Laurdan br In contrast to OPG

In contrast to OPG-rs2073618, the presence of RANKL-rs9533156 heterozygosity with OPG-rs2073617 carrying one or two nonrisk C Laurdan was protective against BC risk in our study.
Table 6 Correlation of Haplotypes With ER/PR Status, Bone Metastasis, and Tumor Size in Breast Cancer Group
Haplotype
Frequency
Total Negative ER/PR Positive ER/PR Adjusted OR
Global
Without Metastasis With Metastasis
Olfat G. Shaker, Mahmoud A. Senousy
SNP-SNP Interactions
Table 7 Protein Interaction With 4 Studied Genes (RANKL, OPG, VDR, and CHI3L1)
Category Protein Interaction With Genes
Genes
Count % P-Value Benjamini
UCSC_TFBS STAT5B
UCSC_TFBS STAT
UCSC_TFBS STAT1
UCSC_TFBS SRY
UCSC_TFBS BACH2
UCSC_TFBS IK3
UCSC_TFBS ROAZ
UCSC_TFBS HAND1E47
UCSC_TFBS RSRFC4
UCSC_TFBS GRE
UCSC_TFBS ER
UCSC_TFBS RP58
UCSC_TFBS TATA
Analysis was performed by David Bioinformatics Resources 6.8, National Institute of Allergy and Infectious Diseases/National Institutes of Health via Gene ID Conversion Tool. List of 4 studied genes was introduced, and protein interaction option by UCSC_TFBS genome browser was chosen.
Notably, the C allele of OPG-rs2073617 was associated with decreased risk of advanced prostate cancer.52 A possible explanation is that rs2073617 SNP is associated with an altered secondary structure, which may cause differences in OPG messenger RNA expression.31 However, the OPG-rs2073617 T/C alleles had no effect on serum OPG in prostate cancer.52 Thus, the mechanism of the protective effect of OPG-rs2073617 should be further investigated.
Reports about the association of CHI3L1 polymorphisms with BC were few. We found significant association between CHI3L1-rs4950928 and BC, where the minor homozygote GG genotype was associated with increased BC risk, whereas the CG heterozygote was protective. In contrast, CHI3L1-rs4950928 was not a significant predisposing factor of BC in a large caseecontrol study.25 Further-more, no association was found for CHI3L1-rs4950928 with glio-blastoma,53 uterine cancer,54 or hepatocellular carcinoma.55 On the other hand, the C allele of CHI3L1-rs4950928 was significantly higher in patients with rectal cancer than those with colon cancer in an Egyptian population.33 These discordant results may be attributable to different tumors, sample sizes, and populations studied.
We observed significant interactions between RANKL-rs9533156 and OPG SNPs with CHI3L1-rs4950928 in relation to BC risk. These interactions are consistent with the link between these genes and diseases characterized by inflammation and tissue
remodeling. High serum YKL-40 level is a nonspecific inflamma-tory marker and was associated with poor prognosis in BC.56,57 Genetic variants of CHI3L1 and RANK/RANKL genes were asso-ciated with inflammatory diseases such as rheumatoid arthritis.58,59 Genetic variants in the OPG locus have been implicated in anky-losing spondylitis.60 RANKL might induce CHI3L1 indirectly e230 - Clinical Breast Cancer February 2019 
through NF-kB signaling.43,44 A cross-talk between OPG and YKL-40 could be through enhancing angiogenesis; both stimulate endothelial cell survival and tube formation by inducing ERK1/2 and Akt phosphorylation.17,61
We demonstrated association of VDR FokI and BsmI poly-morphisms with BC predisposition, with the minor BsmI A (B) allele and AG genotype associated with increased BC risk whereas the minor FokI C (F) allele and the presence of CTþCC genotypes were protective in our studied population. Other genetic variants in VDR, ApaI and TaqI, also conferred high BC susceptibility, particularly in Egyptian women.62 Together, these results support the notion that breast carcinogenesis may be affected by vitamin D/VDR signaling. Previous reports demonstrated inconsistent re-sults about association of FokI and BsmI with BC risk among different populations.22,26-29 This variability among different