A protein in the nucleus of breast cancer cells that plays a role in fueling the growth of aggressive tumors may be a good target for new drugs, reports a research team at the Duke Cancer Institute. The finding, published in the October 18, 2011, print issue of the journal Cancer Cell , presents a potential new way to inhibit breast cancer growth among so-called estrogen receptor negative cancers, which are especially lethal because they don’t respond to current hormone therapies. “This is validation of a new drug target for a subset of breast cancers that have poor treatment options,” said the study’s senior author, Donald McDonnell, PhD , chairman of the Duke Department of Pharmacology and Cancer Biology

For years, researchers have published papers that associate chronic stress with chromosomal damage. Now researchers at Duke University Medical Center have discovered a mechanism that helps to explain the stress response in terms of DNA damage. “We believe this paper is the first to propose a specific mechanism through which a hallmark of chronic stress, elevated adrenaline, could eventually cause DNA damage that is detectable,” said senior author Robert J.

An international team of scientists lead by researchers from Duke University and Johns Hopkins University have discovered a key “switch” in the brain that allows neurons to stop dividing so that these cells can migrate toward their final destinations in the brain. The finding may be relevant to making early identification of people who go on to develop schizophrenia and other brain disorders. “This work sheds light on what has been a big black box in neuroscience,” said Nicholas Katsanis, PhD , co-senior author of the work and Jean and George Brumley Jr., MD, Professor of Developmental Biology, Professor of Pediatrics and Cell Biology.

Under standard laboratory conditions, the human beta-defensin 1 (hBD-1), a human antibiotic naturally produced in the body, had always shown only little activity against microbes.

A curious contagious cancer, found in dogs, wolves and coyotes, can repair its own genetic mutations by adopting genes from its host animal, according to a new study in the journal Science .

The difficult task of sorting and counting prized stem cells and their cancer-causing cousins has long frustrated scientists looking for new ways to help people who have progressive diseases. But in a development likely to delight math teachers, University of Florida researchers have devised a series of mathematical steps that accomplishes what the most powerful microscopes, high-throughput screening systems and protein assays have failed to do — assess how rapidly stem cells and their malignant, stemlike alter egos increase their numbers. The method, published in the online journal PLoS ONE in January, may rev up efforts to develop stem cell therapies for Alzheimer’s, Parkinson’s and other diseases.

Electron microscopes are among the most widely used scientific and medical tools for studying and understanding a wide range of materials, from biological tissue to miniature magnetic devices, at tiny levels of detail.