ライフサイエンスコーパス: melanoma

1 e obtained for TRB CDR3s and NRAS mutants in melanoma.

2 t inhibitors for the treatment of metastatic melanoma.

3 ode biopsy, which showed absence of residual melanoma.

4 the use of neoadjuvant therapy in cutaneous melanoma.

5 or many diseases, including the diagnosis of melanoma.

6 with advanced-ie, unresectable or metastatic-melanoma.

7 iris epithelial neoplasms, melanocytoma, and melanoma.

8 mising potential therapeutic target in uveal melanoma.

9 linical PD-L1 expression scores in malignant melanoma.

10 emic therapies in cutaneous and noncutaneous melanoma.

11 ine-5,6-dione [phendione]) in drug-resistant melanoma.

12 g that PHGDH may be a therapeutic target for melanoma.

13 ntributes to the high rates of metastasis in melanoma.

14 mab, in 2011 for the treatment of metastatic melanoma.

15 NB) is an important prognostic factor for T1 melanoma.

16 ssion of ANGPT2 in a subset of patients with melanoma.

17 enotypically exhausted CD8+ T cells in human melanoma.

18 with metastatic and unresectable BRAF(V600) melanoma.

19 atients with anti-PD-1-refractory metastatic melanoma.

20 r treatment of BRAF(V600E) mutation-positive melanoma.

21 bled killing of autologous and nonautologous melanoma.

22 tasis of breast cancer, prostate cancer, and melanoma.

23 00) mutation-positive advanced or metastatic melanoma.

24 cells as well as Galpha(q/11) mutated uveal melanoma.

25 t thigh lesion confirmed to be biopsy-proven melanoma.

26 change is the most common driver mutation in melanoma.

27 ergize or enhance ACT-based immunotherapy of melanoma.

28 rm surveillance strategies for patients with melanoma.

29 he GEP test in patients with posterior uveal melanoma.

30 hypermutation, and acral, but not cutaneous, melanomas.

31 ted to exacerbate the malignant potential of melanomas.

32 n in patient-derived xenografts and in mouse melanomas.

33 umans prospective study included 6 patients (melanoma, 1; lung, 4; hepatocellular carcinoma, 1).

34 ultiple types of cancer (prostate, lung, and melanoma; 100 samples in total) solely using plasma-deri

35 nts with an untreated conjunctival lesion (5 melanoma, 13 nevus, 7 primary acquired melanosis [PAM])

36 me-dependent increase of HDAC3 and absent in melanoma 2 (AIM2) inflammasome in primary cultured micro

37 in 27.8%, being most common in patients with melanoma (40.9%).

38 2 patients with an untreated iris lesion (10 melanoma, 42 nevus) were included.

39 % [difference, 3.8%; 95% CI, -1.0% to 8.4%]; melanoma: 54.4% vs 35.4% [difference, 19.0%; 95% CI, 9.1

40 [difference, 28.0%; 95% CI, 1.4% to 54.6%]; melanoma: 63.4% vs 36.6% [difference, 26.8%; 95% CI, 17.

41 % [difference, 7.6%; 95% CI, 2.2% to 13.1%]; melanoma: 74.4% vs 59.2% [difference, 15.2%; 95% CI, 3.7

42 ts therapeutic efficacy in controlling mouse melanoma (8-fold reduction in tumor volume), which is as

43 [difference, 34.3%; 95% CI, 10.9% to 57.6%]; melanoma: 80.8% vs 60.5% [difference, 20.3%; 95% CI, 10.

44 dition, codes for both morphologic features (melanoma, 8720-8790) and site (retina, C69.2; choroid, C

45 1% [difference, 4.6%; 95% CI, 3.0% to 6.3%]; melanoma: 91.7% vs 86.2% [difference, 5.5%; 95% CI, 2.2%

46 tandard method (prostate cancer: 198 vs 182; melanoma: 93 vs 74); sensitivity (prostate cancer: 94.7%

47 ) and diminishes growth of NRAS(Q61R)-driven melanoma, a cancer with no effective therapy.

48 erstanding of the genomic landscape of acral melanoma, a rare form of melanoma occurring on palms, so

49 HDI; for the first time to our knowledge in melanoma adjuvant therapy, E1609 has demonstrated a sign

50 elanoma (CM), assess their relationship with melanoma aggressiveness and analyze the factors related

51 lusion, TGF-beta1 levels are associated with melanoma aggressiveness in CM patients and increased in

52 rs or older with resected stage IIIB-C or IV melanoma and an Eastern Cooperative Oncology Group perfo

53 as been approved for treatment of metastatic melanoma and anaplastic thyroid cancer in patients with

54 ing from prostate and lung adenocarcinoma to melanoma and basal cell carcinoma.

