ライフサイエンスコーパス: melanoma

1 he management of individuals at high risk of melanoma.

2 ression in a BRAFV600E-driven mouse model of melanoma.

3 t step toward novel-targeted theranostics in melanoma.

4 nce to the effectiveness of the diagnosis of melanoma.

5 act on the tumorigenic program of metastatic melanoma.

6 line for sentinel lymph node (SLN) biopsy in melanoma.

7 s in monocytes and DCs from human metastatic melanoma.

8 tasis models of 4T1 breast cancer and B16F10 melanoma.

9 ents experienced metastases nor died of iris melanoma.

10 n THOR in zebrafish accelerated the onset of melanoma.

11 survival of patients with widely metastatic melanoma.

12 logical ascorbate to potentiate apoptosis in melanoma.

13 increase odds for development of amelanotic melanoma.

14 potential parameter for targeted therapy in melanoma.

15 n a variety of cancers, including metastatic melanoma.

16 A total of 1059 patients with uveal melanoma.

17 r enucleation as primary treatment for uveal melanoma.

18 s therapeutic potential for the treatment of melanoma.

19 d therapies for commonly mutated BRAF(V600E) melanoma.

20 ipilimumab-refractory patients with advanced melanoma.

21 Incidence and risk factors for melanoma.

22 nown aetiology, not previously identified in melanoma.

23 yclectomy for iris melanoma or presumed iris melanoma.

24 k to identify a gene signature of metastatic melanoma.

25 Age at diagnosis and body site of melanoma.

26 s, and bone marrow, consistent with advanced melanoma.

27 NLRP1 inflammasomes are active in metastatic melanoma.

28 treatment option for patients with advanced melanoma.

29 d nodes in metastatic as compared to primary melanoma.

30 e that has the highest mutation frequency in melanoma.

31 n both mouse embryonic fibroblasts and human melanoma.

32 bination therapy in patients with NF1 mutant melanoma.

33 of diagnosis to 12 months after diagnosis of melanoma.

34 ht be of therapeutic benefit in this type of melanoma.

35 linical outcomes of patients with metastatic melanoma.

36 is a mechanism for vemurafenib resistance in melanoma.

37 adoptively transferred CD8+ T cells against melanoma.

38 noma') is a well-established risk factor for melanoma.

39 een discovered as driver events in malignant melanoma.

40 e used for the treatment of different mutant melanomas.

41 idence rates for over 58,000 newly diagnosed melanomas.

42 y BRAF, but also several NRAS and NF1 mutant melanomas.

43 mpared with volar and subungual/interdigital melanomas.

44 agnosis, 58.3 [16.1] years) and 2917 primary melanomas.

45 d sufficient to activate MAPK in GNAQ mutant melanomas.

46 ained a trunk neural crest gene signature in melanomas.

47 779 [97%]) or malignant (27 [3%]), including melanoma (18 [2.2%]) and lymphoma (9 [1.1%]).

48 ible PYHIN protein family, such as absent in melanoma-2 and IFN-gamma-inducible protein (IFI)16, bind

49 r, eighth edition, staging criteria for iris melanoma, 21 tumors (42%) were T1a, 5 tumors (10%) were

50 From 732 patients diagnosed with uveal melanoma, 311 were treated with brachytherapy.

51 colorectal cancer (70 patients, 286 scans), melanoma (69 patients, 271 scans), and lung cancer (84 p

52 values discriminated metastatic from primary melanoma (87% classification accuracy).

53 han unscreened patients to be diagnosed with melanoma (adjusted risk ratio [RR], 2.4; 95% CI, 1.7-3.4

54 n reducing the viability of some NRAS mutant melanomas, an effect driven by the partial preservation

55 S more potently in colorectal cancer than in melanoma and causes resistance only in the former.

56 anding of signaling and immune regulation in melanoma and implications for responses to treatment, or

57 opriate) in 66% (71/107) and 39% (41/105) of melanoma and NSCLC patients, respectively.

58 aocular tumors in adults and children (uveal melanoma and retinoblastoma, respectively).

59 al nonprostatic cell lines and xenografts of melanoma and small cell lung cancer (SCLC) origin.

