Carcinogenic risk and Bisphenol A exposure: A focus on molecular aspects in endoderm derived glands

•Low-dose BPA-dependent carcinogenesis in endoderm-derived glands is described.•BPA toxicity mechanisms common to organs from the same germ layer are reported.•BPA targets the NRs and stress/NF-kB pathways involved in endoderm carcinogenicity.•Developmental exposure to BPA is a risk for carcinogenesis of endoderm glands.•In vitro toxicogenomics hints mechanisms of BPA carcinogenicity in endoderm glands.

Epidemiological and experimental evidence associates the exposure to Bisphenol A with the increase of cancer risk in several organs, including prostate. BPA targets different pathways involved in carcinogenicity including the Nuclear Receptors (i.e. estrogen and androgen receptors), stress regulated proteins and, finally, epigenetic changes.Here, we analyse BPA-dependent carcinogenesis in endoderm-derived glands, thyroid, liver, pancreas and prostate focusing on cell signalling, DNA damage repair pathways and epigenetic modifications. Mainly, we gather molecular data evidencing harmful effects at doses relevant for human risk (low-doses). Since few molecular data are available, above all for the pancreas, we analysed transcriptomic data generated in our laboratory to suggest possible mechanisms of BPA carcinogenicity in endoderm-derived glands, discussing the role of nuclear receptors and stress/NF-kB pathways. We evidence that an in vitro toxicogenomic approach might suggest mechanisms of toxicity applicable to cells having the same developmental origin.Although we cannot draw firm conclusions, published data summarized in this review suggest that exposure to BPA, primarily during the developmental stages, represents a risk for carcinogenesis of endoderm-derived glands.