o EZH2 inhibitors, we screened a panel of 53 melanoma cell lines for drug sensitivity.

169 transcriptase in real time, we evaluated 60 melanoma cell lines for TERT promoter mutational status,

170 We established a melanoma cell line from a tumor with none of the common

171 , exhibited strong cytotoxicity in the human melanoma cell line G361 that correlated with robust CDK1

172 In melanoma cell lines, Gas6 induced Tyro3 phosphorylation

173 rotein were also elevated in BRAFi-resistant melanoma cell lines generated by long-term in vitro trea

174 TWIST1 protein levels are especially high in melanoma cell lines generated from invasive, premetastat

175 variably inhibited the tumorigenic growth of melanoma cell lines having these three genotypes.

176 A murine melanoma cell line highly metastatic to lymph nodes (B16

177 nificant activity in the Sk-Mel-28 malignant melanoma cell line (IC(50) values of 1.10 and 1.06 muM,

178 ies of 64 metastatic melanoma samples and 20 melanoma cell lines identified increased copy numbers of

179 onducted a microarray on a highly metastatic melanoma cell line in which NFAT1 expression was stably

180 alpha-activated pDCs could also lyse certain melanoma cell lines in a TRAIL-dependent fashion.

181 s were used to compare normal melanocytes to melanoma cell lines in both normoxic and hypoxic conditi

182 r of lncRNAs are differentially expressed in melanoma cell lines in comparison to melanocytes and ker

183 ements of glycolysis in B-Raf(V600E)-mutated melanoma cell lines in response to specific B-Raf inhibi

184 RA1 deletion suppresses cell growth in human melanoma cell lines in vitro and tumor development in vi

185 xpression was identified in human and murine melanoma cell lines, in human malignant melanoma, as wel

186 rounded, amoeboid phenotype in a panel of 16 melanoma cell lines, in mouse melanoma xenografts, and i

187 Melanoma cell lines, including those with ETV1 amplifica

188 erexpression of SOX9 in both human and mouse melanoma cell lines induced cell cycle arrest by increas

189 The TSN from cultured melanoma cell lines induced chemotaxis of monocytes, but

190 Furthermore, SOX9 overexpression in melanoma cell lines inhibited tumorigenicity both in mic

191 1 and MEK162, inhibited the proliferation of melanoma cell lines irrespective of their mutation statu

192 The TSN from uveal melanoma cell lines is capable of affecting the chemotac

193 r matched short-term cultures or in vitro in melanoma cell lines is not caused by acquisition of seco

194 f HCN1 channels by FLNa has been observed in melanoma cell lines, its physiological relevance to neur

195 Comparing four different melanoma cell lines, little overlap of the HLA-bound pep

196 lical endothelial cells (HUVECs) and a human melanoma cell line (Lu1205) increased intercellular adhe

197 the linearity was measured using 4 different melanoma cell lines (M257, M202, M233, and M229).

198 ouse breast cancer cell line EMT-6 and human melanoma cell line MDA-MB-435.

199 cts or downregulated by sh-Jag2 in the uveal melanoma cell lines Mel285, Mel290, 92.1, and OMM1, and

200 The human uveal melanoma cell lines Mel290 and Mel 270, HUVECs, mouse B1

201 ssue, we genetically engineered an HLA-A2(+) melanoma cell line, MEL526, to express GFP or GFP-tagged

202 n isoform 2 was overexpressed in BRAF mutant melanoma cell lines, melanoma cell proliferation and in

203 Shortly after BRAF inhibitor treatment in melanoma cell lines, mutant BRAF bound the ER stress gat

204 In multiple melanoma cell lines, mutant NRas resided in more pronoun

205 To select informative melanoma cell lines, mutational profiles of the clinical

206 Notch and Nodal signaling in the aggressive melanoma cell line MV3 via the activity of an RBPJ-depen

207 regulated by MDM2, and in therapy-resistant melanoma cell lines, nuclear accumulation of MDM2 caused

208 y described herein, we generated B-RAF V600E melanoma cell lines of acquired-resistance to vemurafeni

209 Here we found that melanoma cell lines of multiple genotypes exhibit high b

210 rnover was observed in genetically different melanoma cell lines of varied basal pigmentation states

211 ng of RAF and MEK inhibitors across multiple melanoma cell lines of various genotypes and sensitiviti

