The blastocyte developes embryoblasts and trophoblasts. Cytotrophoblasts cover the whole embryo. Syncytiotrophoblasts will be induced by the products of human endogeneous retroviruses (HERV-W) causing membrane fusion of the cells, thus creating a continuous border between the maternal blood and the fetal circulation, feeding, detoxicating, and regulating its development. The immunological, regulatory, hormonal, etc. changes of the maternal body prevent the impairment of the fetus carrying the paternal haplotype, too. Tumour cells and preneoplastic cells, however, are equally well tolerated by the mother as the fetus itself. Certain maternal tumours possess therefore an epidemiologically measurable peak among the age groups before 50 years of age. Other malignancies are stimulated by the hormonal changes of the pregnants. Others are not stimulated, but the reduced maternal immunological control enables enhanced multiplication of cells. Trophoblasts possess similar growth properties to tumour cells. Tumours of trophoblast origin may appeare during pregnancy and threat the life of both the fetus and mother. The immunological changes of the maternal immune system may increase the number of TREG cells, which might result in immunotolerance to certain tumour antigens extending even to the post partum life. The exacerbating tumours imply different risks to the developping fetus. In addition to the direct impairment of the pregnancy, the maternal tumours have to be diagnosed, and in the majority of the patients also threated. All these medical interventions, even surgical operations have to be done using methodologies, which had been found previously harmless to the developping fetuses. Maternal tumours can methastatise into the placenta and even into the fetal organs. These later consequences will be discussed in this chapter.
|Title of host publication||Maternal Fetal Transmission of Human Viruses and their Influence on Tumorigenesis|
|Number of pages||53|
|ISBN (Print)||9400742150, 9789400742154|
|Publication status||Published - okt. 1 2012|
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