55 e its role in the metastatic cascade of both melanoma and breast cancer cells in vivo.

56 In melanoma and breast cancer models, it is shown that gCM-

57 reatment, and transplant recommendations for melanoma and hematological malignancies.

58 Here, we found that melanoma and lung and breast cancer cells experiencing s

59 In B16-F10 melanoma and MC38 colorectal carcinoma mouse models, rep

60 ionized the clinical management of malignant melanoma and now offer hope to patients with advanced di

61 ated in the presence of E-cadherin in B16F10 melanoma and other cancer cells.

62 sults of immune checkpoint blockade (ICB) in melanoma and other cancers, clinical trials in breast ca

63 in many metastatic human cancers, including melanoma and other nonmelanoma skin cancers.

64 ent strategy for RAF/MEK inhibitor-resistant melanoma and potentially other tumor types.

65 response to immune checkpoint inhibitors in melanoma and small-cell lung cancer.

66 We analyzed ganglioside pattern on four melanoma and two neuroblastoma cell lines by high perfor

67 t ZEB2 is required for outgrowth for primary melanomas and metastases at secondary sites.

68 ations of gamma knife radiosurgery for uveal melanomas and metastases.

69 grades of breast cancers, colorectal cancer, melanoma, and insulinoma) and other diseases including v

70 tic tumors (iris melanoma, ciliary-choroidal melanoma, and melanocytoma) and retinal pigment epitheli

71 ical malignancy, four colorectal cancer, one melanoma, and seven multiple myeloma).

72 oft tissue sarcomas, uterine leiomyosarcoma, melanomas, and radiotherapy-related central nervous syst

73 The melanoma antigen (MAGE) proteins all contain a MAGE homo

74 ptide derived from the cancer testis antigen melanoma antigen-A4 (MAGE-A4).

75 F6 and expressing a transgenic TCR for gp100-melanoma antigen.

76 is study, we investigated a small library of melanoma antigens and the effects of several formulation

77 Among the hallmarks of melanoma are impaired proteostasis and rapid development

78 As such, invasive fronts of human and mouse melanomas are enriched in amoeboid cells that are also k

79 circular RNAs (circRNA) in metastasis, using melanoma as a model aggressive tumor.

80 ically-challenged environments distinguishes melanoma as an ideal model for investigating therapy res

81 d antitumor response to a tissue-restricted, melanoma-associated self-antigen.

82 a lineage approach would uncover metastatic melanoma biology.

83 expression was detected in RIG-Ihi (DDX58hi) melanoma biopsies, correlating with improved patient sur

84 es, including breast, lung, ovary, pancreas, melanoma, bone, and brain tumors.

85 of tumor and microenvironment cell states in melanoma, but little is understood about their function

86 identified in a set of vemurafenib-resistant melanomas, but little is known about how EGFR, or possib

87 cate that GALC may play an oncogenic role in melanoma by modulating the levels of intracellular ceram

88 e multipotency and differentiation status of melanoma can determine ICB benefit.

89 In vivo studies using B16-F10 melanoma cancer cells implanted in C57/BL6 mice demonstr

90 cological, head and neck, lung, lymphoma, or melanoma cancers were eligible.

91 Metastatic melanoma carries a poor prognosis despite modern systemi

92 Consistently, patients with melanoma carrying the APOE4 variant experienced improved

93 e rates and profound regression of malignant melanomas carrying BRAF(V600E) mutations.

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

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

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

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

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

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

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

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

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

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

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

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

106 We posit that melanoma cells acquire metastatic capability by adopting

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 r alterations and the invasive properties of melanoma cells.

132 ties are characteristic of invasive amoeboid melanoma cells.

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

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

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

136 cumulation of acetylated histone H4 in MM96L melanoma cells.

137 complex to promote an invasive phenotype in melanoma cells.

138 ss PARK2 expression and promoter activity in melanoma cells.

139 nd showed antiproliferative activity on A375 melanoma cells.

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

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

142 All melanocytic tumors (iris melanoma, ciliary-choroidal melanoma, and melanocytoma)

143 utations and MDM2 upregulation were found in melanoma clinical samples.

144 active TGF-beta1 in patients with cutaneous melanoma (CM), assess their relationship with melanoma a

145 rning method had a higher sensitivity in the melanoma cohort (71.6% vs 53.7% [difference, 17.9%; 95%

146 857 [79.9%] with European ancestry) and the melanoma cohort included 1295 patients (mean [SD] age at

147 c target to enhance immunotherapy outcome in melanoma, colorectal, and potentially other cancers.

