ライフサイエンスコーパス: melanoma cell

1 and T-cell exclusion within the vicinity of melanoma cells.

2 r, is downregulated in vemurafenib-resistant melanoma cells.

3 as an orchestrator of nuclear morphology in melanoma cells.

4 , and in their absence, T cells did not lyse melanoma cells.

5 ignificantly upregulated in CAFs adjacent to melanoma cells.

6 e assay and chromatin immunoprecipitation in melanoma cells.

7 ranscriptional effector of MAPK signaling in melanoma cells.

8 ce cellular differentiation and apoptosis in melanoma cells.

9 al than controls when implanted with B16.F10 melanoma cells.

10 hat synergize with TTM in BRAF(V600E)-driven melanoma cells.

11 NRas and BRAF at the plasma membrane (PM) of melanoma cells.

12 utophagy blockade only in BRAF(V600E)-mutant melanoma cells.

13 n the formation of invadopodia in metastatic melanoma cells.

14 s proliferation and inhibits invasiveness of melanoma cells.

15 ed a mass spectrometry-based screen in human melanoma cells.

16 CRISPR/Cas9 in human DM93 and murine B16-F1 melanoma cells.

17 ting motility of, podocytes, fibroblasts and melanoma cells.

18 e nanomolar concentration in A375 and B16F10 melanoma cells.

19 migration speed of invadopodia-forming A375 melanoma cells.

20 and autophagosomal genes in melanocytes and melanoma cells.

21 direct transfer of lipids from adipocytes to melanoma cells.

22 on to counter intracellular acidification in melanoma cells.

23 ce using Vemurafenib-sensitive and resistant melanoma cells.

24 MAPK inhibitors when overexpressed in human melanoma cells.

25 is, DNA damage and cell death selectively in melanoma cells.

26 iferation, and particularly invasiveness, of melanoma cells.

27 the population of MITF(high) differentiated melanoma cells.

28 r alterations and the invasive properties of melanoma cells.

29 a novel KIT regulator in KIT-mutant GIST and melanoma cells.

30 ties are characteristic of invasive amoeboid melanoma cells.

31 YAP/TAZ activity in human breast cancer and melanoma cells.

32 BMP signaling suppresses differentiation of melanoma cells.

33 murafenib resistance in BRAF(V600E)- bearing melanoma cells.

34 enhances cisplatin resistance in normal and melanoma cells.

35 of dual targeting of BRAF(V600E) and CDC7 in melanoma cells.

36 genes, individually and together, in B16-F1 melanoma cells.

37 ssion of immune checkpoint molecule PD-L1 in melanoma cells.

38 al, and invasive capacity of patient-derived melanoma cells.

39 r differentiation and drug responsiveness in melanoma cells.

40 fects on both BRAFi-sensitive and -resistant melanoma cells.

41 trategy to reduce the invasive properties of melanoma cells.

42 d protection from intradermal challenge with melanoma cells.

43 t capacity is linked to BRAFi sensitivity in melanoma cells.

44 the cytotoxicity of the drug in BRAF(V600E) melanoma cells.

45 cumulation of acetylated histone H4 in MM96L melanoma cells.

46 complex to promote an invasive phenotype in melanoma cells.

47 ss PARK2 expression and promoter activity in melanoma cells.

48 of glutamine compared to radial growth phase melanoma cells.

49 uppressed invasion within PGC1alpha-silenced melanoma cells.

50 eby enhancing migration and intravasation of melanoma cells.

51 e chromatin occupancy of DDX21 in human A375 melanoma cells.

52 athway-targeted inhibitors and starvation in melanoma cells.

53 e induction of the innate immune response in melanoma cells.

54 at TRAF6 promotes the malignant phenotype of melanoma cells.

55 nd showed antiproliferative activity on A375 melanoma cells.

56 n the metastatic lines of all three pairs of melanoma cells.

57 different from that of either fibroblasts or melanoma cells.

58 ISPR/Cas9-mediated disruption of HER2 in the melanoma cells abrogated the killing effect of the CAR-T

59 We posit that melanoma cells acquire metastatic capability by adopting

60 (Glycoprotein V), GRN (granulin), and MCAM (melanoma cell adhesion molecule) were associated with PL

61 ile, the intervention of TRAF6 expression in melanoma cells affected the activation of CAFs.

