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Increased programmed cell death of the syncytiotrophoblast disrupts the layer, resulting in homeostatic imbalance, which causes placental-derived material to be released into the maternal circulation, including tumor necrosis factor (TNF-alpha) and syncytiotrophoblast microparticles (SBTM) (51)

This is in agreement with previously mentioned studies which had found that high NFkB regulated elevated E2F6 levels in response to TMZ, thus helping maintain GBM viability [74]