Ethanol alters proliferation and differentiation of normal and chromosomally abnormal human embryonic stem cell-derived neurospheres.

Ethanol is a powerful substance and, when consumed during pregnancy, has significant psychoactive and developmental effects on the developing fetus. These abnormalities include growth retardation, neurological deficits, and behavioral and cognitive deficiencies, commonly referred to as fetal alcohol spectrum disorder. The effect of ethanol has been reported to affect cellular development on the embryonic level, however, not much is known about mutations contributing to the influence of ethanol.

Lectins identify glycan biomarkers on glioblastoma-derived cancer stem cells.

Glioblastoma (GBM) is a highly aggressive primary brain tumor with a poor prognosis. Despite aggressive therapy with surgery, radiotherapy, and chemotherapy, nearly all patients succumb to disease within 2 years. Several studies have supported the presence of stem-like cells in brain tumor cultures that are CD133-positive, are capable of self-renewal, and give rise to all cell types found within the tumor, potentially perpetuating growth.

GABRB3 gene expression increases upon ethanol exposure in human embryonic stem cells.

Ionotropic receptors are the target for most mood-defining compounds. Chronic exposure to ethanol (EtOH) alters receptor-mediated responses and the numbers of these channels and specific subunits; as well as induces anxiolytic, sedative, and anesthetic activity in the human brain. However, very little is known regarding the effects of EtOH on ionotropic receptor transcription during early human development (preimplantation).