60 losa cell tumours, and a subset of malignant melanoma and thyroid cancers.

61 vating mutations in BRAF are found in 50% of melanomas and although treatment with BRAF inhibitors (B

62 Abl kinases (Abl/Arg) are activated in melanomas and drive progression; however, their mechanis

63 , our understanding of lymphangiogenesis (in melanomas and other tumour types) is limited by the pauc

64 sis stage, previous treatment for metastatic melanoma, and Eastern Cooperative Oncology Group perform

65 ntly observed in ECs of human carcinomas and melanoma, and in ECs of the pre-metastatic niche in mice

66 diagnosed with melanoma, including multiple melanoma, and in reverse order RR for melanoma in famili

67 ergy metabolism, particularly in BRAF-mutant melanoma, and represent a promising lead for the develop

68 s with red hair are more prone to developing melanoma, and whether the activity of RHC variants might

69 Effective therapies for managing melanoma are limited, so we sought to investigate mensac

70 derlying genetics associated with amelanotic melanoma are unknown.

71 mphoma and a B16 mouse model of subcutaneous melanoma are used to extract a snapshot of tumor-associa

72 ehensive permanent section margin control of melanomas arising in chronically sun-damaged skin on the

73 gnized the cancer germline antigen, MAGE-A3 (melanoma-associated antigen-A3).

74 a-synuclein is highly beneficial to advanced melanoma because it ensures that autophagy is maintained

75 enhances pyroptosis in macrophages, NLRP1 in melanoma behaved differently in the context of cell deat

76 This result may increase the number of early melanomas biopsied and reduce the number of benign lesio

77 In a syngeneic model of melanoma brain metastasis, a combination of MSC-oHSV and

78 ly applicable therapeutic platform to target melanoma brain metastasis.

79 c cancer cell lines, in particular malignant melanoma, breast cancer, and leukemia.

80 es a global phosphoproteomic view of CIBM in melanoma, but also demonstrates that inhibition of BMK1

81 und clinical responses in advanced cutaneous melanoma, but complete remissions are frustrated by the

82 nning beds advances the date of diagnosis of melanoma by at least 2 years.

83 rsor lesion, but it is unknown whether these melanomas can arise from melanocyte stem cells (MCSCs).

84 hat treatment with anle138b leads to massive melanoma cell death due to a major dysregulation of auto

85 cing MEK1/2 and ERK1/2 signaling, inhibiting melanoma cell growth and inducing apoptosis.

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

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

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

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

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

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

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

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

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

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

96 We show a clear dependence of melanoma cell-cell adhesion on pHe and NHE1 as a modulat

97 o-survival role of mitochondrial function in melanoma cells after oncogenic MAPK inhibition.

98 AMIGO2 is upregulated in melanoma cells and tissues compared to human melanocytes

99 aging demonstrates that after extravasation, melanoma cells become pigmented and enact a gene express

100 ficantly (P < 0.001) inhibited the growth of melanoma cells but not normal melanocytes.

101 hat cytoplasmic transfer from macrophages to melanoma cells correlates with melanoma invasion and ari

102 pathways of immunosuppression elaborated by melanoma cells dominate the tumor microenvironment and h

103 tance and contribute to suboptimal growth of melanoma cells following the withdrawal of BRAF inhibiti

104 tumor effects both in vitro and in vivo in a melanoma cells harboring the BRAF fusion.

105 itor Gant61 led to decreased invasion of the melanoma cells in a three-dimensional skin reconstruct m

106 ly, overexpression of miR-200a in metastatic melanoma cells induces cell cycle arrest by targeting CD

107 elanocytes and nevi, and AMIGO2 silencing in melanoma cells induces G1/S arrest followed by apoptosis

108 gulated fusion was investigated by comparing melanoma cells infected with wild-type-like VZV or hyper

109 t be improved by taking the Wnt signature of melanoma cells into account.

