RESUMO
The infection by the human papillomavirus (HPV) is the origin of several cancers around the world. In some areas of Brazil, cervical carcinoma is still the cancer with the highest incidence among women. After epithelial cell transformation by HPV, several molecular events are observed, resulting in the malignant phenotype. In this review we discuss potential molecular targets for therapeutic interventions in human HPV-related carcinomas, with emphasis on cervical cancer, based on the alterations observed in the signaling transduction pathways caused by HPV infection. With a special attention to tyrosine kinase receptors, and other kinases involved in signal transduction and angiogenesis, these pathological alterations are evaluated as novel targets for anticancer therapies in HPV-related carcinomas.