Elsevier

Human Pathology

Volume 26, Issue 12, December 1995, Pages 1291-1292
Human Pathology

Editorial
Hypothesis: The prenatal origins of prostate cancer

https://doi.org/10.1016/0046-8177(95)90291-0Get rights and content

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    According to epidemiological evidence, individuals exposed to famine during early life are at a high risk of developing cardiovascular disease, obesity and type 2 diabetes, schizophrenia, infertility, and some types of malignancy, including breast and prostate cancer (PCa) (Barker et al., 2012; Gardner, 1995; Hoek et al., 1998; Kahn et al., 2010; Keinan-Boker et al., 2009; LH and FW, 1994; Trichopoulos, 1990). Since William Gardner proposed the “Prenatal Origin of PCa” hypothesis in 1995 (Gardner, 1995), epidemiological and experimental studies have been designed to confirm and identify the molecular mechanisms involved in the developmental origins of PCa. In one of the few opportunities to explore how exposure in early life interferes with human PCa, Keinan-Boker et al. (2009) demonstrated an increase in the incidence of PCa in Jewish men exposed to famine and stress in early life during the Holocaust, with exposure at a younger age being associated with higher risk.

  • Developmental changes induced by exogenous testosterone during early phases of prostate organogenesis

    2020, Experimental and Molecular Pathology
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    UGS cells are highly sensitive to steroid hormones and represent a window of susceptibility to endocrine-disrupting chemicals (EDCs), causing deleterious morphogenesis effects, and increasing glandular predisposition to long-term prostatic diseases. The origin of prostate disease in early developmental phases is not a new concept (Gardner, 1995). Previous studies have shown that the androgen-induced program during prostatic development is similar to the program for human prostate cancer, demonstrating that early gland development is a reliable and valid model system for studying mechanisms driving prostate pathogenesis (Schaeffer et al., 2008).

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