62 We propose eradication of amoeboid melanoma cells after surgical removal as a therapeutic s

63 DK was found to control the transcriptome of melanoma cells, allowing for coordinated activation of n

64 EphB4 overexpression in melanoma cells ameliorates the metastatic phenotype and

65 per dermis layer within proximity to in situ melanoma cells, an observation that correlated with dise

66 riptional deregulation of mRNA expression in melanoma cells and assess how these changes facilitate m

67 eased transcriptional activation of c-Jun in melanoma cells and conveyed resistance to BRAF inhibitio

68 in vemurafenib-resistant BRAF(V600E)-mutant melanoma cells and human biopsies, and in silico analysi

69 tively induces apoptosis in BCL2A1-dependent melanoma cells and MCL1-dependent NSCLC cells.

70 Depletion of MITF in melanoma cells and melanocytes attenuates the response t

71 ion via inhibition of autophagy in resistant melanoma cells and mouse xenograft models.

72 equencing profiles of sensitive to resistant melanoma cells and performed pathway analysis.

73 rs, but resulted in depletion of circulating melanoma cells and reduced the metastatic disease burden

74 Wnt5A to facilitate metastatic potential in melanoma cells and rely on Wnt5A for their immunosuppres

75 lecule that mediates the interaction between melanoma cells and stromal fibroblasts, suggesting that

76 and for MC1R-specific cytotoxicity in uveal melanoma cells, and the lanthanum-DOTA-MC1RL analog was

77 In B16 melanoma cells, ArhGAP12 suppresses basal Rac and Cdc42

78 ns exert considerable detrimental effects on melanoma cells at concentrations better tolerated by epi

79 mma, has a role in the immune recognition of melanoma cells by contributing to diversification of the

80 esses the migration and invasion of cultured melanoma cells by modulating the activities of matrix me

81 released upon recognition of the SB-3123(p) melanoma cells by Pmel-1 CD8(+) T-cells.

82 oliferative-to-invasive phenotypic switch in melanoma cells by repressing the expression of the micro

83 d to lysine 27-linked poly-ubiquitination in melanoma cells by the ITCH ubiquitin E3 ligase.

84 e metastatic cascade, and it illuminates how melanoma cells can acquire an early metastatic phenotype

85 Here, we show that melanoma cells can adapt to targeted therapies through a

86 Melanoma cells can switch between a melanocytic and a me

87 ion and a new mechanism for MEKi function in melanoma cells carrying NRas mutations but lacking MEK m

88 In mouse and human melanoma cells CDK5 promotes cell invasiveness by direct

89 amma reduced virus yield only 2-fold in MeWo melanoma cells compared to that of untreated cells.

90 mitochondrial accumulation of polycations in melanoma cells compared with epidermal melanocytes.

91 This latter activity reverses the effect of melanoma cell-conditioned macrophages in blocking NK act

92 ere we show that metabolic differences among melanoma cells confer differences in metastatic potentia

93 ptosis in BRAF inhibitor-naive and resistant melanoma cells containing a BRAF V600E mutation.

94 indicates that a persisting subpopulation of melanoma cells contributes to resistance to targeted the

95 tumor growth in mice bearing ARID2-knockout melanoma cells, correlating with an increase in the infi

96 s of BRAF inhibitor-sensitive and -resistant melanoma cells demonstrated resistance to be associated

97 Six of them were melanoma cells derived from various stages of tumor prog

98 parated by immunocapture into two fractions: melanoma cell-derived exosomes (MTEX) and normal cell-de

99 aracterized Tspan8 for its ability to prompt melanoma cell detachment from their microenvironment and

100 ma patients, and in BRAF inhibitor-resistant melanoma cells displaying a mesenchymal invasive MITF(lo

101 RAD6B knockout or inhibition in metastatic melanoma cells downregulated beta-catenin, beta-catenin-

102 Genetic silencing of PTX3 in invasive melanoma cells dramatically impaired migration and invas

103 iptional programs can become liabilities for melanoma cells due to their acquired dependencies on the

104 sphorylation, reduced invasion, and impaired melanoma cell-endothelial cell interactions.

105 Eradicating all melanoma cells even in drug-sensitive tumors is unsucces

106 Further, in BRAF(V600E)-positive melanoma cells evolved to be resistant to BRAF and/or ME

107 Indeed, malignant melanoma cells exhibit elevated DNFA gene expression aft

108 regulated by a negative feedback mechanism; melanoma cells exposed to IFN upregulate expression of L

109 Importantly, amoeboid melanoma cells express both proliferative and invasive g

110 In vivo, melanoma cells expressing EphA2-S897E or active Cdc42 sh

111 ted significant growth inhibitory effects in melanoma cells expressing high levels of MITF.

