ライフサイエンスコーパス: cutaneous melanoma

1 ilimumab (n = 35, mucosal melanoma; n = 326, cutaneous melanoma).

2 ltrating lymphocytes in breast carcinoma and cutaneous melanoma.

3 e offered the same therapies recommended for cutaneous melanoma.

4 f EZH2 in promoting growth and metastasis of cutaneous melanoma.

5 g RNAs (lincRNAs) associated with metastatic cutaneous melanoma.

6 n tertiary referral centers for treatment of cutaneous melanoma.

7 h vemurafenib for unresectable or metastatic cutaneous melanoma.

8 own about the status of the Hippo pathway in cutaneous melanoma.

9 lation to prior or subsequent development of cutaneous melanoma.

10 urafenib therapy in patients with metastatic cutaneous melanoma.

11 date the role of MMIS within the spectrum of cutaneous melanoma.

12 stic factor for clinically localized primary cutaneous melanoma.

13 ITF(E318K) variant confers moderate risk for cutaneous melanoma.

14 , and somatic LKB1 mutations occur in 10% of cutaneous melanoma.

15 PBL) was associated with a decreased risk of cutaneous melanoma.

16 a clinical determinant for poor prognosis in cutaneous melanoma.

17 rognosis than do patients with metastases of cutaneous melanoma.

18 count is the strongest known risk factor for cutaneous melanoma.

19 ly predicts poor outcome among patients with cutaneous melanoma.

20 asing survival in subgroups of patients with cutaneous melanoma.

21 as definitive procedures for the staging of cutaneous melanoma.

22 n patients undergoing SLN biopsy for primary cutaneous melanoma.

23 d that MAP2 is frequently activated in human cutaneous melanoma.

24 ormonal factors may have a potential role in cutaneous melanoma.

25 s are the most common genetic alterations in cutaneous melanoma.

26 nder is an important factor in patients with cutaneous melanoma.

27 egional lymph nodes of patients with primary cutaneous melanoma.

28 pathogenesis of many tumor types, including cutaneous melanoma.

29 n treating and preventing the progression of cutaneous melanoma.

30 nal epidemiologic studies involving incident cutaneous melanoma.

31 tor for the risk of lymph node metastasis in cutaneous melanoma.

32 linically and genetically distinct from skin cutaneous melanoma.

33 ter resection of thick (> or = 4 mm) primary cutaneous melanoma.

34 ease genes for many human cancers, including cutaneous melanoma.

35 es the ability to noninvasively detect early cutaneous melanoma.

36 or against the use of neoadjuvant therapy in cutaneous melanoma.

37 nsitive and specific method for detection of cutaneous melanoma.

38 icted to be deleterious/damaging are rare in cutaneous melanoma.

39 (10%) had mucosal melanoma and 665 (75%) had cutaneous melanoma.

40 CDK4/6 pathway is frequently dysregulated in cutaneous melanoma.

41 ictor of survival in many cancers, including cutaneous melanoma.

42 patients aged 18 to 79, newly diagnosed with cutaneous melanoma.

43 inical trials utilizing CDK4/6 inhibitors in cutaneous melanoma.

44 homolog (NRAS) are frequent driver events in cutaneous melanoma.

45 as a novel treatment strategy in a subset of cutaneous melanomas.

46 n syndrome and may confer a greater risk for cutaneous melanomas.

47 owing loss of immunostaining for BAP1, and 7 cutaneous melanomas.

48 pathology reports for all ulcerated primary cutaneous melanomas.

49 ons in NRAS and BRAF are found frequently in cutaneous melanomas.

50 contribute to stepwise progression of human cutaneous melanomas.

51 ; <= 1 mm) constitute 70% of newly diagnosed cutaneous melanomas.

52 ng mutations in BRAF than NRAS gene in human cutaneous melanomas.

53 for targeted inhibition of early or invasive cutaneous melanomas.

54 hreonine kinase gene are frequently found in cutaneous melanomas.

55 alteration of PTEN expression in 69 primary cutaneous melanomas.

56 AF were found in benign melanocytic nevi and cutaneous melanomas.

57 fferences in tumorigenesis between uveal and cutaneous melanomas.

58 croenvironment can suppress MCSC-originating cutaneous melanomas.

59 , breakend hypermutation, and acral, but not cutaneous, melanomas.