148 monstrates loss of primary cilia in Spitzoid melanoma compared with Spitz nevi and positions ciliatio

149 ied PhISCS-BnB on a recently published large melanoma dataset derived from the sublineages of a cell

150 pidly after age 50, and nearly two thirds of melanoma deaths are male.

151 lammation is protumorigenic, we transplanted melanoma-derived cells into G2 tert zebrafish embryos an

152 wnstream target of RAC1, in a mouse model of melanoma driven by BRAF(V600E);PTEN loss.

153 the most frequent first primary tumours were melanoma (eight patients, 17.8%), lymphoma (seven patien

154 In patients with melanoma, exosomal PDL1 is also a marker of immune activ

155 The melanoma field has seen an unprecedented set of clinical

156 ecommended in exceptional cases of choroidal melanoma, for which other treatments with greater tumor

157 r cutaneous melanoma than unrelated cases or melanoma-free healthy controls (Bonferroni-corrected t-t

158 Melanomas frequently harbor activating NRAS mutations le

159 model increased the proportion of mice with melanoma, further supporting that DCC is a melanoma tumo

160 gnificant decrease in CI within the spitzoid melanoma group when compared with either the Spitz nevi

161 d cellular processes associated with primary melanoma growth and invasion, including oxidative stress

162 nical Wnt signaling has a profound effect on melanoma growth and is able to counteract Sox10-dependen

163 elated with mitotic index, Breslow index and melanoma growth rate, and were increased in presence of

164 s reduce metastatic burden for patients with melanomas harboring BRAF mutations; however, most eventu

165 pression of the EMT-TF ZEB2 in human primary melanoma has been shown to correlate with reduced invasi

166 Metastatic uveal melanoma has poor overall survival (OS) and no approved

167 s of the stromal-immune interface across 400 melanoma hematoxylin and eosin (H&E) specimens from The

168 Despite advances in therapy for melanoma, heterogeneous responses with limited durabilit

169 We previously identified that the melanoma immune profile (MIP), an IFN-based gene signatu

170 d as an underestimated barrier to successful melanoma immunotherapy.

171 Conditional survival estimates of uveal melanoma improve with time since primary diagnosis.

172 ther explored the associations of these with melanoma in addition to deprivation and socio-economic s

173 sed overall survival in advanced BRAF-mutant melanoma in both therapeutic and adjuvant clinical setti

174 involved in this incompatibility also causes melanoma in hybrids between distantly related species.

175 The point prevalence of uveal melanoma in patients with the germline BAP1 pathogenic v

176 with resected, BRAF(V600)-mutant, stage III melanoma in the phase 3 COMBI-AD trial.

177 Melanoma incidence was lower among exposed individuals (

178 ges in mRNA transcription that in turn drive melanoma initiation and progression.

179 ng efforts have led to the classification of melanoma into four major subtypes (i.e., BRAF-mutant, NR

180 ic SOX2-GLI1 transcriptional complex driving melanoma invasion through the induction of the sialyltra

181 radial to vertical growth, the first step in melanoma invasion, we developed a zebrafish melanoma mod

182 ation and activation that, in turn, promotes melanoma invasion.

183 Cutaneous malignant melanoma is an aggressive cancer of melanocytes with a s

184 Malignant melanoma is an aggressive skin cancer with poor survival

185 Metastatic melanoma is challenging to manage.

186 Growth of anti-PD-1 therapy resistant melanoma is effectively inhibited in Siah2(-/-) mice sub

187 open question in aggressive cancers such as melanoma is how malignant cells can shift the immune sys

188 clinical risk is whether the initial primary melanoma lesion will metastasize and cause advanced dise

189 Tissues adjacent to melanoma lesions (skin) and distant organs (intestine) i

190 Here, using the melanoma lineage survival oncogene MITF as a model, we s

191 th and is able to counteract Sox10-dependent melanoma maintenance both in vitro and in vivo.

192 nd study the role of patrolling monocytes in melanoma metastasis to lungs, we generated C57BL/6J mice

193 a role of JAK3 as a potential suppressor for melanoma metastasis.

194 ed promising outcomes in patients with uveal melanoma metastatic to the liver.

195 melanoma invasion, we developed a zebrafish melanoma model in which constitutive activation of ribos

196 This study utilized a murine melanoma model to evaluate the efficacy of intratumoral

197 Finally, in a murine melanoma model, the frequency of PD-1-expressing tumor-i

198 ote antitumor immune responses in the B16-F0 melanoma model.

