Syndicate content

Archive - Nov 17, 2012


Study Offers Clues to Cause of Brain Tumors in Children

Insights from a genetic condition that causes brain cancer are helping scientists better understand the most common type of brain tumor in children. In new research, scientists at Washington University School of Medicine in St. Louis have identified a cell growth pathway that is unusually active in pediatric brain tumors known as gliomas. They previously identified the same growth pathway as a critical contributor to brain tumor formation and growth in neurofibromatosis-1 (NF1), an inherited cancer predisposition syndrome. "This suggests that the tools we've been developing to diagnose and treat NF1 may also be helpful for sporadic brain tumors," says senior author David H. Gutmann, M.D., Ph.D., the Donald O. Schnuck Family Professor of Neurology. The findings were published online on November 14, 2012 in Genes & Development. NF1 is among the most common tumor predisposition syndromes, but it accounts for only about 15 percent of pediatric low-grade gliomas known as pilocytic astrocytomas. The majority of these brain tumors occur sporadically in people without NF1. Earlier research showed that most sporadic pilocytic astrocytomas possess an abnormal form of a signaling protein known as BRAF. In tumor cells, a piece of another protein is erroneously fused to the business end of BRAF. Scientists suspected that the odd protein fusion spurred cells to grow and divide more often, leading to tumors. However, when they gave mice the same aberrant form of BRAF, they observed a variety of results. Sometimes gliomas formed, but in other cases, there was no discernible effect or a brief period of increased growth and cell division. In other studies, the cells grew old and died prematurely. Dr.

Probing Mystery of the Venus Fly Trap's Botanical Bite

Plants lack muscles, yet in only a tenth of a second, the meat-eating Venus fly trap hydrodynamically snaps its leaves shut to trap an insect meal. This astonishingly rapid display of botanical movement has long fascinated biologists. Commercially, understanding the mechanism of the Venus fly trap's leaf snapping may one day help improve products such as release-on-command coatings and adhesives, electronic circuits, optical lenses, and drug delivery. Now a team of French physicists from the National Center for Scientific Research (CNRS) and Aix-Marseille University in Marseille, France, is working to understand this movement. They will present their findings at the 65th meeting of the American Physical Society's (APS) Division of Fluid Dynamics (DFD), November 18 – 20, 2012, in San Diego, California. The work extends findings by Dr. Yoël Forterre and researchers from Harvard University who discovered several years ago that the curvature of the Venus fly-trap's leaf changes while closing due to a snap-buckling instability in the leaf structure related to the shell-like geometry of the leaves. Mathieu Colombani, a Ph.D. student in Dr. Forterre's laboratory is now conducting experiments to elucidate the physical mechanisms behind this movement. "The extremely high pressure inside the Venus fly trap cells prompted us to suspect that changes with a cell's pressure regime could be a key component driving this rapid leaf movement," he notes. The Colombai team uses a microfluidic pressure probe to target and measure individual cells. This is a tricky experiment because it requires the living plant to be immobilized with dental silicone paste while the probe is inserted using a micromanipulator guided by binoculars. They take pressure measurements before and after leaf closure.

New Discovery Regarding Chromatin Remodeling Complexes

A new discovery from researchers at the Huntsman Cancer Institute (HCI) at the University of Utah concerning a fundamental understanding about how DNA works will produce a "180-degree change in focus" for researchers who study how gene packaging regulates gene activity, including genes that cause cancer and other diseases. The discovery, by Bradley R. Cairns, Ph.D., Senior Director of Basic Science at HCI and a professor in the Department of Oncological Sciences, is reported in the November 11, 2012 online issue of the journal Nature. Dr. Cairns's research focuses on chromatin remodeling complexes (CRCs), which are cellular protein complexes that behave like motors, expanding or compacting different portions of DNA to either express or silence genes, respectively. Before, scientists thought that the motor within CRCs waits at rest until it receives instructions. Dr. Cairns and co-author Dr. Cedric R. Clapier show that the motor within a key CRC responsible for gene packaging and assembly is intrinsically turned on, and instead requires specific instructions to turn it off. "Many articles in the research literature show that CRCs are mutated in cancer cells. They are intimately involved in regulating gene expression—responsible for correctly packaging genes that control growth proliferation and for unpackaging tumor suppressors," said Dr. Cairns. "This research reveals principles by which CRC mutations could cause cancer." Chromosomes are made of long DNA strands compressed around nodes of protein called nucleosomes; when DNA is compressed, the genes in that area are turned off. Some CRCs, called disassembly CRCs, act as motors that unwind sections of DNA chains, making genes active for a given cell process. Another type, called assembly CRCs, rewinds the DNA chain, recompressing it when the process is complete.