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DIAGNOSTIC AND PROGNOSTIC VALUE OF P16INK4A IN PATIENTS WITH CERVICAL INTRAEPITHELIAL NEOPLASIA AND EARLY CERVICAL CANCER

Keywords:

L.I. Korolenkova


Persistent HPV-infection is the main etiological factor of cervical intraepithelial neoplasia (CIN) and cervical cancer. Considering HPV-infection to be very widespread (30–40 % of female population), its outcome to CIN I and later to CIN II–III and cervical cancer is relatively rare. Regression and stabilization of the process are also possible. There is a need for additional studies allowing stratification of women with HPV-infection and CIN regarding risk of progression to CIN III/carcinoma in citu (CIS) and invasive cancer. The major difficulty represents the groups of pa-tients with cytology results ASCUS and LSIL, as well as histologicaly verified CIN II, as they consist of women with both productive and transforming infection. One of the possible approaches is the use of markers of transforming infection, primarily p16INK4a. p16INK4a – cyclin-dependent kinase inhibitor — may be seen as the marker of conversion of productive HPV-infection to transforming stage that clinically corresponds to progression of low-grade neoplasias (CIN I) to high-grade (CIN II-III). This confirms the significant elevation of p16 expression gain in CIN II tissue samples. P16INK4a seems to be especially important in CIN II pa-tients, because not all CIN II potentially progress to CIN III showing the certain rate of spontaneous regression. P16INK4a may be useful for triage of HPV-infected women revealed by cytological and virological screening stages. P16INK4a immunocytochemical staining may serve as a valuable tool in case of viral load persistence after conservative treatment modalities as it helps to differentiate persisting HPV-infection without CIN and CIN progression or recurrence. Taking into account the follow-up longevity of patients treated for high-grade CIN (up to 30 years) P16INK4a may play its role in defining individual outcome and algorithm of follow-up.
References:
May 29, 2020

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