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1 s of age or older with genetically confirmed dystrophic epidermolysis bullosa.
2 al trials of gene therapy for junctional and dystrophic epidermolysis bullosa.
3 angiomas and bone marrow transplantation for dystrophic epidermolysis bullosa.
4 from the skin of two patients with recessive dystrophic epidermolysis bullosa.
5 as been identified as the candidate gene for dystrophic epidermolysis bullosa.
6 res leads to the chronic blistering disease, dystrophic epidermolysis bullosa.
7 1, give rise to the blistering skin disease, dystrophic epidermolysis bullosa.
8 fore allelic with other variants of dominant dystrophic epidermolysis bullosa.
9 s syndrome is a clinical variant of dominant dystrophic epidermolysis bullosa.
10 VII collagen gene (COL7A1) in patients with dystrophic epidermolysis bullosa.
11 ty, especially among patients with recessive dystrophic epidermolysis bullosa.
12 evated in tumours of patients with Recessive Dystrophic Epidermolysis Bullosa, a disease characterize
13 found in the skin of children with recessive dystrophic epidermolysis bullosa after allogeneic bone m
14 reening of COL7A1 mutations in patients with dystrophic epidermolysis bullosa and compared them with
16 n the overwhelming majority of patients with dystrophic epidermolysis bullosa, and most of them in th
18 CFB in invasive cSCCs (n = 71) and recessive dystrophic epidermolysis bullosa-associated cSCCs (n = 1
19 fibroblasts in invasive cSCCs and recessive dystrophic epidermolysis bullosa-associated cSCCs compar
20 utations in cells of patients with recessive dystrophic epidermolysis bullosa can be corrected by hom
21 anchoring fibrils in patients with recessive dystrophic epidermolysis bullosa can be morphologically
22 tein replacement or cell-based therapies for dystrophic epidermolysis bullosa caused by genetic defic
24 idermolysis bullosa; however, many recessive dystrophic epidermolysis bullosa COL7A1 pathogenic nucle
25 ominant (DDEB) and recessive (RDEB) forms of dystrophic epidermolysis bullosa (DEB) and have subseque
33 tations in gene COL7A1 encoding for C7 cause dystrophic epidermolysis bullosa (DEB), a genetic mechan
38 emature stop codon was achieved in recessive dystrophic epidermolysis bullosa fibroblasts, keratinocy
39 with either systemic sclerosis or recessive dystrophic epidermolysis bullosa has led to the common f
40 c genetic treatment strategies for recessive dystrophic epidermolysis bullosa; however, many recessiv
41 obullous disease Hallopeau-Siemens recessive dystrophic epidermolysis bullosa (HS-RDEB) results from
43 n deficiency in generalised severe recessive dystrophic epidermolysis bullosa, in which blood and mar
52 defects (n = 3) or with autosomal recessive dystrophic epidermolysis bullosa (n = 4) were included a
53 ns in genomic DNA predicted severe recessive dystrophic epidermolysis bullosa or junctional epidermol
56 that the high caries experience in recessive dystrophic epidermolysis bullosa patients is probably re
57 of the three techniques we have screened 93 dystrophic epidermolysis bullosa patients yielding an ov
61 f keratinocytes from patients with recessive dystrophic epidermolysis bullosa (RDEB) and normal derma
63 he genetic skin blistering disease recessive dystrophic epidermolysis bullosa (RDEB) develop aggressi
89 s demonstrated in vivo utilizing a recessive dystrophic epidermolysis bullosa (RDEB) knockout mouse m
90 data suggest that individuals with recessive dystrophic epidermolysis bullosa (RDEB) only develop squ
91 man skin fragility disorder coined recessive dystrophic epidermolysis bullosa (RDEB) that is associat
92 trix, we explored their utility in recessive dystrophic epidermolysis bullosa (RDEB), a blistering di
93 Type VII collagen defects cause recessive dystrophic epidermolysis bullosa (RDEB), a blistering sk
94 observations of severe generalized recessive dystrophic epidermolysis bullosa (RDEB), a currently inc
96 eatment is currently available for recessive dystrophic epidermolysis bullosa (RDEB), a severe herita
97 ch as the blistering skin disorder recessive dystrophic epidermolysis bullosa (RDEB), caused by mutat
98 uch as the blistering skin disease recessive dystrophic epidermolysis bullosa (RDEB), which is charac
104 enetic analyses have revealed that recessive dystrophic epidermolysis bullosa results from mutations
106 d healing at 3 and 6 months in patients with dystrophic epidermolysis bullosa was more likely with to
107 n, M2798K, that is associated with recessive dystrophic epidermolysis bullosa, was unable to form ant
108 utions previously disclosed in patients with dystrophic epidermolysis bullosa, we studied how these a
109 rizing conjunctivitis in both eyes caused by dystrophic epidermolysis bullosa who received ophthalmic
110 atitis, psoriasis, infantile hemangiomas and dystrophic epidermolysis bullosa will be discussed.
111 s squamous cell carcinoma pathophysiology in dystrophic epidermolysis bullosa with a focus on known o
112 we treated seven children who had recessive dystrophic epidermolysis bullosa with immunomyeloablativ
113 tations in 13 patients with severe recessive dystrophic epidermolysis bullosa yielding a detection se