ライフサイエンスコーパス: acral

1 4%), amelanotic (2%-8%), spitzoid (<2%), and acral (~1%).

2 Acral and mucosal melanomas arise from sun-protected sit

3 Genetically, acral and mucosal melanomas harbor more alterations of K

4 However, acral and mucosal melanomas were dominated by structural

5 cal trial enrolling patients with metastatic acral and mucosal melanomas, showed an exon 13 K642E mut

6 is of whole-genome sequences from cutaneous, acral and mucosal subtypes of melanoma.

7 in KIT have been identified in melanomas of acral and mucosal types and in those arising in chronica

8 ve response rate to ACT-TIL in patients with acral and nonacral melanomas was 43% and 40%, respective

9 ivo in murine and patient-derived cutaneous, acral and uveal melanoma models.

10 r increases of KIT in 39% of mucosal, 36% of acral, and 28% of melanomas on chronically sun-damaged s

11 cephalopathy, and facial, ocular, dental and acral anomalies.

12 hy and late onset of mild skin fragility and acral blistering.

13 -coding fusions, breakend hypermutation, and acral, but not cutaneous, melanomas.

14 In this classification, primary cutaneous acral CD8(+) T-cell lymphoma and Epstein-Barr virus posi

15 Melanomas arising from mucosal, acral, chronically sun-damaged surfaces sometimes have o

16 Observations: Six patients with a total of 8 acral CTCL lesions received low-dose HDR brachytherapy d

17 es excellent palliation for local control of acral CTCL lesions, offering homogeneous, controlled dos

18 d the role of low-dose HDR brachytherapy for acral CTCL lesions.

19 In a child with a periorificial or acral dermatitis, the diagnosis of zinc, biotin, protein

20 cral melanoma, and outcomes in patients with acral disease were unexpectedly comparable with those of

21 Compared with those with acral disease, patients with nonacral cutaneous melanoma

22 d a molecular classification of inflammatory acral diseases.

23 Twelve patients (75%) displayed cyanotic acral edema of the extremities.

24 Cyanotic acral edema was present in 75% of our patients, a findin

25 t scale, conjunctivitis, and mild facial and acral edema.

26 Other grade III toxicity included acral erythema (n = 1), neuropathy (n = 1), peripheral e

27 e, and studies assessing only nail, mucosal, acral, facial, or metastatic melanomas or melanomas on c

28 of ears, hypoplasia of mammillae, and dorsal acral hypertrichosis.

29 ture in chilblain lesions, accompanied by an acral infiltration of activated plasmacytoid dendritic c

30 to autoamputation, distinctive starfish-like acral keratoses and moderate degrees of deafness.

31 ory Poikiloderma with Hair abnormalities and Acral Keratoses), in four affected individuals from two

32 Acral lentiginous and nodular tumors, male sex, tumor si

33 001) and of the nodular, lentigo maligna, or acral lentiginous histologic subtypes.

34 HR, 8.2; 95% CI, 6.7-10.0) and patients with acral lentiginous histology results (3.3% for acral lent

35 Pathologic diagnoses were: acral lentiginous melanoma (48 patients); subungual mela

36 Acral lentiginous melanoma (ALM) is a rare subtype of ma

37 Patients with metastatic acral lentiginous melanoma (ALM) suffer worse outcomes r

38 Deeper analysis of acral lentiginous melanoma (ALM), a rare sun-shielded me

39 atients of colour predominately present with acral lentiginous melanoma (ALM), the most lethal subtyp

40 ence of the non-lentigo maligna (non-LM)/non-acral lentiginous melanoma (non-ALM) subtypes.

41 0.4 mm, mitotic rate greater than 1/mm2, and acral lentiginous melanoma and lentigo maligna melanoma

42 Acral lentiginous melanoma is a subtype of cutaneous mel

43 Acral lentiginous melanoma lesions < 1.5-mm thick were t

44 Seventy-one percent of patients with acral lentiginous melanoma presented with lesions > or =

45 Multivariable analysis showed that acral lentiginous melanoma, lentigo maligna melanoma, an

46 ngated rete ridges, consistent with invasive acral lentiginous melanoma.

