The association of the programmed cell death-1 PD1.5 C>T polymorphism with cervical cancer risk has not been investigated. In this hospital-based case-control study, we analyzed 256 patients with cervical cancer and 250 healthy controls. Pearson chi-square test was used to examine differences in the distribution of genotypes between cases and controls. Association between the polymorphism and the susceptibility to cervical cancer was evaluated using unconditional logistic regression analysis.
In this study, the ErbB3-binding protein (Ebp1) and p53 protein expression in cervical cancer tissues, and its significance in the prognosis of the disease was investigated. Ebp1 and p53 protein expression was detected by immunohistochemical analysis in cervical cancer tissues (N = 60) and normal tissues adjacent to the cancer tissues (N = 60). The rates of positive Ebp1 and p53 protein expression were 35.0 and 60.0%, respectively. Ebp1 and p53 were overexpressed in cervical cancer tissues, compared to normal tissues (P 0.05).
We selected six tagged single nucleotide polymorphisms (SNPs) in the interleukin 17A (IL-17A) and IL-17F genes, and evaluated the relationship between the six common SNPs and environmental factors in cervical cancer patients. Polymerase chain reaction-restriction fragment length polymorphism was used to detect the IL-17A (rs2275913, rs3748067, and rs3819025) and IL-17F (rs763780, rs9382084, and rs1266828) SNPs. The associations between IL-17A and IL-17F gene polymorphisms and risk of cervical cancer were estimated by conditional logistic regression.
Cervical cancer is associated with abnormal expression of multiple genes. Survivin and Bcl-2 proteins are apoptosis inhibitors. The tumor suppressor gene CD82, which encodes the protein KAI1, is downregulated in cervical cancer, and is associated with differentiation degree. We investigated the expression levels of three proteins and their correlation with metastasis in cervical cancer by comparing them in different cervical lesions.
Development of chemoresistance is a major obstacle that leads to the recurrence and progression of cervical cancer (CC). Autophagy, meaning, “eating of self”, has shown paradoxical functions in tumors. In this study, we first investigated the process of autophagy induction by cisplatin in CC cells. Next, we investigated the role of autophagy in cisplatin-sensitivity of CC cells via blockage of cisplatin-induced autophagy.
In Uyghur women, mortality rates from cervical cancer are amongst the highest in the nation, and genetic susceptibility probably plays a role in the pathogenesis of the disease. We investigated the correlation between polymorphisms of the HLA-DQB1 allele and cervical cancer in Xinjiang Uyghur women. Cervix tissue samples from 80 cases of cervical cancer and 80 cases of cervicitis were genotyped using polymerase chain reaction-sequence-based typing (PCR-SBT) for HLA-DQB1. Two hundred and ninety-six alleles were identified among the 160 cases.
Previous studies have reported that miR-196a is upregulated in cervical cancer tissues and cell lines. However, whether serum miR-196a is increased in patients with cervical cancer or cervical intraepithelial neoplasia (CIN), and its potential clinical value remained unknown. In total, 105 cervical cancer patients, 86 CIN patients, and 50 healthy volunteers were recruited. Quantitative reverse transcription-polymerase chain reaction was performed to compare the serum levels miR-196a in all participants.
The aim of this case-control study was to obtain a comprehensive panel of genetic polymorphisms present only in genes (cytochrome P-450 1A1 - CYP1A1 and catechol-O-methyl transferase - COMT) within the metabolic pathway of sex steroids and determine their possible associations with the presence or absence of cervical cancer.