| Background and ObjectiveEndometrial carcinoma is one of the top three gynecological cancer threatening the health of women. It accounts for 20%-30% of the gynecological cancers. Recent years the outbreak rate was reported the ascending trend. The etiology is still not clear today. It is urgent to explore the risk factors, etiology and outbreak mechanism of endometrial cancer. Reportedly, risk factors of endometrial cancer(for example: fatness, menarche, the age of menopausal, PCOS, et al.) are involved in estrogen. Most studies have showed the initiating of endometrial cancer is concerned with estrogen stimulating endometrium and lack of progesterone. The synthesis and metabolism of estrogen is a complex process. It needs a lot of enzymes. Given estrogen plays a very important role in the development of endometrial cancer, many studies have showed special interests in the metabolic enzymes involved in its metabolic pathways. Genetic polymorphisms could affect their bioactivities and thus change the susceptibility of cancer. Many studies have showed interests in the association between polymorphisms of gynecologic tumors. The correlation between polymorphisms of CYP1B1 and the susceptibility of endometrial cancer was studied in foreign. However, there is still no report in land. With the development of molecular biology, people have realized carcinoma is a genic disease. There are three special genes (promotion genes, suppressor genes, DNA modifying genes) participating in the initiating and developing of tumors. Endometrial carcinoma is also related to the mutation of tumor suppressor genes and the activation of promotion genes. P53 is a kind of tumor suppressor genes, which is correlated with many kinds of cancers. P53 gene is frequently mutated in malignant tumors. We have investigated the studies of the association between p53 gene polymorphism and susceptibility to malignant tumors. So it is needed to investigate the relationship of p53 gene polymorphism with susceptibility to endometrial carcinoma.For the determination of CYP1B1 and p53 genetic polymorphisms and susceptibility to endometrial cancer, polymerase chain reaction-restriction fragment length polymorphism assay was applied. Therefore, this study is important for further understanding on the initiating, developing, susceptibility measurement and prevention for endometrial cancer.Materials and methodsPolymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay was used to detect the genotypes distribution of CYP1B1 Leu432Val, p53Arg72Pro in 76 cases of endometrial cancer and 83 cases of controls. Statistical analysis was performed using the SPSS10.0 software package. The genotypes distribution in the studies was calculated by means of using Chi-square tests. A probability level of 5% was considered as statistically significant. An odds ratio (OR) and 95% confidence interval were used to evaluate the risk of developing endometrial cancer.Results(1) The allele distribution rates of CYP1B1 gene codon 432 in endometrial cancer patients and controls were 44.7%, 55.3% and 64.5%, 35.5% respectively. There was statistical difference in allele distribution between endometrial cancer patients and controls (P<0.05). The G allele was significantly associated with endometrial cancer with an odds ratio (OR) of 2.24(95% confidence interval 1.43-3.52); (2) The genotypes distribution rates were 19.7%, 50.0%, 30.3% and 39.8%, 49.4%, 10.8% respectively between endometrial cancer patients and controls for CYP1B1 gene codon 432. There was statistical difference in genotypes distribution between endometrial cancer patients and controls (P<0.05). The genotype homozygous G/G and heterozygous C/G were associated with a 5.62-fold and 2.04-fold higher risk compared with C/C genotype;(3) The allele distribution rates of p53 gene codon 72 in endometrial cancer patients and controls were 57.2%, 42.8% and 53.6%, 46.4% respectively. There was no statistical difference in allele distribution between endometrial cancer patients and controls for p53 gene codon 72 (P>0.05);(4) The genotypes distribution rates were 43.4%, 27.6%, 29% and 36.1%, 35.0%, 28.9% respectively between endometrial cancer patients and controls for p53 gene codon 72. There was no statistical difference in genotypes distribution between endometrial cancer patients and controls for p53 gene codon 72 (P>0.05).Conclusions(1) CYP1B1 gene codon 432 polymorphism may play a role in the genetic susceptibility to the development of endometrial cancer. Mutated genotype may be associated with a higher risk of endometrial cancer;(2) P53 gene codon 72 polymorphism may not play a role in genetic susceptibility to the endometrial cancer. |
PDF Full Text Request