Although the soluble factor TGF-beta has been shown to suppress the growth of tumor cells in the early stages of breast cancer, high levels of TGF-beta during the later stages of the disease are associated with a poor outcome. A study using human breast cancer samples and mice, which appears online on December 7 in advance of publication in the January print issue of the Journal of Clinical Investigation, indicates that changes in expression of one component of the TGF-beta receptor, T-beta-RIII, might provide a mechanism for the distinct effects of TGF-beta at the different stages of breast cancer.

Scientists from Johns Hopkins and from the University of Milan have effectively proven that they can inhibit lethal human brain cancers in mice using a protein that selectively induces positive changes in the activity of cells that behave like cancer stem cells. The report is published this week in Nature.

Among the many genes packed into each cell of our body, those that get turned on, or expressed, are the ones that make us who we are. Certain proteins do the job of regulating gene expression by clasping onto key spots of DNA -- the nucleic acid that contains the genetic instructions.

The discovery of a DNA marker for two key rust resistance genes is enabling plant breeders around the world to breed more effective rust resistant wheat varieties.

Researchers in the Greene Infectious Disease Laboratory at Columbia University Mailman School of Public Health and their colleagues in the WHO Global Laboratory Network have developed a new tool for pathogen surveillance and discovery—the GreeneChip System. The GreeneChip is the first tool to provide comprehensive, differential diagnosis of infectious diseases, including those caused by viruses, bacteria, fungi, or parasites. In addition, it is the first tool that can be used on a wide variety of samples, including tissue, blood, urine, and stool, allowing for the rapid identification of pathogens in a variety of laboratory and clinical settings.

Researchers have found evidence for a fundamental molecular mechanism underlying the hyperactive high of cocaine. In studies with rats, they have traced the effect to interactions between two types of receiving stations in neurons for nerve signals from their neighbors. The researchers' studies in rats found that when the animals received cocaine, a component of a receptor for the neurotransmitter dopamine tends to grab onto a component of a receptor for glutamate. The result, they found, was interference with normal activation of this glutamate receptor.