47 11 (27%) nodular melanomas, two of 13 (15%) acral lentiginous melanomas, one of one (100%) mucosal m

48 30 (33%) being histologically classified as acral lentiginous melanomas.

49 cral lentiginous histology results (3.3% for acral lentiginous vs 0.9% for superficial spreading; HR,

50 ial spreading, lentigo maligna, nodular, and acral lentiginous.

51 limbs, indicating that melanocytes in these acral locations may be uniquely susceptible to CRKL.

52 ized by cold-induced inflammatory lesions at acral locations presenting in early childhood.

53 al melanoma (UM), mucosal melanoma (MM), and acral melanoma (AM) arise that have distinct genetic pro

54 Acral melanoma (AM) is commonly distinguished from super

55 shown that a particular subtype of melanoma, acral melanoma (AM), has frequent amplification of the C

56 ACT-TIL treatment outcomes of patients with acral melanoma and compared them with contemporaneously

57 esults provide insights into the etiology of acral melanoma and implicate LZTR1 as a key tumor promot

58 ations and structural variation in a primary acral melanoma and its lymph node metastasis.

59 in cutaneous melanoma, BRAF, NRAS and NF1 in acral melanoma and SF3B1 in mucosal melanoma.

60 immunologic basis of responses to ACT-TIL in acral melanoma and to increase the frequency of CRs.

61 Acral melanoma could be distinguished from mucosal melan

62 Acral melanoma is an aggressive type of melanoma with un

63 Acral melanoma is distinct from melanoma of other cutane

64 their mutational status and association with acral melanoma is unclear.

65 cal excision and sentinel node biopsy for an acral melanoma on his left heel.

66 howed that the risk of relapse is greater in acral melanoma patients with high levels of NUAK2 expres

67 with high levels of NUAK2 expression than in acral melanoma patients with low levels of NUAK2 express

68 s of melanoma cells and with the survival of acral melanoma patients.

69 ow that the somatic mutational rates in this acral melanoma sample pair were more comparable to the r

70 phical regions and host factors suggests the acral melanoma subtype is uniquely unrelated to pigmenta

71 Out of 442 included patients, 30 (7%) had acral melanoma while 412 (93%) had nonacral melanoma.

72 se understanding of the genomic landscape of acral melanoma, a rare form of melanoma occurring on pal

73 ective responses in patients with metastatic acral melanoma, and outcomes in patients with acral dise

74 nces favoring nivolumab plus ipilimumab with acral melanoma, BRAF-mutant melanoma, and lactate dehydr

75 Those diagnosed with advanced acral melanoma, mucosal/ocular melanoma, or melanoma of

76 Acral melanoma, the most common melanoma subtype among n

77 sun-exposed skin but far higher than that of acral melanoma.

78 ytes (ACT-TIL) has efficacy in patients with acral melanoma.

79 a unique mutational mechanism that initiates acral melanoma.

80 e well-characterized mutational landscape of acral melanoma.

81 ma and enrichment for CRKL amplifications in acral melanoma.

82 th a greater than fourfold increased risk of acral melanoma.

83 ramme eliminated the anatomic specificity of acral melanoma.

84 as (n = 17), nodular melanomas (n = 17), and acral melanomas (n = 15).

85 ntegrative genomic and clinical profiling of acral melanomas from 104 patients treated in North Ameri

86 We sequenced the DNA of cutaneous and acral melanomas from a large cohort of human patients an

87 Acral melanomas had lower TMB and ultraviolet mutational

88 cription regulator 1 (LZTR1) is amplified in acral melanomas, is required for melanocytes and melanom

89 volar-enriched subpopulation is retained in acral melanomas.

90 logic subtype (P = 0.05) compared with volar acral melanomas.

91 ally map aberrations in the skin adjacent to acral melanomas.

