Overexpression of p16 Protein in Cervical Cancer in Thailand
نویسندگان
چکیده
The main cause of cervical cancer is a sexually transmitted infection by human papillomaviruses (HPVs) (Munoz and Bosch, 1992; Munoz et al., 1992; IARC, 1995; Walboomer et al., 1999). HPV infection has been detected in almost all preneoplastic and neoplastic lesions of the cervix (Zur Hausen, 1996). HPV contributes to neoplastic progression predominantly through the action of two viral oncoproteins, namely E6 and E7. Oncogenes E6 and E7 of HPV have been suggested to play an important role in the differences in oncogenic potential of each HPV subtype in cervical carcinogenesis (HawleyNelson et al., 1989; Munger et al., 1989). The oncoproteins encoded by the E6 and E7 genes have the ability to bind host cell regulatory proteins, especially tumor suppressor gene products p53 and hypophosphorylated retinoblastoma (Rb) protein (pRb). These changes may
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