ライフサイエンスコーパス: melanoma cell line

1 ghly expressing alphavbeta3 human metastatic melanoma cell line.

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

3 olecule into an intracellular structure in a melanoma cell line.

4 ence of ORF23 disrupted capsid assembly in a melanoma cell line.

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

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

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

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

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

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

11 ctivated reporter and increases apoptosis in melanoma cell lines.

12 a cell bank of immunologically characterized melanoma cell lines.

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

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

15 3 is expressed at varying levels in numerous melanoma cell lines.

16 ing also directly decreases proliferation in melanoma cell lines.

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

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

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

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

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

22 -mediated cytolytic activity against various melanoma cell lines.

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

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

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

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

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

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

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

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

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

32 25W was enriched to MAF = 0.65 in the NCI-60 melanoma cell lines.

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

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

35 a cell bank of immunologically characterised melanoma cell lines.

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

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

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

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

40 he increased growth and motility of multiple melanoma cell lines.

41 a phospho-MART-1 peptide identified in both melanoma cell lines.

42 g elevates CTLA-4 expression in two cultured melanoma cell lines.

43 led to inhibit proliferation of VEGFR-2(neg) melanoma cell lines.

44 rs the processing and function of miR-137 in melanoma cell lines.

45 ially blocked the growth of three of the six melanoma cell lines.

46 ase inhibitor sorafenib induces apoptosis in melanoma cell lines.

47 aling pathways up-regulate TAA expression in melanoma cell lines.

48 y 5-AZAdC with a >3-fold increase in 8 of 10 melanoma cell lines.

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

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

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

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

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

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

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

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

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

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

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

60 ell lines with particular selectivity toward melanoma cell lines.

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

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

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

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

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

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

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

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

69 SOCS-1), was reduced in the brain metastatic melanoma cell line A375Br, relative to that in the paren

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

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

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

73 cing CREB expression in two human metastatic melanoma cell lines, A375SM and C8161-c9, suppresses tum

74 The MiTF-positive melanoma cell lines accumulated high levels of apurinic/

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

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

77 Because MAP2 promoter activity levels in melanoma cell lines also correlated with activating muta

78 t Plexin C1 is diminished or absent in human melanoma cell lines; analysis of tissue microarrays of n

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

80 GRM1 was also detected in a subset of human melanoma cell lines and biopsies, suggesting that aberra

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 ance was seen after challenge with different melanoma cell lines and in mice with different genetic b

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

94 AR-1)] is overexpressed in highly metastatic melanoma cell lines and in patients with metastatic lesi

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

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

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

98 Analysis of melanoma cell lines and matched patient samples indicate

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

100 ct endogenous PEDF expression in human uveal melanoma cell lines and mouse melanoma cells.

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

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

103 protein was similarly overexpressed in human melanoma cell lines and primary tumors.

104 in the Hs-294T, A375, and S91 MAGE-positive melanoma cell lines and that members of all three famili

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

106 Four human uveal melanoma cell lines and three cell lines of uveal melano

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 c activity against a panel of chemoresistant melanoma cell lines, and it was found that largazole is

123 nduces apoptosis in BRAFV600E-positive human melanoma cell lines, and systemically administered rIGFB

124 carcinoma, non-small-cell lung carcinoma and melanoma cell lines, and up to 30% of samples from vario

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

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

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

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

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

130 Nelfinavir inhibits the growth of melanoma cell lines at low micromolar concentrations tha

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

132 called ACE 10/10, with the aggressive mouse melanoma cell line B16 showed that they are remarkably r

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

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

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

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

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

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

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

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

141 tibody, inhibits proliferation of VEGFR-2(+) melanoma cell lines by an average of 41%; however, it fa

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

143 Spheroids grown from the human choroidal melanoma cell line C918 were implanted in the superior s

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

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

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

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

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

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

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

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

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

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

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

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

156 ed in B16 murine melanoma cells and in human melanoma cell lines cultured in vitro with either WNT3A

157 In vitro experiments with multiple uveal melanoma cell lines demonstrate that resveratrol causes

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

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

160 Aggressive melanoma cell lines did not respond to treatment with CC

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

162 we show that expression of mature miR-137 in melanoma cell lines down-regulates MITF expression.

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

164 In melanoma cell lines, elevated baseline expression relied

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

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

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

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

169 Pancreatic cancer and melanoma cell lines express PrP.

170 All the primary uveal melanoma cell lines expressed CXCR4 and CCR7 message and

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

172 pared with results following PDT of the same melanoma cell line expressing wild-type survivin.

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

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

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

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

177 In melanoma cell lines, Gas6 induced Tyro3 phosphorylation

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

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

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

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

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

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

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

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

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

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

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

189 metastasis (P < 0.001) of highly metastatic melanoma cell lines in vivo.

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

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

192 Melanoma cell lines, including those with ETV1 amplifica

193 at unlike TRPM1, TRPM7 is expressed in human melanoma cell lines, indicating that these cells may als

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

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

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

197 1 and MEK162, inhibited the proliferation of melanoma cell lines irrespective of their mutation statu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 rmed on autologous cell lines and allogeneic melanoma cell lines originating from other patients.

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

219 Human uveal melanoma cell lines overexpressing the TJ molecule blood

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

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

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

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

224 Upon treatment, melanoma cell lines responded by dramatically increasing

225 ukin-1beta (IL-1beta), while less aggressive melanoma cell lines responded similarly to melanocytes.

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

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

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

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

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

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

232 9, hepatocellular carcinoma cell line HepG2, melanoma cell line SK-MEL-37, and pancreatic carcinoma c

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

234 Human melanoma cell lines, SK-MEL-3 and SK-MEL-28, despite ind

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

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

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

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

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

240 primary and one of the five metastatic uveal melanoma cell lines tested constitutively expressed PD-L

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

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

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

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

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

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

247 al properties and contractility of two human melanoma cell lines that differ in filamin A expression.

248 We developed stable transformant B16-F10 melanoma cell lines that express a ribozyme that targets

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

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

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

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

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

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

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

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

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

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

259 Melanoma cell lines treated with the demethylating agent

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

261 However, all primary and metastatic uveal melanoma cell lines upregulated PD-L1 expression after s

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

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

264 A panel of primary and metastatic uveal melanoma cell lines was evaluated for PD-L1 expression b

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

266 Rnd3 expression in human melanoma cell lines was strongly associated with elevate

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

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

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

270 A) to knock down MMP-1 expression in a human melanoma cell line, we investigated the role of MMP-1 in

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

272 ere, using a collection of established human melanoma cell lines, we defined the reproducibility, abs

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

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

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

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

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

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

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

282 Other melanoma cell lines, which retained some KIT expression

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 sed in primary human malignant melanomas and melanoma cell lines with activated Wnt/beta-catenin sign

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

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

288 genomic strategy to define a novel group of melanoma cell lines with co-overexpression of cyclin-dep

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

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

291 Melanoma cell lines with known sensitivity to BRAF inhib

292 Treatment of melanoma cell lines with PGD2 increased SOX9 expression

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

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

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

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

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

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

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

300 survivin in modulating PDT, we used a human melanoma cell line, YUSAC2/T34A-C4, stably transfected w