110 wn-regulation of microRNA-200a expression in melanoma cells is associated with disease progression an

111 icle hybrids presented here comprised either melanoma cells or prostate cancer cells stably adorned w

112 se type glycans in melanocytes (HEMa-LP) and melanoma cells originating from the radial growth phase

113 We generated A375 melanoma cells resistant to vemurafenib with the goal of

114 We tested 2,368 genes expressed by melanoma cells to identify those that synergize with or

115 Melanoma cells treated using these agents are known to e

116 d the proliferative kinetics of BRAF-mutated melanoma cells treated with the BRAF inhibitor PLX4720 f

117 Deletion of p205 in B16 melanoma cells using CRISPR/Cas9 showed a similar loss o

118 crophages and high uptake by SPARC(+) B16F10 melanoma cells).

119 to detect melanin induction in SKMEL28 human melanoma cells, following inhibition of Hsp90 and BRAF s

120 ovided protection against apoptosis in human melanoma cells, suggesting a suppressive role of NLRP1 i

121 upts the interaction between PHB and CRAF in melanoma cells, thus reducing MEK1/2 and ERK1/2 signalin

122 11, a known metabolic switch in nonpigmented melanoma cells, was severely down-regulated in vitiligo

123 known as JARID1B)-positive subpopulation of melanoma cells, which are slow-cycling and treatment-res

124 metastases in response to challenge with B16 melanoma cells.

125 y are potent against endogenous AC in intact melanoma cells.

126 ed that T-oligo can form G4 in the nuclei of melanoma cells.

127 e myeloid attractant CCL2 in BRAFi-resistant melanoma cells.

128 diate resistance to BRAF inhibitors in human melanoma cells.

129 igenetic modulators against human metastatic melanoma cells.

130 nd relatively selective cytotoxicity against melanoma cells.

131 croM of ascorbate induced apoptosis in A2058 melanoma cells.

132 eres, elicits potent DNA-damage responses in melanoma cells; however, its mechanism of action is larg

133 Genomic analyses of cutaneous melanoma (CM) have yielded biological and therapeutic in

134 int inhibitor response across three separate melanoma cohorts (p=4.7 x 10(-4)).

135 Melanoma, compared with nevus, was associated with older

136 EC N1ICD expression in melanoma correlated with shorter progression-free surviv

137 Here, we found that expression of SDHD in melanoma correlated with the expression of multiple ETS

138 iled to induce complete rejection of HCmel12 melanomas, demonstrating that residual Tregs were able t

139 identified 392 breast cancer-derived and 302 melanoma-derived proteins secreted from highly lung meta

140 r to biopsy a pigmented lesion suggestive of melanoma, dermatologists improved their mean biopsy sens

141 esent work shows the role of SOCS1 in murine melanoma development and the potential of SOCS1-silenced

142 een induction of total PP or PP/Trp53 KO and melanoma development indicates that additional genetic o

143 ods Patients with stage III disease at first melanoma diagnosis (initial; n = 2,042), or who develope

144 g retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5), which

145 The majority of melanomas emerge from clear skin without a precursor les

146 countries with low to moderate incidence of melanoma, except in families and patients with a first m

147 for nevi decreased from 2 days to 1 day, for melanomas from 5 days to 2 days, and for BCC from 2 days

148 administration of ISF35 in subcutaneous B16 melanomas generates tumor-specific, CD8(+) T cells that

149 y, intramuscular delivery of cGAMP inhibited melanoma growth and prolonged the survival of the tumor-

150 Ablation of Tet2 in myeloid cells suppressed melanoma growth in vivo and shifted the immunosuppressiv

151 Using mouse models, we demonstrate that melanoma growth is drastically reduced in mice lacking c

152 of Usp9x and MEK inhibitor fully suppressed melanoma growth.

153 s had curable breast or colorectal cancer or melanoma, had completed treatment (not including endocri

154 lthough the treatment landscape for advanced melanoma has changed since this study was initiated, the

155 In addition to examining melanoma incidence, melanoma hazard ratios and 95% confidence intervals for

156 Further, we report on the anti-melanoma immune response inducing properties of the prom

157 ced tumor cells in raising an effective anti-melanoma immune response.

158 primary outcome of interest was presence of melanoma in a biopsied regional LN.

159 y and feasibility of MILND for patients with melanoma in a group of surgeons newly adopting the proce

160 ltiple melanoma, and in reverse order RR for melanoma in families of multiple discordant cancers.