199 myeloid-derived suppressor cells in various melanoma models.

200 rogression of a mutant Braf;Pten loss-driven melanoma mouse model.

201 rcinomas (n=24), renal carcinomas (n=11), or melanoma (n=44) treated with immunotherapy.

202 with PD-1 blockade in patients with advanced melanoma, non-small cell lung cancer, or bladder cancer.

203 cell carcinoma of the head and neck (SCCHN), melanoma, non-small-cell lung cancer (NSCLC), or urothel

204 vated redox capacity is a general feature of melanomas, not previously observed.

205 types with underlying BRAF driver mutations: melanoma, NSCLC, and ATC.

206 landscape of acral melanoma, a rare form of melanoma occurring on palms, soles or nail beds, whole g

207 tively associated with having a diagnosis of melanoma (odds ratio [OR] 5.01; 95% Confidence Interval

208 Patients with melanoma or a centrally confirmed, PD-L1-positive, relap

209 mRNA expression in paired primary/metastatic melanoma or colorectal cancer cells than those that are

210 radiosurgery as primary treatment for uveal melanoma or uveal metastases.

211 tigation of APOE genotype as a biomarker for melanoma outcome and therapeutic response.

212 t reduces tumor growth of BRAF(V600E)-driven melanoma patient-derived xenografts (PDX) and diminishes

213 rophils, which were expanded in the blood of melanoma patients and detectable in blood and tumors fro

214 our blood vessels are pericyte-FAK negative, melanoma patients are stratified into those with increas

215 LKBH5 gene mutation and expression status of melanoma patients correlate with their response to immun

216 e inhibitors (TKI), the majority of stage IV melanoma patients eventually succumb to the disease.

217 infiltrating T lymphocytes (TILs) from eight melanoma patients for all their class I alleles.

218 erve as important biomarkers for stratifying melanoma patients for immune-checkpoint treatment.

219 atient-derived cells in vitro, as well as in melanoma patients in vivo.

220 ng the outcome of immunotherapy treatment in melanoma patients is challenging.

221 age at diagnosis and the gender of the uveal melanoma patients with BAP1 germline pathogenic variants

222 Melanoma patients' plasma contains exosomes produced by

223 In melanoma patients, a tumor-intrinsic NGFR signature pred

224 atments to bolster the options available for melanoma patients.

225 JAK3 is correlated with poorer prognosis in melanoma patients.

226 ance to glucose deficiency among the studied melanoma phenotypes.

227 role for RAC1 activity in BRAF(V600E)-driven melanoma progression and drug resistance.

228 TCC) expression may serve as a biomarker for melanoma progression and prognosis, and we showed that T

229 onal investigation of cell states throughout melanoma progression and treatment.

230 ession, centrosome number abnormalities, and melanoma progression in cell lines derived from various

231 derstanding the molecular events controlling melanoma progression is of paramount importance for the

232 bout the recently proposed role for STK19 in melanoma progression via a function as an NRAS kinase, s

233 Netrin-1 and its receptor DCC regulate melanoma progression, suggesting therapeutic targeting o

234 in cell lines derived from various stages of melanoma progression.

235 tion-attenuating glycoprotein non-metastatic melanoma protein B (GPNMB) signaling in human PD SN.

236 Genetic risks for cutaneous melanoma range from rare, high-penetrance mutations to c

237 rgets to enhance the effects of BRAFi in any melanoma, regardless of mutational status.

238 Here we report the localization of the melanoma regulatory locus to a single gene, rab3d, which

239 Salvage patterns after melanoma relapse showed significantly higher rates of ip

240 pite the advent of immunotherapy, metastatic melanoma represents an aggressive tumor type with a poor

241 nal to PI3K pathway is essential to overcome Melanoma resistance to fotemustine.

242 Patients with melanoma resistant to RAF/MEK inhibitors (RMi) are frequ

243 uterine, cervical, and esophageal cancer and melanoma, respectively.

244 rferon-beta gene transfer in mouse models of melanoma, resulting in control of tumor progression, but

245 nal-regulated kinase inhibitor resistance in melanoma results in a new transcriptional state associat

246 In men, the incidence of melanoma rises rapidly after age 50, and nearly two thir

247 dence for an association between 25(OH)D and melanoma risk overall.

248 he association between valproic acid use and melanoma risk.

249 otential to revolutionize mouse modeling for melanoma.See related article by Bok et al., p.

