Association of fetal hormone levels with stem cell potential: evidence for early life roots of human cancer.

Intrauterine and perinatal factors have been linked to risk of childhood leukemia, testicular cancer, and breast cancer in the offspring. The pool of stem cells in target tissue has been suggested as a critical factor linking early life exposures to cancer. We examined the relation between intrauterine hormone levels and measurements of stem cell potential in umbilical cord blood.

Stem cells and prenatal origin of breast cancer.

The hypothesis that in utero exposure to pregnancy hormones, notably estrogens, is related to the occurrence of breast cancer in the offspring has been examined in a number of epidemiological and experimental studies. Many studies have provided direct or indirect evidence that supports the hypothesis of an intrauterine component in the origin of breast cancer. Human studies to examine the underlying biological mechanisms, however, have been limited.

Prenatal exposure to ethanol alters the neuroimmune response to a central nervous system wound in the adult rat.

We examined the long-term effects of in utero ethanol exposure on the expression of tumor necrosis factor-alpha (TNF-alpha), glial fibrillary acidic protein (GFAP), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and ED1 in the tissue at the site of a central nervous system (CNS) wound. Adult rats obtained from dams fed control diets or an ethanol diet were fed either control diets or an ethanol diet 5 days before and after infliction of a CNS wound. In pair-fed controls, the expression of TNF-alpha, GFAP, ICAM-1, VCAM-1, and ED1 immunoreactive proteins was increased in the tissue at the wound site when compared with that in nonlesioned tissues.

Ethanol inhibits prolactin- and tumor necrosis factor-alpha-, but not gamma interferon-induced expression of intercellular adhesion molecule-1 in human astrocytoma cells.

In humans, alcohol consumption has multiple effects on the immune system. Despite an increase in our understanding of the effects of alcohol on the immune system, little is known about the effect of alcohol on the neuroimmune response. In the central nervous system (CNS), astrocytes and microglial function as immune effector cells.

Ethanol increases the neurotoxic effect of tumor necrosis factor-alpha in cultured rat astrocytes.

Background: The central nervous system is particularly sensitive to the cytotoxic effect of ethanol. In vivo and in vitro studies indicate that ethanol decreases cell proliferation in a number of cells types, including neurons and glial cells in the central nervous system. The cellular mechanisms involved in ethanol-induced cell toxicity, however, are unclear.