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1 he distinction of melanoma from conventional melanocytic nevi.
2 dded tissue sections in primary melanoma and melanocytic nevi.
3 l-dominant immunity in clinically regressing melanocytic nevi.
4 melanomas are derived directly from benign, melanocytic nevi.
5 alyzed the difference between DNs and common melanocytic nevi.
6 2% of primary melanomas were associated with melanocytic nevi.
7 valence and morphologic features of perianal melanocytic nevi.
8 nomas (primary and metastatic) compared with melanocytic nevi.
9 melanomas compared with primary melanoma and melanocytic nevi.
10 n reported in individual cases of congenital melanocytic nevi.
12 from 100 biopsy-proven lesions, including 55 melanocytic nevi, 20 melanomas, 15 basal cell carcinomas
15 is is involved in persistence of NRAS-driven melanocytic nevi and anticipate that targeted small inte
17 to better understand the characteristics of melanocytic nevi and define pathways of melanocytic tumo
19 haracterized by the sudden onset of numerous melanocytic nevi and have been traditionally described i
20 owed abundant expression of MAP-2 protein in melanocytic nevi and in the in situ and invasive compone
21 Increased expression of miR211-5p stabilizes melanocytic nevi and keeps them in a growth-arrested sta
23 ptosis inhibitor Survivin to be expressed in melanocytic nevi and melanoma but not in normal melanocy
24 K pathway genes are commonly associated with melanocytic nevi and melanoma, whereas germline variants
27 l impression and current knowledge, acquired melanocytic nevi and melanomas may not occur in random l
28 BRAF mutations occur at a high frequency in melanocytic nevi and metastatic lesions, but recent data
29 d malignant melanocytic neoplasms, including melanocytic nevi and primary invasive and metastatic mel
30 ful delivery into a humanized mouse model of melanocytic nevi and results in variant NRAS knockdown i
31 aberration in melanoma that is distinct from melanocytic nevi and should be further evaluated as a di
32 squamous cell carcinoma, actinic keratosis, melanocytic nevi, angiokeratoma, dermatofibroma, solar l
36 icroscope to image in vivo and noninvasively melanocytic nevi at three different stages: common nevi
37 arcinomas, actinic keratoses, atypical nevi, melanocytic nevi, blue nevi, and seborrheic keratoses.
38 confirmatory, showing a strong signal in the melanocytic nevi but progressive signal attenuation with
39 loss abrogates growth arrest of Braf(V600E) melanocytic nevi, but is insufficient for complete progr
40 and -mRNA was characterized in melanomas and melanocytic nevi by immunocytochemistry and in situ reve
41 discriminative genes between DNs and common melanocytic nevi by three independent statistical approa
42 typical moles, are distinguished from common melanocytic nevi by variegation in pigmentation and clin
48 les (PNs) and melanoma arising in congenital melanocytic nevi (CMN) is crucial, as patients with PNs
49 15 Expression was significantly increased in melanocytic nevi compared with melanomas (mean H scores,
53 prone to developing large, markedly atypical melanocytic nevi (EB nevi), which may mimic melanoma cli
61 in the primary melanomas than in the benign melanocytic nevi, however, only p53 over-expression was
63 pproach to small- or medium-sized congenital melanocytic nevi in black children must be different bec
65 the natural history and clinical spectrum of melanocytic nevi in children as well as potentially worr
66 atypical mole phenotype, development of new melanocytic nevi in older individuals is uncommon and co
69 adigm for understanding the growth arrest of melanocytic nevi in vivo termed stable clonal expansion.
71 nevi) from melanoma, we sequenced exomes of melanocytic nevi including dysplastic nevi (n = 19), fol
73 to determine the discriminatory profiles of melanocytic nevi (including dysplastic nevi) from melano
74 t approximately 50% of the existing acquired melanocytic nevi involuted, while the remaining nevi did
78 cal management of large and giant congenital melanocytic nevi (lgCMN) relies heavily upon iterative s
79 expression of PEDF in common and dysplastic melanocytic nevi, melanoma in situ, invasive melanoma, a
82 d gene panel (785 genes) characterization of melanocytic nevi (n = 46) and primary melanomas (n = 42)
83 diatricians to discuss treatment options for melanocytic nevi, nevus sebaceus, port-wine stains, and
84 epts of the risks associated with congenital melanocytic nevi of different sizes and strategies for t
85 utaneous melanoma but infrequently in benign melanocytic nevi or other melanocytic lesions, suggestin
86 es were preferentially represented in benign melanocytic nevi over melanomas and selectively mapped t
88 which growth arrest can be overcome and how melanocytic nevi relate to melanoma are also considered.
90 nome-wide association study on the number of melanocytic nevi reported by 9136 individuals of Europea
93 melanoma is the presence of large numbers of melanocytic nevi so that genes controlling nevus phenoty
94 y role for Wnt signaling in the formation of melanocytic nevi, suggesting that activated Wnt signalin
99 ith dermoscopy are associated with enlarging melanocytic nevi, their actual growth dynamics remain un
101 lesions predisposing to malignancy, such as melanocytic nevi, thyroid nodules, and colonic polyps.
103 stages of malignant progression from common melanocytic nevi to metastatic melanomas and examine the
105 undruggable NRAS(Q61K) in primary cells from melanocytic nevi using small interfering RNA targeted to
107 f BRAF oncogenic mutations was identified in melanocytic nevi, VGP, metastatic melanomas, and melanom
109 sions and Relevance: In this study, perianal melanocytic nevi were common and were associated with pr
111 ry oncogenes, which typically lead to benign melanocytic nevi with characteristic histologic features
112 MN) syndrome is the association of pigmented melanocytic nevi with extra-cutaneous features, classica