Basal cell carcinoma (BCC) is the most common human cancer worldwide, and is a subtype of nonmelanoma skin cancer, characterized by a constantly increasing incidence due to an aging population and widespread sun exposure. Although the mortality from BCC is negligible, this tumor can be associated with significant morbidity and cost. This review presents a literature overview of BCC from pathophysiology to novel therapeutic approaches. Several histopathological BCC subtypes with different prognostic values have been described. Dermoscopy and, more recently, reflectance confocal microscopy have largely improved BCC diagnosis. Although surgery is the first-line treatment for localized BCC, other nonsurgical local treatment options are available. BCC pathogenesis depends on the interaction between environmental and genetic characteristics of the patient. Specifically, an aberrant activation of Hedgehog signaling pathway is implicated in its pathogenesis. Notably, Hedgehog signaling inhibitors, such as vismodegib and sonidegib, are successfully used as targeted treatment for advanced or metastatic BCC. Furthermore, the implementation of prevention measures has demonstrated to be useful in the patient management.
Herlitz junctional epidermolysis bullosa (H-JEB) providesdeposited into the extracellular matrix. Re-expression of a promising model for somatic gene therapy of heritable laminin-5 induced cell spreading, nucleation of hemidesmechano-bullous disorders. This genodermatosis is mosomal-like structures and enhanced adhesion to the culcaused by the lack of laminin-5 that results in absence of ture substrate. Organotypic cultures performed with the hemidesmosomes (HD) and defective adhesion of squamtransduced keratinocytes, reconstituted epidermis closely ous epithelia. To establish whether re-expression of lamiadhering to the mesenchyme and presenting mature heminin-5 can restore assembly of the dermal-epidermal attachdesmosomes, bridging the cytoplasmic intermediate filament structures lacking in the H-JEB skin, we corrected the ments of the basal cells to the anchoring filaments of the genetic mutation hindering expression of the 3 chain of basement membrane. Our results provide the first evilaminin-5 in human H-JEB keratinocytes by transfer of a dence of phenotypic reversion of JEB keratinocytes by laminin 3 transgene. The transduced keratinocytes synsomatic gene therapy and demonstrate that genetic treatthesized a recombinant 3 polypeptide that assembled ment of the mild forms of skin blistering diseases and other with the endogenous laminin ␣3 and ␥2 chains into a bioinherited extracellular matrix pathologies is a realistic goal. logically active laminin-5 that was secreted, processed and
Psoriasis is an immune-mediated skin disease with a genetic predisposition, characterized by regional expansion and activation of T helper (Th)-1, Th-17, and Th-22 cells, releasing high levels of the pro-inflammatory cytokines IFN-γ, TNF-α, IL-17, and IL-22 in the skin [1, 2]. Epidermal keratinocytes respond to this potent pro-inflammatory environment by hyperproliferating and releasing in turn numerous cytokines and chemokines, responsible for the recruitment and inflammatory auto-amplificatory loop in the skin [3]. In
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.