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    In: Journal of Clinical Laboratory Analysis, Wiley, Vol. 32, No. 9 ( 2018-11)
    Abstract: Interleukin‐18‐137G/C, ‐607G/T polymorphisms play multiple roles in various cancers. However, studies focused on its involvement in breast cancer remain controversial, and no study has taken the interaction between interleukin‐18 (IL‐18) gene polymorphism and body mass index (BMI), menopause into consideration. The study investigated the association between IL‐18‐137, ‐607 polymorphisms and risk of breast cancer and a possible interaction between the 2 single nucleotide polymorphisms (SNPs) and BMI, menopause in Chinese Han woman. Methods A total of 488 participants, including 178 patients with breast cancer, 150 patients with benign breast disease and 160 healthy controls were recruited for this study. Polymerase chain reaction (PCR)‐direct sequencing technology was used to identify the genotypes. Results 137 G/C genotype can decrease the risk of breast cancer (OR = 0.54, 95% CI: 0.31‐0.93; P  =   .025). In benign group, subjects with G/C genotype of IL‐18‐137G/C polymorphism had a 1.89‐fold increased risk of developing breast cancer (95% CI = 1.05‐3.41; P  =   .032). Among postmenopausal subjects, people with G/T genotype of IL‐18‐607 polymorphism had a 7.97‐fold increased risk of lymph node metastasis compared with those with T/T homozygotes (95% CI = 1.95‐32.65; P  =   .0045). Among Overweight and obese patients with breast cancer (BMI ≥ 24), people with G/T genotype of IL‐18‐607 polymorphism had a 5.45‐fold increased risk of lymph node metastasis compared with those with T/T homozygotes (95% CI = 1.74‐17.06; P  =   .034). Conclusions IL‐18‐137 G/C genotype may be a protective factor for healthy group, but a risk factor for benign group. IL‐18‐607 G/T genotype have an interaction with menopausal and BMI. The synergetic effect can further increase the risk of lymph node metastasis for breast cancer patients.
    Type of Medium: Online Resource
    ISSN: 0887-8013 , 1098-2825
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2001635-9
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