312P - Molecular and genetic features of squamous cell carcinoma of vulvar cancer depending on HPV status

Background

new prognostic variables can lead to further individualization of vulvar cancer treatment; research in the search for new biomarkers is an urgent area of modern oncology.

Methods

We examined the materials of 76 operations (110 paraffin blocks) for which neoadjuvant treatments were not performed. Mutation tags were evaluated for all tumor samples. When the tumor sample had at least 40% compliance with the mutation process, including overexpression of ARES, hypofunction of the BRCA tumor suppressor and in the presence of a defect of repair compliance, the mutation label was considered positive. An immunohistochemical study was performed with the determination of ligand 1 of programmed cell death (PD-L1) mandatory with CGP, for the selection of patients for immunotherapy. PD-L1 protein expression was determined on 5–micron tissue slices using a DakoPD-L1 IHC22C3 pharmDx analyzer (Agilent, Santa Clara, California) or Ventana (Oro Valley, Arizona) in accordance with the instructions of each manufacturer. Ventana PD-L1 expression is expressed as a percentage of the tumor area positively stained by tumor and immune cells, and DakoPD-L1 as an indicator of the tumor fraction.

Results

We also conducted a correlation study of the relationship between human papillomavirus and the genetic profile of vulvar cancer. Staining of ligand 1 of apoptosis (PD-L1) of squamous cell carcinoma of the vulva, with a negative result for human papillomavirus, showed a higher incidence of this ligand, whereas with positive HPV, the occurrence of PD-L1 was significantly lower. With a positive test for human papillomavirus, mutations in the PI3K/mTOR pathway increased, on the contrary, with a negative test, GA was more often determined in TP53, TERTp, CDKN2A, CCND1, FAT1, NOTCH1, EGFR. PD-L1 receptor expression is more often observed in HPV-negative RV patients compared to HPV-positive ones (7.8 vs. 3.7 p=0.03), while HPV-positive patients were more likely to have STK11 mutation. At the same time, the PIK3CAE545 mutation occurred with the same frequency between the two groups of RV patients.

Conclusions

Thus, this study showed that the presence or absence of human papillomavirus dramatically affects tumor differentiation.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

Hospital Yangi Hayot.

Funding

RSPMCOR Republic of Uzbekistan, MSIC named after P.A. Herzen - the branch of the National Medical Research Center for Radiology of the Ministry of Health of Russia (Moscow, Russian Federation), as well as the Istinye University Clinic (Istanbul, Turkey.

Disclosure

The author has declared no conflicts of interest.