1 However,
acral and mucosal melanomas were dominated by structural
2 cal trial enrolling patients with metastatic
acral and mucosal melanomas, showed an exon 13 K642E mut
3 is of whole-genome sequences from cutaneous,
acral and mucosal subtypes of melanoma.
4 in KIT have been identified in melanomas of
acral and mucosal types and in those arising in chronica
5 r increases of KIT in 39% of mucosal, 36% of
acral,
and 28% of melanomas on chronically sun-damaged s
6 hy and late onset of mild skin fragility and
acral blistering.
7 Melanomas arising from mucosal,
acral,
chronically sun-damaged surfaces sometimes have o
8 Observations: Six patients with a total of 8
acral CTCL lesions received low-dose HDR brachytherapy d
9 es excellent palliation for local control of
acral CTCL lesions, offering homogeneous, controlled dos
10 d the role of low-dose HDR brachytherapy for
acral CTCL lesions.
11 In a child with a periorificial or
acral dermatitis, the diagnosis of zinc, biotin, protein
12 Twelve patients (75%) displayed cyanotic
acral edema of the extremities.
13 Cyanotic
acral edema was present in 75% of our patients, a findin
14 Other grade III toxicity included
acral erythema (n = 1), neuropathy (n = 1), peripheral e
15 of ears, hypoplasia of mammillae, and dorsal
acral hypertrichosis.
16 to autoamputation, distinctive starfish-like
acral keratoses and moderate degrees of deafness.
17 Acral lentiginous and nodular tumors, male sex, tumor si
18 001) and of the nodular, lentigo maligna, or
acral lentiginous histologic subtypes.
19 Pathologic diagnoses were:
acral lentiginous melanoma (48 patients); subungual mela
20 Deeper analysis of
acral lentiginous melanoma (ALM), a rare sun-shielded me
21 Acral lentiginous melanoma lesions < 1.5-mm thick were t
22 Seventy-one percent of patients with
acral lentiginous melanoma presented with lesions > or =
23 ngated rete ridges, consistent with invasive
acral lentiginous melanoma.
24 11 (27%) nodular melanomas, two of 13 (15%)
acral lentiginous melanomas, one of one (100%) mucosal m
25 ial spreading, lentigo maligna, nodular, and
acral lentiginous.
26 ized by cold-induced inflammatory lesions at
acral locations presenting in early childhood.
27 Acral melanoma (AM) is commonly distinguished from super
28 shown that a particular subtype of melanoma,
acral melanoma (AM), has frequent amplification of the C
29 ations and structural variation in a primary
acral melanoma and its lymph node metastasis.
30 in cutaneous melanoma, BRAF, NRAS and NF1 in
acral melanoma and SF3B1 in mucosal melanoma.
31 Acral melanoma could be distinguished from mucosal melan
32 Acral melanoma is distinct from melanoma of other cutane
33 cal excision and sentinel node biopsy for an
acral melanoma on his left heel.
34 howed that the risk of relapse is greater in
acral melanoma patients with high levels of NUAK2 expres
35 with high levels of NUAK2 expression than in
acral melanoma patients with low levels of NUAK2 express
36 s of melanoma cells and with the survival of
acral melanoma patients.
37 ow that the somatic mutational rates in this
acral melanoma sample pair were more comparable to the r
38 th a greater than fourfold increased risk of
acral melanoma.
39 ally map aberrations in the skin adjacent to
acral melanomas.
40 logic subtype (P = 0.05) compared with volar
acral melanomas.
41 T somatic mutations compared to sun-shielded
acral,
mucosal and uveal melanomas.
42 T receptor is mutated in approximately 15%of
acral,
mucosal, and chronic, sun-damaged melanomas.
43 Some melanomas arising from
acral,
mucosal, and chronically sun-damaged sites harbor
44 advanced unresectable melanoma arising from
acral,
mucosal, and chronically sun-damaged sites.
45 neuropathy, corneal anesthesia and scarring,
acral mutilation, cerebral leukoencephalopathy, failure
46 eral and central nervous system involvement,
acral mutilation, corneal scarring or ulceration, liver
47 /interdigital (n = 13) acral skin as well as
acral nevi (n = 24) for clinical, histologic, and molecu
48 from primary tumors and 65.7% (n = 105) were
acral or mucosal by site, whereas in the TCGA-MEL cohort
49 Melanomas that arise on mucosal,
acral,
or CSD skin should be assessed for KIT mutations.
50 iseases of the small nerve fibers that cause
acral pain syndromes, erythromelalgia is not characteriz
51 iseases of the small nerve fibers that cause
acral pain syndromes, erythromelalgia is not characteriz
52 ed PSS can now be clearly distinguished from
acral PSS, caused by mutations in transglutaminase 5.
53 ed by generalized peeling skin, leukonychia,
acral punctate keratoses, cheilitis, and knuckle pads, w
54 PV (n=159), erythrodermic psoriasis (n=23),
acral pustular psoriasis (n=100), or sporadic PRP (n=29)
55 The frequent amplifications in melanomas on
acral sites allowed the detection of single basal melano
56 We show that melanomas on
acral sites have significantly more aberrations involvin
57 s (mucosal sites) and on the hands and feet (
acral sites) in people throughout the world.
58 These results demonstrate that, on
acral sites, melanoma field cells extend significantly i
59 melanomas from palms, soles, and subungual (
acral)
sites; and 20 mucosal melanomas.
60 Melanomas on mucosal membranes,
acral skin (soles, palms, and nail bed), and skin with c
61 (n = 9), and subungual/interdigital (n = 13)
acral skin as well as acral nevi (n = 24) for clinical,
62 Despite the perception that
acral skin is sun-protected, the dominant mutational sig
63 2 primary melanomas (38 from mucosa, 28 from
acral skin, and 18 from skin with and 18 from skin witho
64 Melanomas on dorsal
acral surfaces demonstrated clear differences compared w
65 iosensitive tumor, the complex topography of
acral surfaces presents challenges to achieving homogene