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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.
11 nonsquamous (1 pingueculum, 1 dermolipoma, 2 melanocytic nevi, 1 melanoma).
12 from 100 biopsy-proven lesions, including 55 melanocytic nevi, 20 melanomas, 15 basal cell carcinomas
13      Among children with multiple congenital melanocytic nevi, 25% have no established genetic cause,
14                                              Melanocytic nevi also demonstrated catK expression, but
15 is is involved in persistence of NRAS-driven melanocytic nevi and anticipate that targeted small inte
16 ations of NRAS and BRAF were found in benign melanocytic nevi and cutaneous melanomas.
17  to better understand the characteristics of melanocytic nevi and define pathways of melanocytic tumo
18             These results show that although melanocytic nevi and dysplastic nevi harbor stable genom
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
22                               In this study, melanocytic nevi and malignant melanomas were examined b
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
25 ns of chromosomal aberrations between benign melanocytic nevi and melanoma.
26 ce in growth arrest and tumor suppression in melanocytic nevi and melanoma.
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
33 molecular differences between DNs and common melanocytic nevi are not completely understood.
34                             Giant congenital melanocytic nevi are NRAS-driven proliferations that may
35                                              Melanocytic nevi are the most potent risk factors for me
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
43                          Melanoma and benign melanocytic nevi can overlap significantly in their hist
44                                   Congenital melanocytic nevi (CMN) and infantile hemangiomas are com
45                             Large congenital melanocytic nevi (CMN) are at an increased risk of devel
46                                   Congenital melanocytic nevi (CMN) are pigmented birthmarks that aff
47                                   Congenital melanocytic nevi (CMN) can be associated with neurologic
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,
50                                       A high melanocytic nevi count is the strongest known risk facto
51                                         Most melanocytic nevi develop on sun-exposed skin during chil
52 d molecular bases of acquired and congenital melanocytic nevi during childhood.
53 prone to developing large, markedly atypical melanocytic nevi (EB nevi), which may mimic melanoma cli
54                                     Eruptive melanocytic nevi (EMN) are characterized by the sudden o
55                                       Benign melanocytic nevi frequently emerge when an acquired BRAF
56                                              Melanocytic nevi frequently harbor oncogenic BRAF mutati
57 alogous genotypic profiles for epidermal and melanocytic nevi from recent studies.
58                                     Acquired melanocytic nevi grow and persist in a stable form into
59                                 Melanoma and melanocytic nevi harbor shared lineage-specific antigens
60                                        While melanocytic nevi have been associated with genetic facto
61  in the primary melanomas than in the benign melanocytic nevi, however, only p53 over-expression was
62 opathologic examination revealed remnants of melanocytic nevi in 103 melanomas (54.2%).
63 pproach to small- or medium-sized congenital melanocytic nevi in black children must be different bec
64                  Numbers and distribution of melanocytic nevi in childhood are major indicators of th
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
67 ed to prevalence and morphologic features of melanocytic nevi in the perianal area.
68      We studied 169 patients with congenital melanocytic nevi in this study, 38 of whom were double w
69 adigm for understanding the growth arrest of melanocytic nevi in vivo termed stable clonal expansion.
70 tential of the method to distinguish between melanocytic nevi in vivo.
71  nevi) from melanoma, we sequenced exomes of melanocytic nevi including dysplastic nevi (n = 19), fol
72                                Additionally, melanocytic nevi including dysplastic nevi showed a sign
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
75         Importance: The presence of numerous melanocytic nevi is a significant melanoma risk factor,
76                            A large number of melanocytic nevi is the strongest known risk factor for
77 e relationship between the immune system and melanocytic nevi is unclear.
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
80                                        Human melanocytic nevi (moles) result from a brief period of c
81                           A survey of benign melanocytic nevi (moles), suspected precursors or marker
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
87        We report genome duplication in human melanocytic nevi, reciprocal expression of AURKB and mic
88  which growth arrest can be overcome and how melanocytic nevi relate to melanoma are also considered.
89 compared with those from young, and in human melanocytic nevi relative to normal skin.
90 nome-wide association study on the number of melanocytic nevi reported by 9136 individuals of Europea
91                      The density of acquired melanocytic nevi represents an important risk factor for
92 F1, RAC1, and PTEN, were not found among any melanocytic nevi sequenced.
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
95          This review summarizes the types of melanocytic nevi that are commonly observed in children,
96  the first to characterize certain pigmented melanocytic nevi that may also fit this paradigm.
97                        Spitz nevi are benign melanocytic nevi that overlap histopathologically with m
98 pe characterized by the presence of multiple melanocytic nevi: the atypical mole syndrome.
99 ith dermoscopy are associated with enlarging melanocytic nevi, their actual growth dynamics remain un
100  differentiating dysplastic nevi from common melanocytic nevi through a molecular lens.
101  lesions predisposing to malignancy, such as melanocytic nevi, thyroid nodules, and colonic polyps.
102  in clinical melanoma tissues, compared with melanocytic nevi tissues.
103  stages of malignant progression from common melanocytic nevi to metastatic melanomas and examine the
104 udinal tracking of microscopic structures in melanocytic nevi using RCM is feasible.
105 undruggable NRAS(Q61K) in primary cells from melanocytic nevi using small interfering RNA targeted to
106 ions between primary cutaneous melanomas and melanocytic nevi vary widely between 4% and 72%.
107 f BRAF oncogenic mutations was identified in melanocytic nevi, VGP, metastatic melanomas, and melanom
108                         Phenotypical data on melanocytic nevi were collected from a random sample of
109 sions and Relevance: In this study, perianal melanocytic nevi were common and were associated with pr
110           Despite this, the vast majority of melanocytic nevi, which typically form as a result of BR
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

 
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