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  • br Andreassen CN Alsner J Genetic variants and normal


    [13] Andreassen CN, Alsner J. Genetic variants and normal tissue toxicity after radiotherapy: a systematic review. Radiother Oncol 2009;92:299–309. [14] West CM, Elliott RM, Burnet NG. The genomics revolution and radiotherapy. Clin Oncol 2007;19:470–80. [15] Kerns SL, Ostrer H, Rosenstein BS. Radiogenomics: using CCCP uncoupler to identify cancer patients at risk for development of adverse effects following
    [20] Guerra JL, Gomez D, Wei Q, Liu Z, Wang LE, Yuan X, et al. Association between single nucleotide polymorphisms of the transforming growth factor b1 gene and the risk of severe radiation esophagitis in patients with lung cancer.
    [25] Qiao WB, Zhao YH, Zhao YB, Wang RZ. Clinical and dosimetric factors of radiation-induced esophageal injury: radiation-induced esophageal toxicity. World J Gastroenterol 2005;11:2626–9. [26] Belderbos J, Heemsbergen W, Hoogeman M, Pengel K, Rossi M, Lebesque J. Acute esophageal toxicity in non-small cell lung cancer patients after high dose conformal radiotherapy. Radiother Oncol 2005;75:157–64.
    [27] Singh AK, Lockett MA, Bradley JD. Predictors of radiation-induced esophageal toxicity in patients with non-small-cell lung cancer treated with three-dimensional conformal radiotherapy. Int J Radiat Oncol Biol Phys 2003;55:337–41.
    [28] Ramroth J, Cutter DJ, Darby SC, Higgins GS, McGale P, Partridge M, et al. Dose and fractionation in radiation therapy of curative intent for non-small cell lung cancer: meta-analysis of randomized trials. Int J Radiat Oncol Biol Phys 2016;96:736–47. [29] Zhao L, Sheldon K, Chen M, Yin MS, Hayman JA, Kalemkerian GP, et al. The predictive role of plasma TGF-beta1 during radiation therapy for radiation-induced lung toxicity deserves further study in patients with non-small cell lung cancer. Lung Cancer 2008;59:232–9.
    [30] Yu HM, Liu YF, Cheng YF, Hu LK, Hou M. Effects of rhubarb extract on radiation induced lung toxicity via decreasing transforming growth factor-beta-1 and interleukin-6 in lung cancer patients treated with radiotherapy. Lung Cancer 2008;59:219–26.
    [35] De Jaeger K, Seppenwoolde Y, Kampinga HH, Boersma LJ, Belderbos JS, Lebesque JV. Significance of plasma transforming growth factor-beta levels in radiotherapy for non-small-cell lung cancer. Int J Radiat Oncol Biol Phys 2004;58:1378–87.
    [37] Mosser DD, Morimoto RI. Molecular chaperones and the stress of oncogenesis. Oncogene 2004;23:2907–18. [38] Hacker S, Lambers C, Hoetzenecker K, Pollreisz A, Aigner C, Lichtenauer M, et al. Elevated HSP27, HSP70 and HSP90a in chronic obstructive pulmonary disease: markers for immune activation and tissue destruction. Clin Lab 2009;55:31–40.
    Original Study
    Association of SNP-SNP Interactions Between RANKL, OPG, CHI3L1, and VDR Genes With Breast Cancer Risk in Egyptian Women
    Olfat G. Shaker,1 Mahmoud A. Senousy2
    Genetic susceptibility for breast cancer (BC) is still poorly understood. We investigated the association of single nucleotide polymorphism (SNP)-SNP interactions of 6 SNPs in RANKL, OPG, CHI3L1, and VDR genes
    with BC risk in 115 BC patients and 120 controls using logistic regression models. A stronger combined effect of SNPs via geneegene interaction may predict BC risk. Our data have implications in genetic counseling, BC screening, and prognosis.
    Background: Genetic susceptibility for breast cancer (BC) is still poorly understood. A combination of multiple low-penetrant alleles of cancer-related genes and geneegene interactions (epistasis) contributes to BC risk. Genetic
    variants in receptor activator of nuclear factor kB ligand (RANKL), osteoprotegerin (OPG), chitinase-3elike protein 1 (CHI3L1), and vitamin D receptor (VDR) genes are implicated in breast carcinogenesis; however, the influence of their
    epistatic effects on BC susceptibility has not yet been studied. We investigated the association of single nucleotide polymorphism (SNP)-SNP interactions and haplotypes of 6 SNPs in these 4 genes with the genetic predisposition of BC in Egyptian women. Patients and Methods: Data of 115 BC patients and 120 cancer-free controls were studied. Association tests were conducted using logistic regression models. Results: Individual SNPs showed weak statistical significance with BC susceptibility. The interactions between RANKL-rs9533156 and OPG-rs2073618; OPG-rs2073618 with CHI3L1-rs4950928, VDR-rs2228570 and VDR-rs1544410; OPG-rs2073617 and VDR-rs1544410; VDR-rs2228570 and VDR-rs1544410 were strongly associated with increased BC risk after adjustment for multiple comparisons. No SNPs were in strong linkage disequilibrium. The TCTCTG-rs9533156-rs2073618-rs2073617-rs4950928-rs2228570-rs1544410 haplotype was significantly associated with increased BC risk (adjusted odds ratio ¼ 8.33; 95% confidence interval, 1.32-52.46; P ¼ .025) compared with controls. TCCCTG haplotype stratified BC patients according to estrogen receptor/progesterone receptor status. TCTCTA was positively associated, and TCTCTG and TGTCTG haplotypes inversely correlated with bone metastasis. Bioinformatic analysis revealed 13 proteins commonly interacting with our 4 genes; the most significant was signal transducer and activator