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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
5                                           Of dysplastic nevi, 196 of 580 (34%) showed a positive biop
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
8     Consecutive patient pathology samples of dysplastic nevi and cutaneous melanomas evaluated betwee
9                  MPM images corresponding to dysplastic nevi and melanoma were compared with standard
10 amatic Akt immunoreactivity seen in severely dysplastic nevi and melanomas (66.3% positive).
11 vs lower grade (including mild to moderately dysplastic nevi) and diagnosis of invasive melanoma vs a
12 ons, including melanomas, differently staged dysplastic nevi, and common nevi that were validated by
13 of melanomas arising in a nevus, Spitz nevi, dysplastic nevi, and misdiagnosed lesions.
14          Moderately-to-severely and severely dysplastic nevi are more often associated with melanoma,
15 that Gal-1 ligands were abundant in severely dysplastic nevi, as well as in primary and metastatic me
16 from biopsy-diagnosed moderately-to-severely dysplastic nevi before excision to melanoma in situ afte
17 xpressed in normal cutaneous melanocytes and dysplastic nevi but not in melanoma metastases.
18   The management of clinically atypical nevi/dysplastic nevi (CAN/DN) is controversial, with few data
19                                           In dysplastic nevi cases, the rate of clinically significan
20  analyses of 19 cutaneous malignant melanoma/dysplastic nevi (CMM/DN) kindreds showed significant evi
21 plastic nevi confer a small risk, clinically dysplastic nevi confer substantial risk for melanoma.
22 tions, the presence of clinically identified dysplastic nevi confers greatly increased risk of melano
23 ers of cutaneous melanoma (CM) families with dysplastic nevi (DN) are at high risk of developing CM.
24                                              Dysplastic nevi (DN) is a strong risk factor for cutaneo
25 elanoma, common or congenital nevi (CN), and dysplastic nevi (DN), assessed molecular and genetic pat
26 ly excised, biopsy-proven, mild and moderate dysplastic nevi (DN).
27                                              Dysplastic nevi (DNs), also known as Clark's nevi or aty
28                          Normal and slightly dysplastic nevi exhibited no significant Akt expression,
29  al. approach the problem of differentiating dysplastic nevi from common melanocytic nevi through a m
30 tory profiles of melanocytic nevi (including dysplastic nevi) from melanoma, we sequenced exomes of m
31 ults show that although melanocytic nevi and dysplastic nevi harbor stable genomes with relatively fe
32               Exome sequencing revealed that dysplastic nevi harbored a substantially lower mutationa
33      To portray the mutational repertoire of dysplastic nevi in patients with the dysplastic nevus sy
34     The incidence of moderately and severely dysplastic nevi increased from 1.0% to 7.2% and from 0.6
35                            In the absence of dysplastic nevi, increased numbers of small nevi were as
36 ion of biopsy-diagnosed mildly or moderately dysplastic nevi is unlikely to result in a clinically si
37 quenced exomes of melanocytic nevi including dysplastic nevi (n = 19), followed by a targeted gene pa
38 nsisted of 64 melanocytic lesions, including dysplastic nevi (N=21), primary melanoma (N=20), and met
39 rray analysis of NIK expression reveals that dysplastic nevi (n=22), primary (n=15) and metastatic me
40 o diagnose study cases as mild to moderately dysplastic nevi (odds ratio, 1.26; 95% CI, 0.97-1.64; P
41 ear, then annually thereafter for moderately dysplastic nevi or atypical nevus syndrome; biannually f
42 years, then annually thereafter for severely dysplastic nevi or melanomas in situ; every 3 months for
43  higher number of AP-2-positive cells in the dysplastic nevi (P=0.0013) and primary melanoma (P=0.002
44 cells in the metastatic melanoma compared to dysplastic nevi (P=0.0072) and primary melanoma (P=0.013
45     Additionally, melanocytic nevi including dysplastic nevi showed a significantly lower frequency a
46                                 In contrast, dysplastic nevi showed evidence for genomic instability
47 ents included in situ and invasive melanoma, dysplastic nevi, Spitz nevi, atypical nevus syndrome, fa
48 e following frequencies: annually for mildly dysplastic nevi, Spitz nevi, or solely family history of
49 sue sections of melanoma arising in a nevus; dysplastic nevi; Spitz nevi; and misdiagnosed melanocyti
50 atistical effect of histologic subtype, age, dysplastic nevi syndrome, and associated cancers on muta
51  Gal-3 during the progression from benign to dysplastic nevi to melanoma and further to metastatic me
52                  All diagnoses of clinically dysplastic nevi were confirmed by expert examiners.
53 ges: common nevi without dysplastic changes, dysplastic nevi with structural and architectural atypia