Co-expression of p16(INK4A) and laminin 5 gamma2 by microinvasive and superficial squamous cell carcinomas in vivo and by migrating wound and senescent keratinocytes in culture.

The high frequency of mutation, deletion, and promoter silencing of the gene encoding p16(INK4A) (p16) in premalignant dysplasias and squamous cell carcinomas (SCC) of epidermis and oral epithelium classifies p16 as a tumor suppressor. However, the point during neoplastic progression at which this protein is expressed and presumably impedes formation of an SCC is unknown. Induction of p16 has been found to be responsible for the senescence arrest of normal human keratinocytes in culture, suggesting the possibility that excessive or spatially abnormal cell growth in vivo triggers p16 expression. We examined 73 skin and oral mucosal biopsy specimens immunohistochemically to test this hypothesis. p16 was not detectable in benign hyperplastic lesions, but instead was expressed heterogeneously in some dysplastic and carcinoma in situ lesions and consistently at areas of microinvasion and at superficial margins of advanced SCCs. p16-positive cells in these regions coexpressed the gamma2 chain of laminin 5, identified previously as a marker of invasion in some carcinomas. Normal keratinocytes undergoing senescence arrest in culture proved to coordinately express p16 and gamma2 and this was frequently associated with increased directional motility. Keratinocytes at the edges of wounds made in confluent early passage cultures also coexpressed p16 and gamma2, accompanying migration to fill the wound. These results have identified the point during neoplastic progression in stratified squamous epithelial at which the tumor suppressor p16 is expressed and suggest that normal epithelia may use the same mechanism to generate non-dividing, motile cells for wound repair.

Childhood bullous pemphigoid: a clinicopathologic study and review of the literature.

Bullous pemphigoid (BP) is an acquired bullous disorder that predominantly affects the elderly. It is rare in children but when it occurs, there is considerable clinical and histologic overlap with other acquired or congenital blistering disorders. A definitive diagnosis of childhood BP requires direct immunofluorescence and, in some cases, characterization of the target antigen. Three cases of childhood BP are presented, with their histologic and immunofluorescence findings. The first was a 5-month-old male infant who presented with erythema and bullae of the palms and soles and was found to have linear deposition of IgG and C3 along the dermoepidermal junction on direct immunofluorescence (DIF). Histopathologic examination revealed a subepidermal blister containing eosinophils. Type IV collagen was demonstrated along the floor of the blister cavity by a direct immunoperoxidase technique. The second case was an 8-month-old female infant who presented with a blistering eruption of her palms and soles that then became widespread. Direct immunofluorescence showed linear IgG and C3 at the dermoepidermal junction, with laminin deposition at the base of the blister. The third case was a 7-year-old female with bullae and erosions on the vulva and vaginal mucosa. A subepidermal blister was seen on microscopic examination whereas immunofluorescence demonstrated linear IgG and C3 deposition at the basement membrane zone (BMZ). A literature review uncovered 50 cases of childhood BP confirmed by direct or indirect immunofluorescence, or both, and often with evidence of autoantibodies against either the 180 kD or the 230 kD human bullous pemphigoid antigens (BP180 or BP230). This review was used to delineate characteristics of childhood BP, including the newly proposed subtypes: infantile BP and childhood localized vulval BP. Infantile BP presents within the first year of life and is characterized by BP-like lesions on erythematous or normal acral skin. Localized vulval BP is a self-limited, nonscarring BP-like process that involves only the vulva. Both subtypes are normally self-limited and respond well to either topical or systemic steroids, if treatment is initiated before the disease becomes widespread.

Cromomicosis: informe de cinco casos con énfasis histopatológico y terapéutico / Chromomycosis: report of five cases with emphasis terapeutic and histopathological

La cromomicosis es una micosis subcutánea y cutánea crónica que predomina en las áreas tropicales y subtropicales. Determinar las características epidemiológicas, clínicas e histopatológicas de los pacientes diagnosticados como cromomicosis; con énfasis en los datos histopatológicos y terapéuticos. Se informan cinco pacientes estudiados entre 1987 y 1997; 3 hombres y dos mujeres con una evolución promedio de 15,8 años. La topografía fue extremidades inferiores y superiores, y un caso diseminada a cara, tronco y extremidades superiores, manifestándose en todos los casos como placas verrucosas. En todos los casos se aisló Fonsecaea pedrosoi. En cuanto a distribución geográfica, 2 pacientes eran de Oaxaca y el resto de Puebla, Tamaulipas y Chiapas respectivamente. En el estudio histopatológico se demostraron cambios proliferativos en la epidermis, constituidos por acantosis e hiperplasia pseudoepiteliomatosa aguda y crónica; así como proliferación vascular y fibrosis: Se pudieron observar células fumagoides tanto dentro de células gigantes multinucleadas, en forma libre, como en los microabscesos de neutrófilos. Las modalidades terapéuticas se basaron en su mayoría en la combinación de procedimientos médicos y quirúrgicos. Debido al número de pacientes incluidos en este estudio, solo podemos describir las características clínicas, histopatológicas y etiología de la cromomicosis. Así mismo podemos concluir que no existe un tratamiento de elección, y que la combinación de procedimientos quirúrgicos y médicos siguen siendo la mejor opción en la cromomicosis