1970
Porokeratosis--a mutant clonal keratosis of the epidermis. I. Histogenesis
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Cited by 87 publications
(29 citation statements)
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“…Histopathologic examination of the improved lesions revealed the disappearance of parakeratosis and residual but less stacked pictures of the cornoid lamella. Although the therapeutic mechanisms of etretinate in this genetic disease are unknown, these histologic changes suggest that the drug may normalize the disordered process of keratinization, but can not completely eliminate the expression of the mutant gene (9). A similar suggestion for the action mechanisms of the drug has been given by Kariniemi,Stubb and Lassus (5), who observed visible but small and shallow figures of the cornoid lamella in biopsy specimens taken after two months of therapy with etretinate.…”
Section: Commentmentioning
confidence: 68%
“…Histopathologic examination of the improved lesions revealed the disappearance of parakeratosis and residual but less stacked pictures of the cornoid lamella. Although the therapeutic mechanisms of etretinate in this genetic disease are unknown, these histologic changes suggest that the drug may normalize the disordered process of keratinization, but can not completely eliminate the expression of the mutant gene (9). A similar suggestion for the action mechanisms of the drug has been given by Kariniemi,Stubb and Lassus (5), who observed visible but small and shallow figures of the cornoid lamella in biopsy specimens taken after two months of therapy with etretinate.…”
Section: Commentmentioning
confidence: 68%
“…6 It is proposed that the findings of early focal apoptosis of keratinocytes in the lesional epidermis of the porokeratosis underneath the cornoid lamella accompanied by dysregulation of keratin formation could play a role in the pathogenesis of the disorder. 7 A study of 33 cases of the various types of porokeratoses, showed increased p53 and decreased mdm2 and p21 expression within keratinocytes underlying cornoid lamella -the phenotypic expression of a rapidly cycling cell population with faulty p53 function.…”
Section: Resultsmentioning
confidence: 99%
“…Histologically, EPPP papular lesions usually have dense superficial perivascular mononuclear inflammatory infiltrates with eosinophils [ 14 , 15 ]. Reed and Leone suggested localized keratinocytic clones cause epidermal dysplasia [ 16 ]. Secondary amyloid deposition is rare in EPPP, but positive staining for 34BE12 suggests that amyloid materials originate from degenerating epidermal keratinocytes [ 4 ].…”
Section: Discussionmentioning
confidence: 99%
