Article Text
Abstract
Introduction/Background In the presence of high risk HPV, E7 oncogene causes the overexpression of p16 and Ki-67 is an indicator for cell proliferation. This study aims to evaluate HPV positive women in aspect of p16 and Ki-67 presence in tissues.
Methodology This is a retrospective review of 287 patients who tested positive for HPV DNA.
Results Colposcopic biopsies revealed normal histopathological findings in 28 patients (9.8%), cervicitis in 48 patients (16.7%), cervical intraepithelial lesion (CIN) 1 in 178 patients (62.0%), CIN2 in 26 patients (9.1%), CIN3 in four patients (1.4%) and carsinoma in situ (CIS) in three patients (1.0%). Cervical tissue positivity for p16 was 2.6% in patients with benign histopathological findings, 16.3% in patients with CIN1, 92.3% in patients with CIN2, 100% in patients with CIN3 and 100% in patients with CIS. Cervical tissue positivity for Ki-67 was 42.1% in patients with benign histopathological findings, 77.5% in patients with CIN1, 96.1% in patients with CIN2, 100% in patients with CIN3 and 100% in patients with CIS. The sensitivity and specificity of p16 positivity for CIN1, CIN2, CIN3 and CIS were 25.1% (95% CI: 19.4%–31.5%) and 97.4% (95% CI: 90.8%–99.7%) respectively. When p16 positivity was combined with Ki-67 positivity, the sensitivity decreased to 20.4% (95% CI: 15.2%–26.5%) and the specificity was 97.4% (95% CI: 90.8%–99.7%). The sensitivity and specificity of p16 positivity for CIN2, CIN3 and CIS were 93.9% (95% CI: 79.8%–99.3%) and 90.6% (95% CI: 86.3%–93.9%) respectively. When p16 positivity was combined with Ki-67 positivity, the sensitivity decreased to 90.9% (95% CI: 75.7%–98.1%) and the specificity increased to 94.1% (95% CI: 90.5%–96.7%).
Conclusion The presence of p16 and Ki-67 in cervical tissues has a significant role in the detection of precancerous lesions and may help to predict the progression of precancerous lesions into malignancy.
Disclosure Nothing to disclose.