250 ucted neoadjuvant ICB trial in patients with melanoma showed via targeted expression profiling(17) th

251 ociated lymphocytes, most prominent in uveal melanoma, showed positive results for PAX8.

252 ergistic effect on breast cancer (MCF-7) and melanoma (SK-MEL-5) was proven.

253 cles contain melanosome markers suggesting a melanoma-specific mechanism of EV release, regulated by

254 age III cohort versus the AJCCv8 cohort, the melanoma-specific survival (MSS) rates at 5 years were 6

255 25(OH)D was associated with higher risks of melanoma (SRR (95% CI) per 30 nmol = 1.42 (1.17-1.72)) a

256 from an open reading frame downstream of the melanoma stem cell marker gene ABCB5.

257 g and stromal barrier, which represented the melanoma stromal microenvironment.

258 on Cancer (AJCC) stage, Collaborative Ocular Melanoma Study (COMS) size, tumor largest basal diameter

259 re-existing NGFR(hi) multitherapy-refractory melanoma subpopulation, which ought to be eliminated to

260 regions and host factors suggests the acral melanoma subtype is uniquely unrelated to pigmentation.

261 By extending our analyses to other melanoma subtypes in The Cancer Genome Atlas, we predict

262 l secondary loci for a total of 85 cutaneous melanoma susceptibility loci.

263 otably, ARID2 mutations are more frequent in melanoma than PBRM1 mutations.

264 tly higher mean polygenic load for cutaneous melanoma than unrelated cases or melanoma-free healthy c

265 ICIs) have achieved unprecedented results in melanoma, the biological features of the durable respons

266 ent a novel therapeutic target in metastatic melanoma, the most lethal form of skin cancer.

267 mide, thus providing novel opportunities for melanoma therapy.

268 the early progression of noninvasive primary melanoma to an invasive state is poorly understood.

269 ling, improves the response of patients with melanoma to checkpoint immunotherapy(1,2).

270 etastases are less responsive than cutaneous melanoma to chemotherapy or immune checkpoint inhibitors

271 ations that drive the progression of primary melanoma to metastatic disease have been studied extensi

272 utcome of patients with metastatic cutaneous melanoma to the vitreous.

273 Melanomas treated with the 10-mm plaque were smaller (me

274 f this signaling axis as a viable option for melanoma treatment.

275 t the role of the miR-211-DUSP6-ERK5 axis in melanoma tumor growth and suggest a mechanism for the de

276 h melanoma, further supporting that DCC is a melanoma tumor suppressor.

277 lation led to ~70% regression of established melanoma tumor.

278 ug in suppressing the growth of subcutaneous melanoma tumors and prolonging survival.

279 ion is identified in immune responsive human melanoma tumors.

280 as a potential dietary intervention to block melanoma tumour growth and sensitize tumours to targeted

281 Uveal melanoma (UM) is a currently untreatable form of melanom

282 Uveal melanoma (UM) is the most common intraocular tumour in a

283 stemic treatment of patients with metastatic melanoma using immune checkpoint and tyrosine kinase inh

284 eterogeneity within individual patients with melanoma using multiplatform analysis of commonly mutate

285 subsequent neoplasm, especially sarcoma and melanoma, was significant, evidence supporting routine t

286 Finally, in human melanoma we show that when 50% or more tumour blood vess

287 A total of 6863 cases of uveal melanoma were identified.

288 Eyes with melanoma were imaged with OCTA before treatment and at 1

289 IC (without in-transit metastasis) cutaneous melanoma were randomly assigned to receive pembrolizumab

290 amyloid observed in PD, is also elevated in melanoma, where its expression is inversely correlated w

291 ed to patients with BRAF wild-type cutaneous melanoma, while those three regimens or combination BRAF

292 noma (UM) is a currently untreatable form of melanoma with a 50% mortality rate.

293 nvolving patients who had resected stage III melanoma with BRAF V600E or V600K mutations, 12 months o

294 patients were aged 18-80 years with stage IV melanoma with no evidence of disease after surgery or ra

295 s with non-small-cell lung cancer (NSCLC) or melanoma with untreated brain metastases to determine th

296 ab demonstrates activity in metastatic uveal melanoma, with deep and sustained confirmed responses.

297 efficiently and inefficiently metastasizing melanomas, with circulating lactate being a more promine

298 ry to hypoxic (FME) and normoxic (LOX) human melanoma xenografts in a murine window chamber model.

299 the aggressive growth of BRAF(V600E)-mutant melanoma xenografts in vivo.

300 sensitivity to T cell attack in vitro and in melanoma xenografts.