161 reported a significantly increased risk for melanoma in people with Parkinson's disease.

162 Melanoma in situ (MIS) is increasing in incidence, and e

163 great promise in the treatment of malignant melanoma in the last few years, with these drugs now com

164 Melanomas in PP;Trp53-deficient mice lacked either Ras o

165 cancers, other than hematologic cancers and melanoma, in multistate cohort studies.

166 tion than previous screening programs and if melanoma incidence and thickness differed in screened vs

167 tes showed substantial increases in invasive melanoma incidence for tumors of all thicknesses in all

168 In addition to examining melanoma incidence, melanoma hazard ratios and 95% confi

169 des durable antitumor activity in metastatic melanoma, including complete response (CR) in about 15%

170 ers of first-degree relatives diagnosed with melanoma, including multiple melanoma, and in reverse or

171 le RAF-driven, autochthonous murine model of melanoma incorporating a fluorescent reporter allele (td

172 itive phenotypic index, and prior amelanotic melanoma increase odds for development of amelanotic mel

173 The number of nevi-associated melanomas increased from 15.5% to 33.3%.

174 in estimating lymph node positivity in thin melanoma independent of traditional pathologic factors.

175 acrophages to melanoma cells correlates with melanoma invasion and arises as a result of intimate cel

176 The melanoma involved the choroid (938/1059, 89%), ciliary b

177 Melanoma is a complex and genomically diverse malignancy

178 Melanoma is a heterogeneous tumor with different subpopu

179 Melanoma is a lethal form of skin cancer.

180 s challenge the belief that metastatic uveal melanoma is immunotherapy resistant and support the furt

181 sion of major histocompatibility class II in melanoma is linked to favorable disease outcome.

182 Melanoma is one of the deadliest cancers, yet the cells

183 ined risk factor and precursor for cutaneous melanoma is the dysplastic nevus.

184 A family history of cutaneous melanoma ('melanoma') is a well-established risk factor for melanom

185 ns in CDKN2A are frequently identified among melanoma kindreds and are associated with increased atyp

186 ith previously treated or untreated advanced melanoma led to subsequent clinical development, includi

187 luated tumor specimens from 65 patients with melanoma, lung nonsquamous, squamous cell lung or head a

188 and neck has favorable recurrence rates when melanoma margins are difficult to assess, and recurrence

189 Forty patients with uveal melanoma (mean age, 57.98+/-14.75 years) were included i

190 .4; P < .001) and to have a thinner invasive melanoma (median thickness, 0.37 mm vs 0.65 mm; P < .001

191 A family history of cutaneous melanoma ('melanoma') is a well-established risk factor

192 ll as the diverse presentation of intestinal melanoma metastases and the diagnostic and therapeutic d

193 The treatment of intestinal melanoma metastases has changed due to the introduction

194 e intensity was observed within the group of melanoma metastases.

195 es and corresponding enzymes associated with melanoma metastasis in patient samples.

196 nefit achieved through surgical resection of melanoma metastatic to the abdominal viscera in patients

197 f myeloid-derived suppressor cells (MDSC) in melanoma microenvironment is supported by chemokine rece

198 Identifying patients at risk of amelanotic melanoma might enable earlier diagnosis and improved sur

199 Malignant melanoma (MM) is the most aggressive form of skin cancer

200 ICAM-1 as a potential target for metastatic melanoma (MM).

201 he clinical armamentarium against metastatic melanoma (MMel).

202 Using mouse melanoma models, we report that CD8(+) TILs enhance pero

203 at full-body skin examination (FBSE) reduces melanoma morbidity or mortality has prompted an "I" rati

204 ing tumor growth in the BRAF V600E/PTEN-null melanoma mouse model.

205 were initiated at 3.0 mg/kg in patients with melanoma (n = 16) and renal cell carcinoma (RCC; n = 15)

206 ion of melanocytic nevi (n = 46) and primary melanomas (n = 42).

