[1] Jemal A, Murray T, Samuels A, et al. Cancer statistics. 2003. CA Cancer J Clin, 2003; 53, 5-26. doi:  10.3322/canjclin.53.1.5
[2] The National Cancer Institute website. http://seer.cancer.gov/statfacts/html/prost.html[2015-10].
[3] Lamont KR, Tindall DJ. Minireview:Alternative activation pathways for the androgen receptor in prostate cancer. Mol Endocrinol, 2011; 25, 897-907. doi:  10.1210/me.2010-0469
[4] Safety Assessment of Di(2-ethylhexyl) phthalate (DEHP)Released from PVC Medical Devices. http://www.fda.gov/downloads/MedicalDevices/DeviceRegulationandGuidance/GuidanceDocuments/UCM080457.pdf [2015-10].
[5] Lottrup G, Andersson AM, Leffers H, et al. Possible impact of phthalates on infant reproductive health. Int J Androl, 2006; 29, 172-80; discussion 81-5. doi:  10.1111/ija.2006.29.issue-1
[6] Zhao Y, Ao H, Chen L, et al. Mono-(2-ethylhexyl) phthalate affects the steroidogenesis in rat Leydig cells through provoking ROS perturbation. Toxicol In Vitro, 2012; 26, 950-5. doi:  10.1016/j.tiv.2012.04.003
[7] Ming-Yue MA, Zhang YM, Guo L, et al. Effects of DEHP and MEHP on apoptosis of leydig cells of mice. Industrial Health & Occupational Diseases, 2012; 339-41. (In Chinese) http://en.cnki.com.cn/Article_en/CJFDTOTAL-GYWZ201206007.htm
[8] Erkekoglu P, Rachidi W, Yuzugullu OG, et al. Induction of ROS, p53, p21 in DEHP-and MEHP-exposed LNCaP cells-protection by selenium compounds. Food Chem Toxicol, 2011; 49, 1565-71. doi:  10.1016/j.fct.2011.04.001
[9] Yao PL, Lin YC, Richburg JH. Mono-(2-ethylhexyl) phthalate (MEHP) promotes invasion and migration of human testicular embryonal carcinoma cells. Biol Reprod, 2012; 86, 160, 1-10. https://tools.niehs.nih.gov/portfolio/index.cfm/portfolio/publicationDetail/id/1885827
[10] Zhang HY, Zhang W, Bao TY, et al. Relationship between environmental endocrine disruptor DEHP and prostatic hyperplasia in rats. Journal of Modern Urology, 2009; 347-9. (In Chinese) http://med.wanfangdata.com.cn/Paper/Detail?id=PeriodicalPaper_xdmnwkzz200905008
[11] Yong W, Jiao C, Jianhui W, et al. Mono-2-ethyhexyl phthalate advancing the progression of prostate cancer through activating the hedgehog pathway in LNCaP cells. Toxicol In Vitro, 2016; 32, 86-91. doi:  10.1016/j.tiv.2015.12.012
[12] Jaenisch R, Bird A. Epigenetic regulation of gene expression:how the genome integrates intrinsic and environmental signals. Nat Genet, 2003; 33, 245-54. doi:  10.1038/ng1089
[13] Ehrlich M. DNA hypomethylation in cancer cells. Epigenomics, 2009; 1, 239-59. doi:  10.2217/epi.09.33
[14] Jones PA, Baylin SB. The epigenomics of cancer. Cell, 2007; 128, 683-92. doi:  10.1016/j.cell.2007.01.029
[15] Du P, Ye HR, Gao J, et al. Methylation of PTCH1a gene in a subset of gastric cancers. World J Gastroenterol, 2009; 15, 3799-806. doi:  10.3748/wjg.15.3799
[16] Hinoue T, Weisenberger DJ, Pan F, et al. Analysis of the association between CIMP and BRAF in colorectal cancer by DNA methylation profiling. PLoS One, 2009; 4, e8357. doi:  10.1371/journal.pone.0008357
[17] Wolf I, Bose S, Desmond JC, et al. Unmasking of epigenetically silenced genes reveals DNA promoter methylation and reduced expression of PTCH in breast cancer. Breast Cancer Res Treat, 2007; 105, 139-55. doi:  10.1007/s10549-006-9440-4
[18] Lof-Ohlin ZM, Levanat S, Sabol M, et al. Promoter methylation in the PTCH gene in cervical epithelial cancer and ovarian cancer tissue as studied by eight novel Pyrosequencing(R) assays. Int J Oncol, 2011; 38, 685-92. https://core.ac.uk/download/pdf/33995555.pdf
[19] Zhu Y, James RM, Peter A, et al. Functional Smoothened is required for expression of GLI3 in colorectal carcinoma cells. Cancer Lett, 2004; 207, 205-14. doi:  10.1016/j.canlet.2003.10.025
