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1 vi, large nondysplastic nevi, and clinically dysplastic nevi.
2 ze the role of keratinocyte dysplasia within dysplastic nevi.
3 Indices corresponding to common nevi (0-1), dysplastic nevi (1-4), and melanoma (5-8) were significa
4 he spectrum of melanocyte transformation (16 dysplastic nevi, 11 melanomas in situ, 107 invasive prim
6 ing subtypes were more often associated with dysplastic nevi (20% and 18%, respectively) (P = .002),
7 munoreactivity, was observed in 1 of 16 (6%) dysplastic nevi, 3 of 11 (27%) melanomas in situ, and 81
11 ons, including melanomas, differently staged dysplastic nevi, and common nevi that were validated by
14 that Gal-1 ligands were abundant in severely dysplastic nevi, as well as in primary and metastatic me
15 from biopsy-diagnosed moderately-to-severely dysplastic nevi before excision to melanoma in situ afte
17 The management of clinically atypical nevi/dysplastic nevi (CAN/DN) is controversial, with few data
19 analyses of 19 cutaneous malignant melanoma/dysplastic nevi (CMM/DN) kindreds showed significant evi
20 plastic nevi confer a small risk, clinically dysplastic nevi confer substantial risk for melanoma.
21 tions, the presence of clinically identified dysplastic nevi confers greatly increased risk of melano
22 ers of cutaneous melanoma (CM) families with dysplastic nevi (DN) are at high risk of developing CM.
27 al. approach the problem of differentiating dysplastic nevi from common melanocytic nevi through a m
28 tory profiles of melanocytic nevi (including dysplastic nevi) from melanoma, we sequenced exomes of m
29 ults show that although melanocytic nevi and dysplastic nevi harbor stable genomes with relatively fe
32 The incidence of moderately and severely dysplastic nevi increased from 1.0% to 7.2% and from 0.6
34 ion of biopsy-diagnosed mildly or moderately dysplastic nevi is unlikely to result in a clinically si
35 quenced exomes of melanocytic nevi including dysplastic nevi (n = 19), followed by a targeted gene pa
36 nsisted of 64 melanocytic lesions, including dysplastic nevi (N=21), primary melanoma (N=20), and met
37 rray analysis of NIK expression reveals that dysplastic nevi (n=22), primary (n=15) and metastatic me
38 ear, then annually thereafter for moderately dysplastic nevi or atypical nevus syndrome; biannually f
39 years, then annually thereafter for severely dysplastic nevi or melanomas in situ; every 3 months for
40 higher number of AP-2-positive cells in the dysplastic nevi (P=0.0013) and primary melanoma (P=0.002
41 cells in the metastatic melanoma compared to dysplastic nevi (P=0.0072) and primary melanoma (P=0.013
42 Additionally, melanocytic nevi including dysplastic nevi showed a significantly lower frequency a
43 ents included in situ and invasive melanoma, dysplastic nevi, Spitz nevi, atypical nevus syndrome, fa
44 e following frequencies: annually for mildly dysplastic nevi, Spitz nevi, or solely family history of
45 sue sections of melanoma arising in a nevus; dysplastic nevi; Spitz nevi; and misdiagnosed melanocyti
46 atistical effect of histologic subtype, age, dysplastic nevi syndrome, and associated cancers on muta
47 Gal-3 during the progression from benign to dysplastic nevi to melanoma and further to metastatic me
49 ges: common nevi without dysplastic changes, dysplastic nevi with structural and architectural atypia
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