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• W1968640856 abstract "The scientific community now recognizes that exposure to certain environmental chemicals can adversely affect the developing organism, and subsequently result in a lifetime risk of chronic disease (the developmental basis of adult health and disease). Prenatal exposure to diethylstilbestrol (DES) was the first documented example where exposure of the fetus resulted in long-term changes in the offspring that were not apparent until much later in life, usually after the onset of puberty. Diethylstilbestrol was prescribed for pregnant women from the late 1940s to 1970s, with the mistaken belief that it would prevent miscarriage. World-wide estimates suggest that 2 to 8 million pregnancies may have been treated with DES. Today, we know DES as a “transplacental carcinogen,” because it crossed the mother's placenta and caused reproductive cancer in her offspring. Although the prevalence of neoplasia is estimated to be very low in the DES-exposed population (0.1%), numerous other abnormalities including subfertility/infertility have a high prevalence (>90%) and occur in both sons and daughters. Together, these reproductive tract abnormalities comprise “the DES syndrome” (1Newbold R. Lessons learned from perinatal exposure to diethylstilbestrol (DES).Toxicol Appl Pharmacol. 2004; 199: 142-150Crossref PubMed Scopus (236) Google Scholar). For over 3 decades, research from our lab and others using experimental animals have replicated the changes observed in DES-exposed humans. In some cases, experimental animals have predicted changes later found in DES-exposed humans such as oviductal malformations (2Newbold R.R. Tyrey S. Haney A.F. McLachlan J.A. Developmentally arrested oviduct: a structural and functional defect in mice following prenatal exposure to diethylstilbestrol.Teratology. 1983; 27: 417-426Crossref PubMed Scopus (51) Google Scholar), and increased incidence of uterine fibroids (3Baird D.D. Newbold R. Prenatal diethylstilbestrol (DES) exposure is associated with uterine leiomyoma development.Reprod Toxicol. 2005; 20: 81-84Crossref PubMed Scopus (81) Google Scholar, 4Cook J.D. Davis B. Cai S.I. Barrett J.C. Conti C.J. Walker C.L. Interaction between genetic susceptibility and early-life environmental exposure determines tumor-suppressor-gene penetrance.Proc Natl Acad Sci USA. 2005; 102: 8644-8649Crossref PubMed Scopus (85) Google Scholar, 5McLachlan J.A. Newbold R.R. Bullock B.C. Long-term effects on the female mouse genital tract associated with prenatal exposure to diethylstilbestrol.Cancer Res. 1980; 40: 3988-3999PubMed Google Scholar). Molecular studies have shown that many of the DES-associated structural and cellular abnormalities are caused by altered programming of genes such as Hox and Wnt, which play important roles in reproductive tract differentiation (6Miller C. Degenhardt K. Sassoon D.A. Fetal exposure to DES results in de-regulation of Wnt7a during uterine morphogenesis.Nat Genet. 1998; 20: 228-230Crossref PubMed Scopus (126) Google Scholar, 7Pavlova A. Boutin E. Cunha G. Sassoon D. Msx1 (Hox-7.1) in the adult mouse uterus: cellular interactions underlying regulation of expression.Development. 1994; 120: 335-345PubMed Google Scholar, 8Taylor H.S. Vanden Heuvel G.B. Igarashi P. A conserved Hox axis in the mouse and human female reproductive system: late establishment and persistent adult expression of the Hoxa cluster genes.Biol Reprod. 1997; 57: 1338-1345Crossref PubMed Scopus (347) Google Scholar). Through the years, not only have we gained insights into the mechanisms involved in DES-associated abnormalities, but we have also learned that many problems incurred by DES-exposed men and women may be examples of developmental (prenatal/neonatal/early childhood) exposure to other environmental chemicals with endocrine-disrupting activity. Environmental “hormone mimics,” whether synthetic or naturally occurring, can disrupt developing organ systems and, like DES, cause abnormalities that may not be apparent until much later in life (9Colborn T. Dumanoski D. Myers J.P. Our stolen future. Penguin Books USA, New York1996Google Scholar). In fact, developmental exposure to endocrine-disrupting chemicals has been proposed to be linked to endometriosis, fibroids, and breast cancer in women, poor sperm quality and increased incidence of cryptorchism in men, and subfertility/infertility in men and women. It is interesting to note that abnormalities characterizing the DES syndrome are similar to those described following exposure to other endocrine-disrupting chemicals (1Newbold R. Lessons learned from perinatal exposure to diethylstilbestrol (DES).Toxicol Appl Pharmacol. 2004; 199: 142-150Crossref PubMed Scopus (236) Google Scholar). Prenatal DES exposure is a continuing story, with indications that vaginal cancer continues to be found in daughters as they age. Further, second-generation effects are surfacing with reports of increased menstrual irregularities (10Titus-Ernstoff L. Troisi R. Hatch E.E. Wise L.A. Palmer J. Hyer M. et al.Menstrual and reproductive characteristics of women whose mothers were exposed in utero to diethylstilbestrol (DES).Int J Epidemiol. 2006; 35: 862-868Crossref PubMed Scopus (73) Google Scholar) and ovarian cancer (11Blatt J. Van Le L. Weiner T. Sailer S. Ovarian carcinoma in an adolescent with transgenerational exposure to diethylstilbestrol.J Pediatr Hematol Oncol. 2003; 25: 635-636Crossref PubMed Scopus (71) Google Scholar) in DES granddaughters, and increased hypospadias in DES grandsons (12Brouwers M.M. Feitz W.F. Roelofs L.A. Kiemeney L.A. de Gier R.P. Roeleveld N. Hypospadias: a transgenerational effect of diethylstilbestrol?.Hum Reprod. 2006; 21: 666-669Crossref PubMed Scopus (116) Google Scholar, 13Klip H. Verloop J. van Gool J.D. Koster M.E. Burger C.W. van Leeuwen F.E. Hypospadias in sons of women exposed to diethylstilbestrol in utero: a cohort study.Lancet. 2002; 359: 1102-1107Abstract Full Text Full Text PDF PubMed Scopus (243) Google Scholar). These transgenerational findings are consistent with changes previously reported in DES-exposed mice (14Newbold R.R. Hanson R.B. Jefferson W.N. Bullock B.C. Haseman J. McLachlan J.A. Increased tumors but uncompromised fertility in the female descendants of mice exposed developmentally to diethylstilbestrol.Carcinogenesis. 1998; 19: 1655-1663Crossref PubMed Scopus (172) Google Scholar, 15Newbold R.R. Hanson R.B. Jefferson W.N. Bullock B.C. Haseman J. McLachlan J.A. Proliferative lesions and reproductive tract tumors in male descendants of mice exposed developmentally to diethylstilbestrol.Carcinogenesis. 2000; 21: 1355-1363Crossref PubMed Google Scholar). This has important implications because it suggests that maternal exposure to an endocrine-disrupting substance like DES, can directly alter the reproductive tract of the person exposed as a fetus, and also the affect the health of another generation. Although we do not fully understand the mechanisms involved in the transmission of disease from one generation to another, it likely involves persistent epigenetic changes in some genes such that the fate of tissues or organs are altered. This is an important area of new investigation and critical research direction." @default.
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• W1968640856 title "Prenatal exposure to diethylstilbestrol (DES)" @default.
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• W1968640856 doi "https://doi.org/10.1016/j.fertnstert.2008.01.062" @default.
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