60 All patients had clinically node-negative cutaneous melanoma (1.5 to 4.0 mm).

61 3,158 patients aged 1 to 19 years, 96.3% had cutaneous melanoma, 3.0% had ocular melanoma, and 0.7% h

62 al, and dark homogeneous streaks) of primary cutaneous melanomas; 3 melanomas per pattern were tested

63 pathology was CRC = 54, non-CRC = 37 (ocular/cutaneous melanoma = 32, cholangiocarcinoma = 3, appendi

64 s, we found significantly elevated risks for cutaneous melanoma (380% increase) and prostate cancer (

65 ancer (100% vs 65.9%, P = .06), particularly cutaneous melanoma (62.5% vs 9.9%, P < .001) and ocular

66 oximately 8% of cancer samples, primarily in cutaneous melanomas (70%).

67 d protein expression in 137 invasive primary cutaneous melanomas (71 superficial spreading melanomas,

68 Diagnoses included conjunctival and eyelid cutaneous melanoma (85 and 42 patients, respectively), s

69 In human cutaneous melanomas, adipocyte-selective FABP4 transcrip

70 e third most commonly mutated codon in human cutaneous melanoma, after BRAF V600 and NRAS Q61.

71 h investigating the link between arsenic and cutaneous melanoma, although arsenic has been associated

72 a phase III trial in patients with resected cutaneous melanoma (American Joint Committee on Cancer 7

73 that is associated with a high penetrance of cutaneous melanoma and chronic lymphocytic leukemia.

74 tient who received a diagnosis of metastatic cutaneous melanoma and developed melanoma-associated ret

75 trol study examining the association between cutaneous melanoma and environmental arsenic exposure am

76 these signatures onto the collection of TCGA cutaneous melanoma and found that poorly differentiated

77 hnology to study gene expression patterns in cutaneous melanoma and highlight recent advances concern

78 for the majority of BRAF mutations found in cutaneous melanoma and is also commonly found in nevi.

79 We conclude that loss of NF1 is common in cutaneous melanoma and is associated with RAS activation

80 is the most common driver mutation in human cutaneous melanoma and is frequently accompanied by loss

81 sought to determine the frequency of RETp in cutaneous melanoma and its functional responsiveness to

82 o maligna melanoma (LMM) comprises 4%-15% of cutaneous melanoma and occurs less commonly than superfi

83 a genome-wide association pooling study for cutaneous melanoma and performed validation in samples t

84 ators of the immune response against primary cutaneous melanoma and predict their impact on patient s

85 histochemical staining of both primary human cutaneous melanoma and pulmonary metastases revealed CXC

86 s after wide local excision of thick primary cutaneous melanoma and sentinel lymphadenectomy.

87 unlight exposure that most increases risk of cutaneous melanoma and the role of diet.

88 is is a critical event in the development of cutaneous melanoma and ultimately an indicator of poor p

89 ne mutation in BAP1 associated with multiple cutaneous melanomas and classic dysplastic nevus syndrom

90 rigenicity) in thin (< or = 1.00 mm) primary cutaneous melanomas and examined their association with

91 veal melanomas are molecularly distinct from cutaneous melanomas and lack mutations in BRAF, NRAS, KI

92 frequencies of associations between primary cutaneous melanomas and melanocytic nevi vary widely bet

93 P1 mutations with a propensity for uveal and cutaneous melanomas and other internal malignancies have

94 lanoma, is proposed in cases with 2 invasive cutaneous melanomas and/or related cancers in the same p

95 discovery set of 73 benign nevi, 76 primary cutaneous melanoma, and 11 in-transit melanoma metastase

96 ors (lung adenocarcinoma, mammary carcinoma, cutaneous melanoma, and uveal melanoma), we demonstrate

97 BRAF mutations are frequent in cutaneous melanomas, and BRAF inhibitors (BRAFi) have sh

98 interleukin-8, has been detected in primary cutaneous melanomas, and the importance of these mediato

99 Cutaneous melanomas are notorious for their tendency to

100 Cutaneous melanomas arise through causal pathways involv

101 Cutaneous melanomas arise with histopathological and mol

102 (lymph node metastases >1 mm), IIIB, or IIIC cutaneous melanoma as per American Joint Committee on Ca

103 syndrome, including mesothelioma and ocular/cutaneous melanomas, as well as renal, breast, lung, gas

104 cents diagnosed with sporadic single-primary cutaneous melanoma at age 20 years or younger, adult pat

105 No patient had a personal history of cutaneous melanoma, autoimmune disease, or cutaneous vit

106 tients who underwent SLN mapping for primary cutaneous melanoma between January 1996 and July 2005 we

107 y signature is remarkably conserved in human cutaneous melanoma biopsies, arguing for COX activity as

