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 urafenib therapy in patients with metastatic cutaneous melanoma.

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

4 stic factor for clinically localized primary cutaneous melanoma.

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

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

7 a clinical determinant for poor prognosis in cutaneous melanoma.

8 rognosis than do patients with metastases of cutaneous melanoma.

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

10 ly predicts poor outcome among patients with cutaneous melanoma.

11 asing survival in subgroups of patients with cutaneous melanoma.

12 as definitive procedures for the staging of cutaneous melanoma.

13 n patients undergoing SLN biopsy for primary cutaneous melanoma.

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

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

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

17 egional lymph nodes of patients with primary cutaneous melanoma.

18 pathogenesis of many tumor types, including cutaneous melanoma.

19 n treating and preventing the progression of cutaneous melanoma.

20 nal epidemiologic studies involving incident cutaneous melanoma.

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

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

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

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

25 (10%) had mucosal melanoma and 665 (75%) had cutaneous melanoma.

26 to recurrence and survival in patients with cutaneous melanoma.

27 f vascularity on the outcome associated with cutaneous melanoma.

28 analysis of the SLN in patients with primary cutaneous melanoma.

29 ses (TNM) categories and stage groupings for cutaneous melanoma.

30 dm2, in the tumorigenesis and progression of cutaneous melanoma.

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

32 e primary causal agent in the development of cutaneous melanoma.

33 neous melanomas, and in metastatic uveal and cutaneous melanoma.

34 tivation of RAS have been described in human cutaneous melanoma.

35 enter are sufficient for mastery of LM/SL in cutaneous melanoma.

36 10q in 83 individuals with sporadic primary cutaneous melanoma.

37 e by DNA methylation in 30 cases of sporadic cutaneous melanoma.

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

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

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

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

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

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

44 nsitive and specific method for detection of cutaneous melanoma.

45 n tertiary referral centers for treatment of cutaneous melanoma.

46 h vemurafenib for unresectable or metastatic cutaneous melanoma.

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

48 lation to prior or subsequent development of cutaneous melanoma.

49 pathology reports for all ulcerated primary cutaneous melanomas.

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

51 contribute to stepwise progression of human 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 croenvironment can suppress MCSC-originating cutaneous melanomas.

58 fferences in tumorigenesis between uveal and cutaneous melanomas.

59 with complete penetrance and without primary cutaneous melanomas.

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

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

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

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

64 3,158 patients aged 1 to 19 years, 96.3% had cutaneous melanoma, 3.0% had ocular melanoma, and 0.7% h

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

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

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

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

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

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

71 k4a-deficient background develop spontaneous cutaneous melanomas after a short latency and with high

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

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

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

75 the preoperative evaluation of patients with cutaneous melanoma and for intraoperative identification

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

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

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

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

80 tein-2 (TRP-2), as it is highly expressed in cutaneous melanoma and melanocytes.

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

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

83 alysis can identify unrecognized subtypes of cutaneous melanoma and predict experimentally verifiable

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

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

86 trials in the treatment of disorders such as cutaneous melanoma and skin wounding, with 20% of all ge

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 Malignant cutaneous melanomas and metastases were taken directly f

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

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

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

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

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

99 l melanomas, in the vertical growth phase of cutaneous melanomas, and in metastatic uveal and cutaneo

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

101 Cutaneous melanomas are notorious for their tendency to

102 that the two genetic changes, in a subset of cutaneous melanomas, are functionally overlapping.

103 Cutaneous melanomas arise through causal pathways involv

104 Cutaneous melanomas arise with histopathological and mol

105 mor-suppressor gene(s) in the development of cutaneous melanoma as well as a variety of other forms o

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

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

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

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

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

111 e arms 6q, 9p, and 10q, occurs frequently in cutaneous melanoma but infrequently in benign melanocyti

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

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

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

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

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

117 Chemoprevention of cutaneous melanoma can become a valid strategy complemen

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

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

120 ighly aggressive and poorly aggressive human cutaneous melanoma cell lines (established from the same

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

122 Ectopic expression of PTEN in several cutaneous melanoma cell lines suppressed colony formatio

123 mutations and analyzed the RAS status of 53 cutaneous melanoma cell lines, 18 glioma cell lines, and

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

125 d from ocular melanoma tumors; and (iii) two cutaneous melanoma cell lines.

