Modern outlooks on prevalence of ESR1 and PRG polymorphism in women of reproductive age with endometrial hyperplasia

Prevalence of proliferative processes is very high nowadays. Moreover, such processes easily transform into malignant ones. However, pathogenesis of endometrial hyperplasia (EH) is not fully understood. Imbalance of estrogen and progesterone, as well as estrogen and progesterone receptors is the reason for hyperplastic process onset in hormone-dependent tissues. Currently, there are no markers that could serve as objective predictors for EH development. It is unclear, whether EH transforms into cancer or spontaneously improves. The purpose of the study is to determine prevalence of ESR1 and PRG polymorphism in women of reproductive age with endometrial hyperplasia. Materials and Methods. Trial subjects (n=143) were divided into three groups: Group 1 consisted of 53 patients with glandular and glandular-cystic EH without atypia; Group 2 contained 34 patients with atypical EH; Group 3 was the control group. Polymerase chain reaction of DNA synthesis was used to conduct molecular and genetic loci study. Statistical analysis of the data obtained was performed with SAS JMP 11 and Statistica 10. Results. Mutant CC-allele of PvuII ESR1 polymorphism was found in every fourth woman with glandular endometrial hyperplasia and in every third patient with atypical endometrial hyperplasia. Prevalence of GG genotype of XbaI ESR1 polymorphism did not have any statistically significant differences in comparison with the control group. Mutant TT-allele of Val660Leu PRG polymorphism in glandular endometrial hyperplasia was 1.8 times more common in experimental groups than in the control one. Homozygous AA-genotype of 331G/A PRG polymorphism was not identified in women with endometrial hyperplasia. Conclusion. In endometrial hyperplasia, prevalence of mutant CC-allele of PvuII C/T ESR1 polymorphism leads to a decrease in ERa sensitivity, whereas prevalence of mutant TT-allele of Val660Leu PRG polymorphism leads to impaired sensitivity and a decrease in the biosynthesis rate of progesterone receptors. EH etiology and pathogenesis in women of reproductive age still remains the subject for future scientific research.