RESUMO
BACKGROUND: p53 is a key regulator of the cellular stress response. p53 modulates the transcription of several genes. OBJECTIVES: To examine the influence of p53 on expression of heat shock protein 72 (HSP72). METHODS: Two model systems were used. (i) HSP72 expression was studied by Western blot on extracts from p53-proficient or p53-deficient primary mouse keratinocytes, and (ii) archival human anogenital skin from fibroepithelial polyps, human papillomavirus (HPV) 16/18-associated lesions or squamous cell carcinomas (SCCs) was subjected to immunostaining for HSP72. RESULTS: Basal HSP72 expression was higher in keratinocytes from p53-deficient than from p53-proficient mice. Immunostaining for HSP72 was higher in HPV 16/18 lesions and SCCs, which have reduced p53 protein. CONCLUSIONS: p53 status may influence the basal level of HSP72.
Assuntos
Genes p53/fisiologia , Proteínas de Choque Térmico/metabolismo , Queratinócitos/metabolismo , Animais , Western Blotting , Carcinoma de Células Escamosas/metabolismo , Técnicas de Cultura de Células , Proteínas de Choque Térmico HSP72 , Melanoma/metabolismo , Camundongos , Proteínas de Neoplasias/metabolismo , Papillomaviridae , Infecções por Papillomavirus/metabolismo , Neoplasias Cutâneas/metabolismo , Infecções Tumorais por Vírus/metabolismoRESUMO
Vasculitis is an uncommon paraneoplastic syndrome, and acute renal failure is an unusual presentation of leukemia. We report a case of B-cell chronic lymphocytic leukemia that presented with acute renal failure caused by biopsy-proven lymphocytic vasculitis that subsequently was shown to be T-cell-mediated and systemic at autopsy.