212 h mutagenic exposure than in the genome of a melanoma cell line or the transcriptome of melanoma shor

213 bserved in vivo upon exposure of BRAF-mutant melanoma cell lines or patient-derived xenograft models

214 o overcome PLX4032/vemurafenib resistance in melanoma cell lines or short-term culture where the resi

215 Additionally, over half of melanoma cell lines overexpressed MERTK compared with no

216 Human uveal melanoma cell lines overexpressing the TJ molecule blood

217 Here we acquire this insight in a melanoma cell line panel by tracking metabolic flux usin

218 Bioinformatic analysis of multiple melanoma cell lines points to an inverse expression patt

219 Reexpressing DCC in human melanoma cell lines promoted tumor cell death and tumor

220 A transplantable mouse MPNST-like melanoma cell line recapitulated mast cell recruitment i

221 on of endogenous RasGRP3 expression in these melanoma cell lines reduced Ras-GTP formation as well as

222 ort that TTM inhibited transformed growth of melanoma cell lines resistant to BRAF or MEK1/2 inhibito

223 Upon treatment, melanoma cell lines responded by dramatically increasing

224 a cDNA library generated from the autologous melanoma cell line resulted in the isolation of a mutate

225 Bves overexpression in uveal melanoma cell lines resulted in increased expression of

226 nt of direct patient-derived tissue, but not melanoma cell lines, resulted in short-term antagonistic

227 rate that the exogenous expression of LXN in melanoma cell lines results in a significant inhibition

228 Finally, we showed that chimera-derived melanoma cell lines retain regulatory allele competency

229 A BRAF(V600E) mutant melanoma cell line, SB-3123(p) which is resistant to Pme

230 In melanoma cell lines, SD-208 blocked TGF-beta induction o

231 Importantly, melanoma cell lines selected for resistance to BRAFi+MEK

232 We tested the method using the COLO-829 melanoma cell line sequenced to 40-fold coverage.

233 expressed B4GALNT1 in GM2/GD2-negative human melanoma cell line (SH4) and confirmed production of GM2

234 d displays antiproliferative efficacy in the melanoma cell line SK-MEL-2 but showed only weak antitum

235 9, hepatocellular carcinoma cell line HepG2, melanoma cell line SK-MEL-37, and pancreatic carcinoma c

236 cDNA (hIFNbeta) was used to transduce human melanoma cell lines SK-MEL-05 and SK-MEL-147 (both wild

237 In the mGlu1 receptor-expressing melanoma cell lines SK-MEL-2 (SK2) and SK-MEL-5 (SK5), w

238 co-culture experiment with human metastatic melanoma cell line (SKMEL- 147) and immortalized keratin

239 which are from assays performed on purified melanoma cell lines, suggest that the TERT promoter harb

240 blocked ERK phosphorylation and growth in a melanoma cell line, suggesting that it may provide a hig

241 ion in cultured normal human melanocytes and melanoma cell lines supported our immunohistochemical fi

242 anoma, whereas stable suppression of Phip in melanoma cell lines suppressed metastatic potential and

243 ctedly, introduction of plexin B1 into human melanoma cell lines suppressed, rather than activated, t

244 Overexpression of DBT kills all four melanoma cell lines tested regardless of the presence of

245 death via apoptotic mechanisms in nearly all melanoma cell lines tested, regardless of the BRAF or NR

246 EK and mTOR1,2 inhibition in all NRAS mutant melanoma cell lines tested, suggesting that PI3K signali

247 Our results show that in 11 of 12 melanoma cell lines tested, UV photoproduct repair occur

248 tal cell surface expression of CD74 in human melanoma cell lines tested.

249 ath compared with a negative control in most melanoma cell lines tested.

250 se inhibitor RAF265 in a BRAF (V600E) mutant melanoma cell line that is resistant to this drug.

251 alpha (TNF)-induced NF-kappaB activation in melanoma cell lines that express filamin A (FLNA).

252 sistance to PDT was investigated in a set of melanoma cell lines that markedly differ in the levels o

253 emokine protein array identified a subset of melanoma cell lines that produced a similar broad array

254 erences were found in human NRAS(Q61) mutant melanoma cell lines that were also more sensitive to pha

255 nhibition remodeled the signaling network of melanoma cell lines that were BRAF mutant and PTEN null.

