A collaborative study conducted at the Frederick National Lab and published in Cancer Research has provided new insight as to why elevated estrogen levels are associated with an increased risk of breast cancer.

In the past, nonhuman primate research has relied on only a few infectious molecular clones for numerous diverse research projects including pathogenesis, preclinical vaccine evaluations, transmissions, and host vs. pathogen interactions. But new data suggests that there is a selected phenotype of the simian immunodeficiency virus (SIV) that causes infection.

Until recently, researchers studying RAS, a family of proteins involved in transmitting signals within cells, believed that the exchange of guanosine 5’-diphosphate (GDP) by guanosine triphosphate (GTP) was sufficient to activate the protein. Once activated, RAS can cause unintended and overactive signaling in cells, which can lead to cell division and, ultimately, cancer.

Many aspects of how infectious viruses assemble in cells have yet to be completely deciphered. However, as reported in a recent Journal of Virology paper, researchers may be one step closer to understanding how HIV-1, the virus that causes AIDS, assembles and replicates.

When Alison Rattray and colleagues in the Gene Regulation and Chromosome Biology Laboratory (GRCBL) examined a mutant yeast cell they had isolated in a screen, they noticed something strange. The DNA exhibited a “very specific, but weird, rearrangement,” she explained.