108 enes included BRAF, CDKN2A, NRAS and TP53 in cutaneous melanoma, BRAF, NRAS and NF1 in acral melanoma

109 f postmitotic neurons, is induced in primary cutaneous melanoma but is absent in metastatic melanomas

110 duce profound clinical responses in advanced cutaneous melanoma, but complete remissions are frustrat

111 incorporated the importance of ulceration in cutaneous melanoma, but have focused on the number of me

112 topical application of imiquimod suppresses cutaneous melanoma by TLR7-dependent recruitment and tra

113 f the Hippo pathway effectors YAP and TAZ in cutaneous melanoma" by Nallet-Staub et al., 2013, provid

114 The survival of patients with cutaneous melanoma can be accurately predicted using jus

115 Chemoprevention of cutaneous melanoma can become a valid strategy complemen

116 Cancers, including cutaneous melanoma, can cluster in families.

117 Participants included 368 cutaneous melanoma cases and 373 colorectal cancer contr

118 a low tumorigenic and non-metastatic primary cutaneous melanoma cell line generated angiogenic tumors

119 The primary cutaneous melanoma cell lines SB2 and MeWo were repeated

120 otal of 14 Braf-mutant and 3 wild-type human cutaneous melanoma cell lines.

121 ulator of AZD6244 sensitivity in Braf-mutant cutaneous melanoma cells and the novel regulation of PTE

122 lls directed against HER2 can kill uveal and cutaneous melanoma cells in vitro and in vivo.

123 over, ectopic expression of MUC18 in primary cutaneous melanoma cells leads to increased tumor growth

124 we have shown that short exposure of primary cutaneous melanoma cells to dacarbazine resulted in the

125 examined the plasticity of human metastatic cutaneous melanoma cells with respect to vascular functi

126 397 and Tyr576, in only aggressive uveal and cutaneous melanoma cells, which correlates with their in

127 ic melanoma cells when compared with that in cutaneous melanoma cells.

128 se fibrovascular patterns (both in uveal and cutaneous melanoma), cellular and extracellular composit

129 designed to assess the associations between cutaneous melanoma (CM) and exposure to nonsteroidal ant

130 shared epidemiological risk factors between cutaneous melanoma (CM) and UM, in this study we have se

131 a field synopsis of genetic associations of cutaneous melanoma (CM) by systematically retrieving and

132 ferentiative effects in both melanocytes and cutaneous melanoma (CM) cells mediated through the vitam

133 Uveal melanoma (UM) and cutaneous melanoma (CM) differ significantly in their ep

134 Genomic analyses of cutaneous melanoma (CM) have yielded biological and ther

135 Cutaneous melanoma (CM) is the most lethal skin cancer.

136 morphisms (SNPs) with overall survival among cutaneous melanoma (CM) patients.

137 levels of active TGF-beta1 in patients with cutaneous melanoma (CM), assess their relationship with

138 ration is an important prognostic factor for cutaneous melanoma (CM).

139 ients with obstructive sleep apnea (OSA) and cutaneous melanoma (CM).

140 codon 72 variant is associated with risk of cutaneous melanoma (CM).

141 in ocular melanoma specimens and in the BAP1 cutaneous melanoma (CM)/ocular melanoma predisposition s

142 rs of the immune response in a large primary cutaneous melanoma cohort.

143 roximately 65% decrease in early or invasive cutaneous melanoma compared with inhibition of each sing

144 oles and approximately 60% of early invasive cutaneous melanomas contain a T1799A B-Raf mutation ((V6

145 omatic mutations in this community sample of cutaneous melanomas, contrary to earlier reports.

146 Although positive cutaneous melanoma control cell lines harbored the T1796

147 ions have been found in a high proportion of cutaneous melanomas, cutaneous nevi, and papillary thyro

148 Analysis of The Cancer Genome Atlas cutaneous melanoma data set showed that high GILT mRNA e

149 adult patients with sporadic single-primary cutaneous melanoma diagnosed at age 35 years or older, a

150 and Melanoma (GEM) Study, with first primary cutaneous melanoma diagnosed in the year 2000 and analyz

151 In cutaneous melanoma, driver mutations in NRAS and BRAF pr

152 of all Swedish women who were diagnosed with cutaneous melanoma during their reproductive period, fro

153 ent pathology samples of dysplastic nevi and cutaneous melanomas evaluated between September 1, 1999

154 nd, phase 3 trial in patients with stage III cutaneous melanoma (excluding lymph node metastasis </=1