112 f CAV1 immunoprecipitates from B16F10 murine melanoma cells expressing or not E-cadherin.

113 n metastasis: EVs from the IGF2BP1 knockdown melanoma cells failed to promote metastasis, whereas EVs

114 diagnostic and therapeutic radionuclides to melanoma cells for imaging and therapy.

115 e to the lymphatic environment thus protects melanoma cells from ferroptosis and increases their abil

116 Oleic acid protected melanoma cells from ferroptosis in an Acsl3-dependent ma

117 the unique composition of lymph may protect melanoma cells from ferroptosis-a form of iron-dependent

118 Melanoma cells from lymph nodes were more resistant to f

119 The CAR-T cells were also able to kill melanoma cells from patients resistant to adoptive T-cel

120 se and that MEK/ERK signaling pathways shift melanoma cells from proliferation to invasion.

121 astases after intravenous injection than did melanoma cells from subcutaneous tumours.

122 reas EVs isolated from IGF2BP1-overexpressed melanoma cells further accelerated EV-induced metastasis

123 PARK2 overexpression reduces melanoma cell growth in vitro and in vivo and induces ap

124 FLG and DST support melanoma cell growth in vitro and in vivo.

125 The MHC class I Ag presentation pathway in melanoma cells has a well-established role in immune-med

126 The highly malignant NME1(LOW) variant of melanoma cells has potential to provide novel therapeuti

127 idative stress and form more metastases than melanoma cells in blood.

128 esses tumor metastasis of B16F10 and YUMM1.7 melanoma cells in both C57BL/6Ncrl and NOD-scid IL2Rgamm

129 Thereby, FR suppressed the proliferation of melanoma cells in culture and inhibited the growth of Ga

130 Here we show that melanoma cells in lymph experience less oxidative stress

131 , migration, and invasion of mouse and human melanoma cells in multiple in vitro assays.

132 The adaptability of melanoma cells in nutrient- and therapeutically-challeng

133 a vector provides extensive killing of human melanoma cells in vitro and a potent anti-tumor effect i

134 efficiently abrogate SOX10 protein in human melanoma cells in vitro and in melanoma mouse models in

135 ed against HER2 can kill uveal and cutaneous melanoma cells in vitro and in vivo.

136 roblasts promoted the malignant phenotype of melanoma cells in vitro and in vivo.

137 egulator of metabolism in BRAF(V600E)-mutant melanoma cells in vitro.

138 and PGE2 were also observed in NRF2-deleted melanoma cells in vivo.

139 onic acid (DIDS)-dependent pH(i) recovery in melanoma cells, in response to intracellular acidificati

140 ogical inhibition of BRAF-V600E or ERK1/2 in melanoma cells increases PARK2 expression.

141 phagy, whereas the overexpression of MITF in melanoma cells increases the number of autophagosomes bu

142 enhances cisplatin resistance in normal and melanoma cells independently of beta-catenin.

143 Moreover, the EVs from IGF2BP1 knockdown melanoma cells inhibited fibronectin deposition and accu

144 r cells (EO771 mammary carcinoma and B16-F10 melanoma cells) injected into wild-type and MNX mice (i.

145 A methylation in the critical protumorigenic melanoma cell-intrinsic genes including PD-1 (PDCD1), CX

146 veals that tumor-derived PTX3 contributes to melanoma cell invasion via targetable inflammation-relat

147 mesenchymal-to-amoeboid transition promoted melanoma cell invasion, survival under shear stress, adh

148 ment from their microenvironment and trigger melanoma cell invasiveness, but the signaling events by

149 turn, apoptotic killing of a wide variety of melanoma cells, irrespectively of their stage, mutationa

150 High expression of AXL in melanoma cells is associated with high expression of inv

151 induced increases of TGF-beta1 expression in melanoma cells is attenuated in the presence of high lep

152 Here, we report that growth of BRAF-mutant melanoma cells is inhibited, up to complete rejection, i

153 the MHC class II Ag presentation pathway in melanoma cells is less clear.