207 except in families and patients with a first melanoma occurrence before age 40 years in whom the rule

208 cantly raised odds of diagnosis of ulcerated melanoma (odds ratio 2.90, 95% confidence interval 1.07-

209 d primary status (single or multiple primary melanoma); odds ratios (ORs) and 95% CIs are reported.

210 Melanoma of the skin is a common cancer only in European

211 a personal history were more likely to have melanoma on the head and neck (21% vs 15%, P = .003).

212 hose with many nevi were more likely to have melanoma on the trunk (41% vs 29%, P < .001), those with

213 Melanomas on dorsal acral surfaces demonstrated clear di

214 history of melanoma were more likely to have melanomas on the limbs (57% vs 42%, P < .001), and those

215 main immediate early AP-1 member induced by melanoma oncogenes.

216 Melanoma onset was accelerated in kit(lf); Tg(mitfa:BRAF

217 n vivo, expression of wild-type BRAF delayed melanoma onset, but only in a kit-dependent manner.

218 patients with advanced-stage tumors, such as melanoma or lung cancer.

219 eyes with previous iridocyclectomy for iris melanoma or presumed iris melanoma.

220 iagnosed with an in situ or invasive primary melanoma over a 12-month period from October 2006 to 200

221 of (clinically and dermoscopically) SK-like melanomas, patient demographics, and interobserver agree

222 y activation that is observed in a cohort of melanoma patients after vemurafenib treatment.

223 rolizumab, starting with a small pilot of 19 melanoma patients and eventually defining a pan-tumor T

224 the CD73-adenosinergic pathway is active in melanoma patients and whether adenosine restricts the ef

225 Given many BRAF-mutated melanoma patients experience disease progression with ta

226 A retrospective study was conducted for iris melanoma patients from 3 regional ophthalmologic centers

227 me B imaging paradigm, biopsy specimens from melanoma patients on checkpoint inhibitor therapy were a

228 We also detected CD73 upregulation in melanoma patients progressing under adoptive T-cell tran

229 alysis of the largest yet-reported cohort of melanoma patients reveal how tumor and immunity co-evolv

230 In two independent cohorts of melanoma patients treated with anti-CTLA4 and anti-PD1,

231 In specimens from breast cancer and melanoma patients, CD39(+)CD8(+) T cells were present wi

232 vels are associated with reduced survival of melanoma patients, implying that this mechanism also dri

233 atment expression as a biomarker to stratify melanoma patients.

234 clinical responses in a subset of metastatic melanoma patients.

235 The Melanoma Patterns of Care study was a population-based o

236 as a "cell cycle brake" that is lost during melanoma progression to metastasis and provides the abil

237 an embryonic cell gene signature to promote melanoma progression, thus providing potential opportuni

238 h P-cadherin expression correlate with human melanoma progression, whereas elevated P-cadherin levels

239 -mediated immunity to provide tumor (B16-ova-Melanoma) protection in around 40% of vaccinated mice an

240 The melanoma recognition is still difficult, and generally,

241 n MMel.The clinical management of metastatic melanoma requires predictors of the response to checkpoi

242 In melanoma, resistance to targeted therapy has been linked

243 coding and non-coding mutations in cutaneous melanoma resolved novel signatures of mutagenesis attrib

244 For mucosal and cutaneous melanoma, respectively, the incidence of grade 3 or 4 tr

245 The whole-genome mutation landscape of melanoma reveals diverse carcinogenic processes across i

246 Our findings suggest that lithium may reduce melanoma risk and associated mortality.

247 mportant pathways (such as melanogenesis) in melanoma risk assessment.

248 a mouse model of adoptive T cell therapy for melanoma, Runx3-deficient CD8(+) tumour-infiltrating lym

249 a for phenotypes, MC1R genotype, and primary melanomas scored for histopathologic pigmentation.

250 Analyses of the melanoma secretome and validation in clinical specimens

251 ening technique for non-Hodgkin lymphoma and melanoma skin cancer.

252 all six genes were significant in predicting melanoma specific survival (MSS) in a univariate analysi

253 iting revealed that AMIGO2 is regulated by a melanoma-specific BRD2/4-bound promoter and super-enhanc

254 Melanoma-specific mortality for the MMS group was 2 vs 1

255 dissection was not associated with increased melanoma-specific survival among 1934 patients with data

256 a were incident patients with a diagnosis of melanoma stage 0 to III and with continuous insurance en

257 b and Dabrafenib due to metastatic cutaneous melanoma stage IV.

