Background: Polychemotherapy in ovarian cancer (OC) is the second major component of treatment.
However, treatment with cytostatics is stopped in 25% of cases because of significant side effects. It is shown
that concentration of certain cytokines and their balance is largely formed in accordance with a genetic
Objective: The objective of the study was to evaluate the cytokine status of blood serum of patients with ovarian
cancer with different tumor response to neoadjuvant chemotherapy (NACT).
Method: Patients received 2 courses NACT according to the scheme AP. The levels of IL-1β and IL-1Ra, IL-10,
TNF-α in blood serum were determined by solid phase ELISA. For molecular genetic studies we selected
polymorphic variants in the promoters of the gene represented in dbS`NP NCBI and SNP500 Cancer databases.
Results: The sharply declined in patients with ovarian cancer compared with the normal, level of IL-1β correlates
with increased levels of IL-1RA. It is found that 75% of patients who had progression of the disease after NACT
bear CT genotype of gene IL-1β associated with a low expression of the cytokine, while the TT genotype,
providing a high level of the expression of IL-1β gene had met only 25% among patients in this group. At the
same time 70% of patients with a complete response are the carriers of the T allele, while a complete response
was associated with a higher level of IL-1β than in the progression group.
Low secretion of TNF-α in all types of tumor response when testing TNF-α G-308A gene polymorphisms was
associated with carriage of GA and AA genotypes, which are associated with low production of this cytokine.
Increased compared to the control IL-10 production in patients with ovarian cancer associated with genotype
replacement at position 1082 G/A IL-10 gene, which occured in 10% of patients with a complete response and
25% of patients with tumor progression after NACT.
Conclusion: All the studied polymorphisms of IL-1β, IL-10 and TNF-α genes in patients with OC are associated
with the level of these cytokines and tumor NACT response.