154 Melanoma cells lacking functional Elkin1 exhibit defecti

155 ession of active noncanonical EphA2-S897E in melanoma cells led to a mesenchymal-to-amoeboid transiti

156 Functionally, overexpression of KDM5B in melanoma cells led to broadening of their oxidative meta

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 Treatment of melanoma cell lines expressing endogenous AT2R with eith

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 enib diminishes the metabolic flexibility of melanoma cells, making them unable to shift between glyc

210 Upon growth challenge, Rac1(P29S)-harboring melanoma cells massively upregulate lamellipodia formati

211 the surface and biomechanical properties of melanoma cells, measured by mass spectrometry (ToF-SIMS)

212 Preventing melanoma cell mechanical reprogramming might be a promis

213 hat extracellular vesicles (EVs) secreted by melanoma cells mediate the effects of IGF2BP1 on metasta

214 in endothelial cells, incubated with the B16 melanoma cell medium for 2 hours, expressed decreased le

215 miR-211 deficiency rendered melanoma cells metabolically vulnerable by attenuating m

216 d modulates cellular adhesions and regulates melanoma cell migration and cell-cell interactions.

217 In vitro, IFNgamma reduced melanoma cell migration, cell-cycle activity, and basal

218 4 and MYD88 knockdown inhibited PTX3-induced melanoma cell migration, suggesting that PTX3 functions

219 cytostatic stress-resulted sEVs facilitated melanoma cell migration; all sEV groups supported microt

220 fter secondary envelopment in fibroblasts or melanoma cells, multiple infectious VZV particles accumu

221 No significant cell shearing of uveal melanoma cells occurred in vitro with 25 G, 27 G, or 30

222 hat block paradoxical signaling in malignant melanoma cells occurring through this drug target.

223 etected on tape-stripped samples with murine melanoma cells of different concentrations.

224 Melanoma cells of high metastatic potential demonstrate

225 lore how the stiffness of the ECM influences melanoma cells of varying metastatic potential.

226 Cancer cells, including melanoma cells, often metastasize regionally through the

227 veal low, medium, and large deformability of melanoma cells originating from vertical growth phase (V

228 Murine melanoma cells overexpressing VDR produced fewer pulmona

229 ompetent mice with mouse melanomas, had more melanoma cells per microlitre in tumour-draining lymph t

230 geneity, based on transcriptionally distinct melanoma cell phenotypes.

231 Melanoma cells preserve intracellular pH (pH(i)) within

232 Conversely, its genetic silencing increases melanoma cell proliferation and reduces cell death.

233 SMI#9 treatment inhibited melanoma cell proliferation but not normal melanocytes.

234 It inhibited colorectal cancer and melanoma cell proliferation much more effectively than i

235 ro suggest that these genes may also support melanoma cell proliferation through angiogenesis-indepen

236 SCD) and that SCD is required for MITF(High) melanoma cell proliferation.

237 DK on human lymphatic endothelial (HLEC) and melanoma cell proliferation.

238 ain of Zeb2 expression in pulmonary-residing melanoma cells promoted the development of macroscopic l

239 uences bone metastasis formation by altering melanoma cell repulsion/adhesion to bone endothelial cel

240 ith this model, miR-211 expression increased melanoma cell resistance to both the inhibitors, and thi

241 tors), and DNFA expression remains higher in melanoma cells resistant to vemurafenib treatment than i

242 ncoding mDia1 and -3 formins in B16-F1 mouse melanoma cells revealed enhanced frequency of cells disp

243 Melanoma cells secrete their own ECM proteins, an event

244 tify SMIM10, a mitochondrial protein that in melanoma cells selectively downregulates BRAFV600E RNA a

245 the PRMT5-MDM4 axis is essential for robust melanoma cell sensitivity and provide preclinical eviden

246 onserved IFN-gamma transcriptome response in melanoma cells serves to amplify the antitumor immune re

247 Melanoma cells shift between epigenetic-metabolic states

248 Upon SMIM10 overexpression, BRAFV600E melanoma cells show disrupted mitochondrial structure/fu

249 Vertical growth phase human melanoma cells show higher oxygen consumption and prefer

250 Human melanoma cells (SK-MEL-28) transfected with APCN cDNA ac

251 case study owing to the presence of distinct melanoma cell states.

