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The expression of ΔNp63 and ΔNp73 as early markers in cervical carcinoma

C71 Abstract Cervical cancer (CXCA) is a major cause of cancer death among women worldwide. It is well established that viral oncoprotein E6 and E7 from high risk HPV is a necessary cause of cervical cancer development by interfering apoptosis and cell cycle via p53 and pRb inactivation. Both p63 and p73 share significant homology in structure and function to p53; however, p63 and p73 can encode truncated N-terminal isoforms (ΔNp63 and ΔNp73) which can inhibit transactivating function of full length isoforms (TAp63 and TAp73). In this study, we attempt to investigate the correlation between overexpression of ΔNp63 and ΔNp73 in cervical dysplasia (n=98) and invasive cervical cancer (n=98) compared to normal cervix (n=54), using immunohisochemistry (IHC) technique. Our data demonstrated significant association between the expression of ΔNp63 and ΔNp73 in both cervical dysplasia ( P P 2 ) test. Additionally, the expression of ΔNp63 and ΔNp73 was further analyzed between low grade squamous intra-epithelials lesion (LSIL) and high grade squamous intra-epithelials lesion (HSIL) compared to normal cervix. Association was significantly found between LSIL and normal cervix ( P