155 ed, phase 3 trial in patients with stage III cutaneous melanoma (excluding lymph node metastasis </=1

156 luded stage IV or locally advanced stage III cutaneous melanoma, expression of HLA*A0201, an absence

157 for only about half of all densely affected cutaneous melanoma families, and the causes of familial

158 erved a female advantage in the prognosis of cutaneous melanoma, for which behavioral factors or an u

159 18 non-Hispanic white patients with invasive cutaneous melanoma from melanoma clinics in Philadelphia

160 18 non-Hispanic white patients with invasive cutaneous melanoma from melanoma clinics in Philadelphia

161 that enrolled patients with incident primary cutaneous melanomas from population-based and hospital-b

162 These findings provide insights into cutaneous melanoma genetic architecture, reinforcing the

163 Despite remarkable progress in cutaneous melanoma genomic profiling, the mutational lan

164 Patients with one primary localised cutaneous melanoma greater than 2 mm in Breslow thicknes

165 The necessary margin of excision for cutaneous melanomas greater than 2 mm in thickness is co

166 if they were age 18 to 70 years with primary cutaneous melanoma >/= 1.0 mm Breslow thickness and unde

167 0-case learning phase, patients with primary cutaneous melanoma (> or =1 mm with Clark level > or =II

168 Although 70% of cutaneous melanomas harbor activating mutations in the B

169 markable outcomes for patients with advanced cutaneous melanoma harboring a BRAF(V600E) mutation.

170 K kinases hold promise for the management of cutaneous melanomas harboring BRAF mutations.

171 gical factors such as ultraviolet radiation, cutaneous melanoma has a strong genetic component.

172 In recent years, the incidence of cutaneous melanoma has increased more than that of any o

173 The incidence of cutaneous melanoma has increased over the past several d

174 Cutaneous melanoma has the lowest survival rate of all f

175 ars, the treatment of patients with advanced cutaneous melanoma has undergone substantial changes.

176 Cutaneous melanomas have been found to express several i

177 tolerance against skin cancers, particularly cutaneous melanoma, have been a great challenge, given t

178 MMB was associated with improved survival in cutaneous melanoma: hazard ratio (HR) = 0.71 [0.60-0.85]

179 h premalignant and malignant stages of human cutaneous melanoma histogenesis and investigated its pot

180 -7 (FABP7) has been shown to be expressed in cutaneous melanoma; however, its role in tumor progressi

181 a (NHL) have an increased risk of developing cutaneous melanoma; however, risks associated with speci

182 surveillance of individuals at high risk for cutaneous melanoma improves early detection and reduces

183 reported susceptibility locus for ocular and cutaneous melanoma in Danish families.

184 Cutaneous melanoma in patients aged 1 to 19 years was mo

185 l, eligible patients had surgically resected cutaneous melanoma in the following categories: (1) T2bN

186 econstruction after wide excision of primary cutaneous melanoma in the head and neck region.

187 eport that repetitive UV exposure of primary cutaneous melanomas in a genetically engineered mouse mo

188 Cutaneous melanoma incidence is increasing.

189 vitreous debris in the context of metastatic cutaneous melanoma includes intravitreal metastasis, and

190 A total of 39,049 incident patient cases of cutaneous melanoma, including 36,694 in NHWs; 127 in Afr

191 le of ultraviolet radiation (UV) exposure in cutaneous melanoma induction, we studied xeroderma pigme

192 Cutaneous melanoma is a highly aggressive tumor that is

193 Cutaneous melanoma is a type of cancer with an inherent

194 High-mitotic-rate primary cutaneous melanoma is associated with aggressive histolo

195 The relationship of vitiligo to cutaneous melanoma is believed to be due to an immune re

196 Cutaneous melanoma is epidemiologically linked to ultrav

197 Early detection of cutaneous melanoma is essential, as prognosis with metas

198 Although the global incidence of cutaneous melanoma is increasing, survival rates for pat

199 Cutaneous melanoma is one of the most aggressive cancers

200 Incidence and mortality of cutaneous melanoma is rising rapidly in the United State

201 A well-defined risk factor and precursor for cutaneous melanoma is the dysplastic nevus.

202 core principle in the management of primary cutaneous melanoma is wide surgical excision, but occasi

203 The mainstay of management of primary cutaneous melanoma is wide surgical excision, but occass

204 ighly metastatic cancer that, in contrast to cutaneous melanoma, is largely unresponsive to checkpoin

205 Virus-specific CD8(+) TILs migrated into cutaneous melanoma lesions during acute infection with e

206 pts were detected in acute myeloid leukemia, cutaneous melanoma, low- and high-grade gliomas of the b

207 phatic metastasis to the breast from primary cutaneous melanoma mainly from the anterior trunk inferi

208 A family history of cutaneous melanoma ('melanoma') is a well-established ri

209 expression in most primary melanomas and all cutaneous melanoma metastases.