252 increased lung colonization from circulating melanoma cells, suggesting that the prometastatic functi

253 hat SMIM10 exerts an oncosuppressive role in melanoma cells.Taken together, our results unveil the po

254 esence of mechanically activated currents in melanoma cells that are dependent on TMEM87a, which we h

255 ow that a subpopulation of BRAF(V600) mutant melanoma cells that tolerates exposure to BRAF and MEK i

256 analyses and RNAseq on two panels of primary melanoma cells that were either sensitive or resistant t

257 high Tspan8 expression level, conferring to melanoma cells the invasive properties required for tumo

258 ed the abundance of the TGF-beta receptor in melanoma cells, thereby enhancing cellular responsivenes

259 -lysine)s, prevent vemurafenib resistance in melanoma cells through induction of mitochondrial bioene

260 Additionally, metastatic human melanoma cells/tissues exhibited diminished levels of JA

261 shed levels of JAK3 mRNA relative to primary melanoma cells/tissues.

262 ontrast, genetic targeting of MDK sensitized melanoma cells to anti-PD-1/anti-PD-L1 treatment.

263 ks the slow-cycling phenotype and sensitizes melanoma cells to BRAF/MEK inhibition.

264 y targeting therapies mechanically reprogram melanoma cells to confer a drug-protective matrix enviro

265 atical flux balance analyses in BRAF-mutated melanoma cells to discover that elevated antioxidant cap

266 nificantly reduces the ability of aggressive melanoma cells to enter the blood stream, colonize dista

267 Knockdown of FTO sensitizes melanoma cells to interferon gamma (IFNgamma) and sensit

268 c42EP5 is consistently required for amoeboid melanoma cells to invade and migrate into collagen-rich

269 Here we used ribosome profiling in melanoma cells to investigate the effects of prolonged I

270 -specific inhibitors limit the adaptation of melanoma cells to multiple stresses including BRAF-MEK i

271 indings reveal a biomechanical adaptation of melanoma cells to oncogenic BRAF pathway inhibition, whi

272 inhibitors synergistically sensitized uveal melanoma cells to PLX51107 treatment.

273 The ability of melanoma cells to switch from melanocytic to mesenchymal

274 romoted metastatic initiation by sensitizing melanoma cells to TGF-beta.

275 ay sensitize previously resistant metastatic melanoma cells to therapy.

276 d quantitative (phospho)-proteomics of human melanoma cells treated with either dabrafenib, a BRAF in

277 anistically, autocrine production of PTX3 by melanoma cells triggered an IKK/NFkappaB signaling pathw

278 In vivo fate mapping made clear that melanoma cells undergo a conversion in state where ZEB2

279 ic state on the immune response, we examined melanoma cells upon metabolic perturbations or CRISPR-Ca

280 Here, we show that EV from Ret mouse melanoma cells upregulate the expression of programmed c

281 EV from human melanoma cells upregulated PD-L1 and immunosuppression o

282 l therapeutic targets in KIT-mutant GIST and melanoma cells using a human tyrosine kinome siRNA scree

283 Survival of uveal melanoma cells was evaluated in vitro following needle a

284 expression in murine B16-F10 and human A2058 melanoma cells was investigated following its silencing

285 Growth of ERbeta-positive breast cancer and melanoma cells was significantly decreased by treatment

286 Here, we show that PGC1alpha expression in melanoma cells was silenced by chromatin modifications t

287 using a genome-wide CRISPR screen in B16.SIY melanoma cells, we confirm Ifngr2 and Jak1 as important

288 roblasts and immune cells in the presence of melanoma cells, we generate a reconstructed TME that clo

289 Using SK-MEL 28 human melanoma cells, we show that endogenous alpha-syn is pre

290 In wild-type mice injected with melanoma cells, we show that the stem cell transcription

291 focused phototoxicity effects in which human melanoma cells were killed after 5 min of light exposure

292 and to promote proliferation and invasion of melanoma cells, whereas the ubiquitination-deficient BRA

293 IFNgamma also increased PD-L1 levels on the melanoma cells, which may counterbalance some of the ben

294 row in two-dimensional in vitro assays using melanoma cells with fluorescent cell-cycle indicators an

295 man melanoma biopsies revealed that amoeboid melanoma cells with high Myosin II activity are predomin

296 Treatment of MAPK inhibitor-resistant melanoma cells with MDM2 inhibitor Nutlin-3A restored FB

297 Patient-derived melanoma cells with silenced HLA-I APM escaped recogniti

298 reas PTEN levels increased with treatment of melanoma cells with the histone deacetylase inhibitor LB

299 tor vemurafenib and in vemurafenib-resistant melanoma cells, with miR-211 loss rendering them more dr

300 nd confers resistance to targeted therapy in melanoma cells, xenograft mouse models, and patient samp