Abstract
The idea that exposure to adverse environmental conditions and lifestyle choices during pregnancy can result in fetal programming that underlies disease susceptibility in adulthood is now widely accepted. Fetal alcohol exposed offspring displays many behavioral and physiological abnormalities including neuroendocrine–immune functions, which often carry over into their adult life. Since the neuroendocrine–immune system plays an important role in controlling tumor surveillance, fetal alcohol exposed offspring can be vulnerable to develop cancer. Animal studies have recently showed increased cancer growth and progression in various tissues of fetal alcohol exposed offspring. I will detail in this chapter the recent evidence for increased prostate carcinogenesis in fetal alcohol exposed rats. I will also provide evidence for a role of excessive estrogenization during prostatic development in the increased incidence of prostatic carcinoma in these animals. Furthermore, I will discuss the additional possibility of the involvement of impaired stress regulation and resulting immune incompetence in the increased prostatic neoplasia in the fetal alcohol exposed offspring.
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Acknowledgment
This work was partly supported by National Institute of Health grants R37AA08757 and R01AA11591. Prostate research works were conducted in our laboratory by Drs. Sengottuvelan Murugan, Changqing Zhang, Sepideh Mojtahedzadeh, and Nadka Boyadjieva.
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Sarkar, D.K. (2015). Fetal Alcohol Exposure Increases Susceptibility to Carcinogenesis and Promotes Tumor Progression in Prostate Gland. In: Vasiliou, V., Zakhari, S., Seitz, H., Hoek, J. (eds) Biological Basis of Alcohol-Induced Cancer. Advances in Experimental Medicine and Biology, vol 815. Springer, Cham. https://doi.org/10.1007/978-3-319-09614-8_23
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