Results 81 to 90 of about 4,117 (196)
Advances in cell sources, bioengineering, and manufacturing are reshaping the design of skin substitutes. This review highlights emerging strategies driving skin tissue engineering and discusses their potential to enable safer, reproducible, and clinically accessible skin substitutes for regenerative medicine.
Gilles Lemaître +7 more
wiley +1 more source
We integrated 14 single‐cell RNA‐seq datasets and 18 bulk cohorts to define eight CAF subtypes in GI cancers. myCAF1 and myCAF2 promoted immunosuppressive, poor‐prognosis niches, whereas iCAF1 was linked to favorable prognosis and antitumor immunity.
Huaitao Wang +7 more
wiley +1 more source
Integrated Immune, Epithelial and Lipid Pathways in NSAID‐Exacerbated Respiratory Disease
ABSTRACT NSAID‐exacerbated respiratory disease (N‐ERD) is a chronic inflammatory disorder characterized by asthma, chronic rhinosinusitis with nasal polyps and respiratory reactions to cyclooxygenase‐1 inhibiting nonsteroidal anti‐inflammatory drugs (NSAID).
Piotr Szatkowski, Lucyna Mastalerz
wiley +1 more source
Antisense oligonnucleotide treatment of COL7A1 causes non-specific splice modifications
Recessive dystrophic epidermolysis bullosa (RDEB) is an inherited disease caused by bi‐allelic mutations in the COL7A1, which results in severe blistering of the skin and mucous membranes. Current therapies treat the symptoms but not the disease.
West, K.A., Wilton, S.D., Fletcher, S.
core
Schematic overview of progression from differentiated thyroid carcinoma (DTC) to anaplastic thyroid carcinoma (ATC). ATC primarily develops via two pathways: the BRAF p.V600E‐mutated papillary thyroid carcinoma (PTC) pathway and the RAS‐mutated pathway. The origin and progression of BRAF/RAS‐wildtype ATC remain unclear.
Toru Odate, Tetsuo Kondo
wiley +1 more source
Genome editing represents a promising strategy for the therapeutic correction of COL7A1 mutations that cause recessive dystrophic epidermolysis bullosa (RDEB).
Webber, Beau R. +14 more
core +1 more source
Revertant Mosaicism Due to a Second-Site Mutation in COL7A1 in a Patient with Recessive Dystrophic Epidermolysis Bullosa [PDF]
Despite the high incidence of revertant mosaicism (35%) in patients with the genetic skin disease epidermolysis bullosa (EB) due to correcting mutations in the genes COL17A1 and LAMB3, revertant mosaicism has not been described for COL7A1 until recently.
Cuadrado-Corrales, Natividad +18 more
core +1 more source
Identification of COL7A1 as a prognostic biomarker in lung squamous cell carcinoma
Abstract The Collagen Type VII Alpha 1 Chain (COL7A1) is associated with a variety of cancers, however, COL7A1 gene expression in human lung squamous cell carcinoma (LUSC) and its prognostic value have not been well studied. In this study, we used bioinformatics database to analyze the relationship between COL7A1 expression and survival in LUSC
Weihao Song +9 more
openaire +1 more source
In the absence of a positive family history, it is often difficult to determine whether a single case of mild-to-moderately severe dystrophic epidermolysis bullosa (DEB) represents autosomal recessive or de novo dominant disease.
Mellerio, J E +7 more
core +1 more source
Dystrophic Epidermolysis Bullosa
Epidermolysis bullosa is a rare inherited blistering disease with an incidence of 8-10 per million live births. Dystrophic epidermolysis bullosa is a type of epidermolysis bullosa caused by mutation in type VII collagen, COL7A1.
Randhir Sagar Yadav +4 more
doaj +1 more source