258 In melanoma that arose from DPN we find additional oncogeni

259 astasis and provides the ability to identify melanomas that are highly proliferative and more prompte

260 When analysis was limited to melanomas that were </=2 mm thick and had </=2 mitoses/m

261 In human melanoma, the Na(+)/H(+) exchanger NHE1 is an important

262 D-1) was ineffective against BRAFi-resistant melanomas, the addition of MDSC depletion/blockade (anti

263 sic components of resistance in BRAF-mutated melanoma; the model describes tumor-stroma dynamics both

264 r anti-programmed death-1 therapy in mucosal melanoma to date.

265 describe the dermoscopic features of SK-like melanomas to understand their clinical morphology.

266 Melanoma transformation is unlikely to be due to height

267 Continuous BRAF inhibition of BRAF mutant melanomas triggers a series of cell state changes that l

268 aling, thereby inhibiting BRAF(V600E)-driven melanoma tumor growth.

269 MDSC from melanoma tumor models decreased the levels of proliferat

270 how a high propensity of 4-(11)C-MBZA toward melanoma tumor.

271 ne epigenetic analysis of patient metastatic melanoma tumors taken prior to checkpoint blockade, whic

272 he human eIF1A NTT are associated with uveal melanoma (UM).

273 in GNAQ or GNA11 occurs in over 80% of uveal melanomas (UMs) and activates MAPK.

274 tients with a clinically diagnosed choroidal melanoma underwent complete 25-gauge posterior vitrectom

275 valuation of a (11)C-labeled probe to target melanoma using PET.

276 s benign seborrheic keratoses; and malignant melanomas versus benign nevi.

277 The impact of age at first melanoma was observed only in those younger than 40 year

278 ogic pigmentation between incident and prior melanomas was analyzed using an exact logistic regressio

279 When applied to mutant BRAF melanoma, we found that our approach exhibited significa

280 e checkpoint blockade therapy for metastatic melanoma, we found that tumor aneuploidy inversely corre

281 ocytic nevi (including dysplastic nevi) from melanoma, we sequenced exomes of melanocytic nevi includ

282 scriptomic data set derived from 703 primary melanomas, we showed that all six genes were significant

283 1 consecutive patients with metastatic uveal melanoma were enrolled between June 7, 2013, and Sept 9,

284 h histologically confirmed metastatic ocular melanoma were enrolled.

285 cs between those who did and did not develop melanoma were examined, and a survival analysis was perf

286 %, P < .001), those with a family history of melanoma were more likely to have melanomas on the limbs

287 However, acral and mucosal melanomas were dominated by structural changes and mutat

288 ex) and MC1R status with incident amelanotic melanomas were evaluated using logistic regression model

289 of nevi per patient, 19 [range, 8-81]), all melanomas were labeled UDN and as morphologically suspic

290 ful criteria in correctly diagnosing SK-like melanomas were the presence of blue-white veil, pseudopo

291 ary clinical case: a patient with metastatic melanoma who developed disease recurrence following an i

292 ed the cases of two patients with metastatic melanoma who developed fatal myocarditis during ipilimum

293 improved survival in patients with advanced melanoma with BRAF V600 mutations.

294 patients with completely resected, stage III melanoma with BRAF V600E or V600K mutations to receive o

295 significantly longer in patients with uveal melanoma with high nuclear BAP1 stain (P = 0.004).

296 nd Ets-1 levels are coincidently elevated in melanoma with highest levels detected in metastatic tumo

297 The detection of ulceration in melanomas with thicker than 1 mm increased from 24.0% to

298 dels: 4T1 and MCF-7 breast carcinoma, B16F10 melanoma, WT-GBM glioma and MKN45-P gastric carcinoma.

299 able to detect alphavbeta3 integrin in human melanoma xenografts in a selective fashion.

300 promising therapeutic agents for metastatic melanoma, yet their mechanism of action remains unclear.