210 Cutaneous melanoma metastatic to the vitreous is very ra

211 nal disease control in patients with primary cutaneous melanomas more than 4 mm thick.

212 te resection of lymph nodes (ie, the primary cutaneous melanoma must have been completely excised wit

213 (n = 60 [28%]), mesothelioma (n = 48 [22%]), cutaneous melanoma (n = 38 [18%]), and renal cell carcin

214 s of 8 patients with retinal metastasis from cutaneous melanoma (n = 4), breast cancer (n =2), esopha

215 lectronic laboratory databases, and incident cutaneous melanomas (n = 14,056) were identified from an

216 RETp was assessed in 71 non-desmoplastic cutaneous melanomas (non-DMs) and 70 desmoplastic melano

217 econstruction after wide excision of primary cutaneous melanoma of the extremities.

218 mized phase III trial included patients with cutaneous melanoma of the trunk and extremities who were

219 RNA samples from ten primary cutaneous melanomas of similar depth of invasion were an

220 basin cannot be predicted correctly (eg, in cutaneous melanoma on the trunk), the use of indocyanine

221 is a rare intraocular tumor that, similar to cutaneous melanoma, originates from melanocytes.

222 In following > 10,000 patients with cutaneous melanoma over the past 30 years, our instituti

223 The significant increase in cutaneous melanomas over the past 30 years has led to st

224 emonstrates that RETp is frequently found in cutaneous melanoma, particularly desmoplastic subtypes,

225 Cutaneous melanomas, particularly the desmoplastic subty

226 with identifying potential new pathways for cutaneous melanoma pathogenesis.

227 MEK inhibitors improve survival in cutaneous melanoma patients but show only modest efficac

228 d from whole-exome sequencing analysis of 98 cutaneous melanoma patients from 27 families.

229 In conclusion, CTC number in metastatic cutaneous melanoma patients is prognostic for OS with a

230 ysis of 2,183 population-ascertained primary cutaneous melanoma patients, clinical, demographic, and

231 enomic surrogate of poor disease outcome for cutaneous melanoma patients.

232 ne variants have also been found in familial cutaneous melanoma pedigrees, but their contribution to

233 (lymph node metastases >1 mm), IIIB, or IIIC cutaneous melanoma, per American Joint Committee on Canc

234 ed for its functional and prognostic role in cutaneous melanoma progression.

235 lation of TSG may play a significant role in cutaneous melanoma progression.

236 uated outcomes in 2001 patients with primary cutaneous melanomas randomly assigned to undergo wide ex

237 Genetic risks for cutaneous melanoma range from rare, high-penetrance muta

238 Patients with resected stage II-III cutaneous melanomas remain at high risk for metastasis a

239 Most genetic susceptibility to cutaneous melanoma remains to be discovered.

240 Diagnosis of cutaneous melanoma requires accurate differentiation of

241 dscape of coding and non-coding mutations in cutaneous melanoma resolved novel signatures of mutagene

242 For mucosal and cutaneous melanoma, respectively, the incidence of grade

243 A patient with metastatic cutaneous melanoma responsive to immunotherapy experienc

244 A database query of patients with cutaneous melanoma returned 1158 patients with primary l

245 The major genetic determinants of cutaneous melanoma risk in the general population are di

246 s, both of which have been shown to increase cutaneous melanoma risk.

247 igmented skin lesions and early diagnosis of cutaneous melanoma should be expanded to ABCDE (to inclu

248 cm) excision margins in patients with thick cutaneous melanomas showed that narrow margins were asso

249 A similar pattern was observed for risk of cutaneous melanoma (SIR: CLL/SLL = 1.92, FL = 1.60, DLBC

250 studied the transcriptome landscape of skin cutaneous melanoma (SKCM) using 103 primary tumor sample

251 rized the mutational landscape of human skin cutaneous melanoma (SKCM) using data obtained from The C

252 Trametinib and Dabrafenib due to metastatic cutaneous melanoma stage IV.

253 1 potential secondary loci for a total of 85 cutaneous melanoma susceptibility loci.