256 First, we identified NRAS-mutant melanoma cell lines that were dependent on NRAS for prol

257 entiated THP-1 and HTB-66 cells, an invasive melanoma cell line, through extracellular matrix was inh

258 ance in newly characterized metastatic uveal melanoma cell lines to clinical-grade MEK inhibitors, tr

259 ere, we chronically expose (patient-derived) melanoma cell lines to differentiation antigen-specific

260 Applying this platform in melanoma cell lines to profile the immunopeptidome respo

261 tin limited the responses of these PTEN-null melanoma cell lines to vemurafenib, with enhanced cytoto

262 In vivo studies using either a melanoma cell line (transduced alpha(v)beta(6) expressio

263 n 15,500 genes individually in a BRAF(V600E) melanoma cell line treated with RAF, MEK, ERK or combine

264 Melanoma cell lines treated with the demethylating agent

265 CD2 surface levels and enabled killing of a melanoma cell line typically resistant to CD16-deficient

266 Accordingly, NFAT1 depletion in metastatic melanoma cell lines was associated with reduced IL8 and

267 A series of 13 melanoma cell lines was briefly exposed to a BRAF inhibi

268 A subset of acquired drug-resistant melanoma cell lines was sensitive to Gamitrinib.

269 A panel of human melanoma cell lines was transfected with siRNA to induce

270 Fn14 expression in approximately 60% of the melanoma cell lines we tested, including both B-Raf WT a

271 n primary melanocytes and a highly pigmented melanoma cell line, we demonstrate that reduced expressi

272 Furthermore, using melanoma cell line, we show that KLK7-mediated cleavage

273 ing siRNA-mediated knockdown across multiple melanoma cell lines, we determined that loss of GABPA re

274 In this study, across 60 melanoma cell lines, we find bimodal expression patterns

275 ECM results of tape-stripped different human melanoma cell lines were confirmed by previous studies b

276 Four human uveal melanoma and three mouse melanoma cell lines were found to express PEDF mRNA.

277 ensitivity profiling revealed that PTEN(LOF) melanoma cell lines were sensitive to PI3Kbeta inhibitor

278 To develop this approach, melanoma cell lines were treated with AKT inhibitor AZD5

279 nografts involving inflammatory prostate and melanoma cell lines, whereas it is ineffective in noninf

280 ly in over 70% of melanoma tumors and 80% of melanoma cell lines, whereas such correlation does not e

281 produce robust calcium mobilization in human melanoma cell lines which can be blocked by the CXCR4-se

282 set of perturbation experiments in SKMEL-133 melanoma cell lines, which are resistant to the therapeu

283 Here, we investigated a panel of melanoma cell lines wild type for BRAF and NRAS to deter

284 ion and protein synthesis in patient-derived melanoma cell lines with acquired resistance to combined

285 Human melanoma cell lines with and without the IL-18 receptor

286 accinia virus (GLV-1h68) and radiotherapy in melanoma cell lines with BRAF mutant, Ras mutant or wild

287 down significantly inhibits proliferation of melanoma cell lines with different oncogenic mutations w

288 Treatment of neuroblastoma and melanoma cell lines with fenretinide, bortezomib, or tha

289 Melanoma cell lines with known sensitivity to BRAF inhib

290 ll proliferation was assessed using HLEC and melanoma cell lines with patient sera under both normoxi

291 Treatment of melanoma cell lines with PGD2 increased SOX9 expression

292 Cotreatment of BRAF-mutated melanoma cell lines with phenformin and PLX4720 resulted

293 Melanoma cell lines with RETp, RET wild type (RETwt), BR

294 Studies in four melanoma cell lines with various genetic backgrounds sho

295 In this study we demonstrate that ~50-60% of melanoma cell lines with vemurafenib resistance acquired

296 Co-treatment of melanoma cell lines with WNT3A-conditioned media and rec

297 -related proteins were variably expressed in melanoma cell lines, with 42% expressing activated phosp

298 Specifically, we demonstrate that melanoma cell lines, with acquired in vitro-induced vemu

299 molar cellular potency against a mutant BRAF melanoma cell line, WM266.4.

300 gene expression analyses revealed that human melanoma cell lines WM793 and especially WM239 (vertical