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

127 Moreover, UV-B irradiation of primary cutaneous melanoma cells induces IL-8 mRNA and protein p

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

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

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

131 397 and Tyr576, in only aggressive uveal and cutaneous melanoma cells, which correlates with their in

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

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

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

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

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

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

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

139 Members of cutaneous melanoma (CM) families with dysplastic nevi (D

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

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

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

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

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

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

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

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

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

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

150 Although positive cutaneous melanoma control cell lines harbored the T1796

151 osomal aberrations in Spitz nevi and primary cutaneous melanomas could represent a basis for developi

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

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

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

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

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

157 Within the set of human primary cutaneous melanomas examined, melastatin expression appe

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

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

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

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

162 of mice with 7,12-dimethylbenz(a)anthracene, cutaneous melanomas formed in 12% (17/145) of the Tyr-MI

163 valuated by in situ hybridization in primary cutaneous melanoma from 150 patients with localized dise

164 18 non-Hispanic white patients with invasive cutaneous melanoma from melanoma clinics in Philadelphia

165 18 non-Hispanic white patients with invasive cutaneous melanoma from melanoma clinics in Philadelphia

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

167 tine histopathologic analysis of 417 primary cutaneous melanomas from the University of California at

168 ive human intraocular (uveal) and metastatic cutaneous melanomas generally lack evidence of significa

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

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

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

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

173 0-case learning phase, patients with primary cutaneous melanoma (> or =1 mm with Clark level > or =II

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

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

176 A mouse model of cutaneous melanoma has been generated previously through

177 The analysis of genetic changes in primary cutaneous melanoma has been limited by the need for fixa

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

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

180 iligo, therapy-induced hypopigmentation, and cutaneous melanoma has not been well studied.

181 Cutaneous melanoma has the lowest survival rate of all f

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

183 Cutaneous melanomas have been found to express several i

184 s was selected using these criteria: primary cutaneous melanoma having a thickness > or =1 mm with a

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

186 -7 (FABP7) has been shown to be expressed in cutaneous melanoma; however, its role in tumor progressi

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

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

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

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

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

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

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

194 Cutaneous melanoma incidence is increasing.

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

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

197 Cutaneous melanoma is a highly aggressive tumor that is

198 Cutaneous melanoma is a type of cancer with an inherent

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

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

201 Cutaneous melanoma is epidemiologically linked to ultrav

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

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

204 Incidence of cutaneous melanoma is rising especially steeply, with mi

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

206 The mainstay of treatment of cutaneous melanoma is surgical excision.

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

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

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

210 enforced expression of MCAM/MUC18 in primary cutaneous melanoma led to increased tumor growth and met

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

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

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

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

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

216 nes, 18 glioma cell lines, and 17 uncultured cutaneous melanoma metastasis.

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

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

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

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

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

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

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

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

225 as to investigate the surgical management of cutaneous melanomas of the hands and feet.

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

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

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

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

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

231 Cutaneous melanomas, particularly the desmoplastic subty

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

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

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

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

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

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

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

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

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 oma, the nonmetastatic MCAM-negative primary cutaneous melanoma SB-2 cells were transfected with MCAM

248 Stable transfection of primary cutaneous melanoma SB-2 cells with the dominant-negative

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

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

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

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

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

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

255 activated RAS to promote the development of cutaneous melanomas that are clinically indistinguishabl

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

257 ising in congenital nevi, as well as primary cutaneous melanomas that were not associated with a CMN.

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

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

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

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

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

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

264 In cutaneous melanoma, tumor depth remains the best biologi

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

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

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

268 All patients with clinically node-negative cutaneous melanoma undergoing SLN biopsy from 1991 to 19

269 1A CpG island was investigated in metastatic cutaneous melanomas using methylation-specific PCR; regi

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

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

272 traviolet radiation (UVR)-induced metastatic cutaneous melanoma was produced without the use of chemi

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

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

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

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

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

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

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

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

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

282 One hundred and six patients with localized cutaneous melanoma were studied.

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

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

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

286 m the previously reported changes in primary cutaneous melanoma, which show frequent deletions of chr

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

288 The records of 344 patients with primary cutaneous melanoma who underwent lymphatic mapping and S

289 All patients with primary cutaneous melanoma who underwent SLNB from 1991 through

290 consecutive patients with localized primary cutaneous melanoma who underwent SLNB were identified.

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

292 nd junction and if untreated develop primary cutaneous melanoma with a mean onset age of approximatel

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 Patients with cutaneous melanoma with Breslow's depth greater than 1 m

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

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

298 (95% CI, 5.1 to 7.5 months) for mucosal and cutaneous melanoma, with objective response rates of 23.

299 (95% CI, 8.9 to 16.7 months) for mucosal and cutaneous melanoma, with objective response rates of 37.

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