254 significantly higher mean polygenic load for cutaneous melanoma than unrelated cases or melanoma-free

255 translation of CAR-T cells against uveal and cutaneous melanoma that do not respond to TIL therapy or

256 identified in metastatic unknown primary and cutaneous melanomas that lacked BRAFV600 and NRAS mutati

257 , data presented by Dhal et al. show that in cutaneous melanomas the KIT promoter is a target for hyp

258 For patients with primary cutaneous melanoma, the risk of sentinel node (SN) metas

259 therapies have shown efficacy in metastatic cutaneous melanoma, their use in ocular variants has bee

260 found that LNK is significantly elevated in cutaneous melanoma; this elevation is correlated with hy

261 tations) are present in hairy-cell leukemia, cutaneous melanoma, thyroid carcinomas and, less commonl

262 y and distribution of T cells within primary cutaneous melanoma tissue correlate with survival of met

263 hough UM metastases are less responsive than cutaneous melanoma to chemotherapy or immune checkpoint

264 We used a polygenic risk score for cutaneous melanoma to compare families without known hig

265 bowel is common because of the tendency for cutaneous melanoma to metastasise to the gastrointestina

266 ent, and outcome of patients with metastatic cutaneous melanoma to the vitreous.

267 This is a study of 29 patients with advanced cutaneous melanoma treated with ipilimumab.

268 ng of tumor-related gene promoter regions in cutaneous melanoma tumors has not been reported.

269 Over half of cutaneous melanoma tumors have BRAF(V600E/K) mutations.

270 tion (MSP) in 15 melanoma cell lines and 130 cutaneous melanoma tumors.

271 ons are significantly less frequent in other cutaneous melanoma types and if present arise late in pr

272 1A CpG island was investigated in metastatic cutaneous melanomas using methylation-specific PCR; regi

273 The SIR for cutaneous melanoma was 2.2 (95% CI 1.0-4.4; n=8), and on

274 mitosis per square millimeter in the primary cutaneous melanoma was associated with decreased surviva

275 pregnancy on the risk of death in women with cutaneous melanoma was suggested historically by anecdot

276 ad undergone complete resection of stage III cutaneous melanoma, we randomly assigned them to receive

277 ic murine melanoma model, which mimics human cutaneous melanoma, we tested effects of ultralow noncyt

278 e, in genetically engineered mouse models of cutaneous melanomas, we sought to better understand the

279 The demographics and presentation of cutaneous melanoma were age related; younger children we

280 y for regional LN metastasis associated with cutaneous melanoma were examined.

281 Cancer stage (AJCC) stage IIB, IIC, and III cutaneous melanoma were randomly allocated (1:1), via a

282 IIB, or IIIC (without in-transit metastasis) cutaneous melanoma were randomly assigned to receive pem

283 Patients with a primary cutaneous melanoma were randomly assigned to wide excisi

284 A total of 101 patients with metastatic cutaneous melanoma were recruited prospectively.

285 Four patients with advanced cutaneous melanoma were treated with a mitogen-activated

286 ncident genetic alterations found in primary cutaneous melanomas, were first introduced into human me

287 ; range 7-28), thus radically different from cutaneous melanoma, where hundreds of exonic DNA insults

288 iated by a mutation in GNAQ or GNA11, unlike cutaneous melanomas, which usually harbour a BRAF or NRA

289 ith resected stage IIIA/B/C/D BRAF wild-type cutaneous melanoma, while either of those two agents or

290 d be offered to patients with BRAF wild-type cutaneous melanoma, while those three regimens or combin

291 ried for all patients with SLNs positive for cutaneous melanoma who subsequently underwent completion

292 eyes of an 80-year-old male with metastatic cutaneous melanoma, who developed paraneoplastic vitelli

293 ajor genes involved in familial and sporadic cutaneous melanoma with an emphasis on CDKN2A, CDK4, MC1

294 hat a 1 cm excision margin is inadequate for cutaneous melanoma with Breslow thickness greater than 2

295 Consecutive patients with cutaneous melanoma with sentinel lymph nodes resected fr

296 determinant of individual susceptibility to cutaneous melanoma, with fair skinned subjects at highes

297 (95% CI, 5.1 to 7.5 months) for mucosal and cutaneous melanoma, with objective response rates of 23.

298 (95% CI, 8.9 to 16.7 months) for mucosal and cutaneous melanoma, with objective response rates of 37.

299 vitreous debris in the context of metastatic cutaneous melanoma would benefit from evaluation by an o

300 The clinical management of cutaneous melanoma would benefit significantly from a be