[20] Rodriguez J, Frigola J, Vendrell E, et al. Chromosomal instability correlates with genome-wide DNA demethylation in human primary colorectal cancers. Cancer Res, 2006; 66, 8462-9468. doi:  10.1158/0008-5472.CAN-06-0293
[21] Wilson AS, Power BE, Molloy PL. DNA hypomethylation and human diseases. Biochim Biophys Acta, 2007; 1775, 138-62. https://www.ncbi.nlm.nih.gov/pubmed/17045745
[22] Cravo M, Pinto R, Fidalgo P, et al. Global DNA hypomethylation occurs in the early stages of intestinal type gastric carcinoma. Gut, 1996; 39, 434-8. doi:  10.1136/gut.39.3.434
[23] Soares J, Pinto AE, Cunha CV, et al. Global DNA hypomethylation in breast carcinoma:correlation with prognostic factors and tumor progression. Cancer, 1999; 85, 112-8. doi:  10.1002/(ISSN)1097-0142
[24] Kim KY, Kim DS, Lee SK, et al. Association of low-dose exposure to persistent organic pollutants with global DNA hypomethylation in healthy Koreans. Environ Health Perspect, 2010; 118, 370-4. https://experts.umn.edu/en/publications/association-of-low-dose-exposure-to-persistent-organic-pollutants
[25] Rusiecki JA, Baccarelli A, Bollati V, et al. Global DNA hypomethylation is associated with high serum-persistent organic pollutants in Greenlandic Inuit. Environ Health Perspect, 2008; 116, 1547-52. doi:  10.1289/ehp.11338
[26] Yang H, Liu Y, Bai F, et al. Tumor development is associated with decrease of TET gene expression and 5-methylcytosine hydroxylation. Oncogene, 2013; 32, 663-9. doi:  10.1038/onc.2012.67
[27] Yegnasubramanian S, Haffner MC, Zhang Y, et al. DNA hypomethylation arises later in prostate cancer progression than CpG island hypermethylation and contributes to metastatic tumor heterogeneity. Cancer Res, 2008; 68, 8954-67. doi:  10.1158/0008-5472.CAN-07-6088
[28] Brothman AR, Swanson G, Maxwell TM, et al. Global hypomethylation is common in prostate cancer cells:a quantitative predictor for clinical outcome? Cancer Genet Cytogenet, 2005; 156, 31-6. doi:  10.1016/j.cancergencyto.2004.04.004
[29] Bedford MT, van Helden PD. Hypomethylation of DNA in pathological conditions of the human prostate. Cancer Res, 1987; 47, 5274-6. https://www.ncbi.nlm.nih.gov/pubmed/2443238
[30] Nestor CE, Ottaviano R, Reddington J, et al. Tissue type is a major modifier of the 5-hydroxymethylcytosine content of human genes. Genome Res, 2012; 22, 467-77. doi:  10.1101/gr.126417.111
[31] Li W, Liu M. Distribution of 5-hydroxymethylcytosine in different human tissues. J Nucleic Acids, 2011; 2011, 870726. http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.349.7087
[32] Haffner MC, Chaux A, Meeker AK, et al. Global 5-hydroxymethylcytosine content is significantly reduced in tissue stem/progenitor cell compartments and in human cancers. Oncotarget, 2011; 2, 627-37. doi:  10.18632/oncotarget.v2i8
[33] Rusyn I, Kadiiska MB, Dikalova A, et al. Phthalates rapidly increase production of reactive oxygen species in vivo:role of Kupffer cells. Mol Pharmacol, 2001; 59, 744-50. https://hero.epa.gov/hero/index.cfm/reference/details/reference_id/630937
[34] Valinluck V, Tsai HH, Rogstad DK, et al. Oxidative damage to methyl-CpG sequences inhibits the binding of the methyl-CpG binding domain (MBD) of methyl-CpG binding protein 2 (MeCP2). Nucleic Acids Res, 2004; 32, 4100-8. doi:  10.1093/nar/gkh739
[35] Mimeault M, Moore E, Moniaux N, et al. Cytotoxic effects induced by a combination of cyclopamine and gefitinib, the selective hedgehog and epidermal growth factor receptor signaling inhibitors, in prostate cancer cells. Int J Cancer, 2006; 118, 1022-31. doi:  10.1002/ijc.21440
[36] Narita S, So A, Ettinger S, et al. GLI2 knockdown using an antisense oligonucleotide induces apoptosis and chemosensitizes cells to paclitaxel in androgen-independent prostate cancer. Clin Cancer Res, 2008; 14, 5769-77. doi:  10.1158/1078-0432.CCR-07-4282