Despite years of public health campaigns warning of the dangers of smoking when pregnant, many women are unaware of the risk or find themselves unable to quit. As a result, far too many babies are still being exposed in the womb to toxins that enter their mothers’ bloodstreams when they inhale cigarette smoke. Among the many infant and child health problems that have been linked to maternal smoking are premature birth, low birth weight, asthma, reduced lung function, sudden infant death syndrome (SIDS), and cleft lip and/or palate.
Now, a large international study involving NIH-supported researchers provides a biological mechanism that may explain how exposure to cigarette toxins during fetal development can produce these health problems . That evidence centers on the impact of the toxins on the epigenome of the infant’s body tissues. The epigenome refers to chemical modifications of DNA (particularly methylation of cytosines), as well as proteins that bind to DNA and affect its function. The genome of an individual is the same in all cells of their body, but the epigenome determines whether genes are turned on or off in particular cells. The study found significant differences between the epigenetic patterns of babies born to women who smoked during pregnancy and those born to non-smokers, with many of the differences affecting genes known to play key roles in the development of the lungs, face, and nervous system.
Once in a while a research publication reveals an entirely new perspective on a fundamental issue in biology or medicine. Today’s blog is about such a paper. The story, though complex, is very significant.
The choreography of human brain development is amazing, but quite mysterious. Today’s post highlights a study  that reveals the locations of some of the chemical choreographers that collaborate with DNA to orchestrate these fancy moves in the brain. Continue reading →
Caption: Histologic image of clear cell kidney cancer Slide courtesy of W. Marston Linehan, National Cancer Institute, NIH
Understanding how cancer cells shift into high gear—what makes them become more aggressive and unresponsive to treatment—is a key concern of cancer researchers. A new study reveals how this escalation occurs in the most common form of kidney cancer: clear cell renal cell carcinoma (ccRCC). The study shows that ccRCC tumors acquire specific mutations that encourage uncontrollable growth and shifts in energy use and production .
Conducted by researchers in the NIH-led The Cancer Genome Atlas (TCGA) Research Network, the study compared more than 400 ccRCC tumors from individual patients with healthy tissue samples from the same patients. Researchers were looking for differences in the gene activity and proteins in healthy vs. tumor tissue. Continue reading →