92 mmune activation in nodular melanomas versus acral melanomas.

93 T somatic mutations compared to sun-shielded acral, mucosal and uveal melanomas.

94 T receptor is mutated in approximately 15%of acral, mucosal, and chronic, sun-damaged melanomas.

95 Some melanomas arising from acral, mucosal, and chronically sun-damaged sites harbor

96 advanced unresectable melanoma arising from acral, mucosal, and chronically sun-damaged sites.

97 Responses were evident across patients with acral, mucosal, and cutaneous melanoma.

98 neuropathy, corneal anesthesia and scarring, acral mutilation, cerebral leukoencephalopathy, failure

99 eral and central nervous system involvement, acral mutilation, corneal scarring or ulceration, liver

100 /interdigital (n = 13) acral skin as well as acral nevi (n = 24) for clinical, histologic, and molecu

101 DESIGN, SETTING, AND PARTICIPANTS: Acral nevi specimens (n = 50) that had been obtained for

102 from primary tumors and 65.7% (n = 105) were acral or mucosal by site, whereas in the TCGA-MEL cohort

103 Melanomas that arise on mucosal, acral, or CSD skin should be assessed for KIT mutations.

104 iseases of the small nerve fibers that cause acral pain syndromes, erythromelalgia is not characteriz

105 iseases of the small nerve fibers that cause acral pain syndromes, erythromelalgia is not characteriz

106 mal cornification in lamellar ichthyosis and acral peeling skin syndrome, respectively; loss of TG3 c

107 such as the scalp, face, external genitalia, acral, periumbilical, and perineal areas.

108 M1b disease and cutaneous versus mucosal or acral primaries.

109 ed PSS can now be clearly distinguished from acral PSS, caused by mutations in transglutaminase 5.

110 ed by generalized peeling skin, leukonychia, acral punctate keratoses, cheilitis, and knuckle pads, w

111 further disease alleles in one subject with acral pustular psoriasis (c.2031-2A>C;c.2031-2A>C) and i

112 PV (n=159), erythrodermic psoriasis (n=23), acral pustular psoriasis (n=100), or sporadic PRP (n=29)

113 erythematous base and not restricted to the acral region or within psoriatic plaques." CONCLUSIONS A

114 The frequent amplifications in melanomas on acral sites allowed the detection of single basal melano

115 We show that melanomas on acral sites have significantly more aberrations involvin

116 s (mucosal sites) and on the hands and feet (acral sites) in people throughout the world.

117 These results demonstrate that, on acral sites, melanoma field cells extend significantly i

118 factor (IGF) signalling and drive tumours at acral sites.

119 melanomas from palms, soles, and subungual (acral) sites; and 20 mucosal melanomas.

120 Melanomas on mucosal membranes, acral skin (soles, palms, and nail bed), and skin with c

121 (n = 9), and subungual/interdigital (n = 13) acral skin as well as acral nevi (n = 24) for clinical,

122 Despite the perception that acral skin is sun-protected, the dominant mutational sig

123 Acral skin may develop nevi, but their mutational status

124 as well as 5 healthy nonacral and 10 healthy acral skin samples.

125 study, nevi arising on mostly sun-protected acral skin showed a rate of BRAF mutation similar to tha

126 Acral skin showed a unique immune environment, likely co

127 2 primary melanomas (38 from mucosa, 28 from acral skin, and 18 from skin with and 18 from skin witho

128 utaneous melanomas, 30 (75%) were located on acral skin, despite only 10 of 30 (33%) being histologic

129 Compared to healthy acral skin, PPP, palmPP, and DPE displayed a broad overl

130 noma arises throughout the body, whereas the acral subtype arises on the palms of the hands, soles of

131 retrospectively identified patients who had acral subtype on the basis of clinicopathologic data ava

132 Melanomas on dorsal acral surfaces demonstrated clear differences compared w

133 iosensitive tumor, the complex topography of acral surfaces presents challenges to achieving homogene