At least with mouse models of inflammation, there's apparently no concern about what conclusions are legitimate to draw from a correlation between those models and inflammation in humans.
The current thinking about mutations in cancer cells holds that there are two types – driver mutations that are behind cancer growth because they give tumor cells a growth advantage, and passenger mutations that are along for the ride. "Historically, passenger mutations have been largely ignored," Leonid Mirny told BioWorld Today, because cancer development is seen largely as "a series of unfortunate events" in the form of accumulating driver mutations.
Fibrosis is a silent killer in more ways than one. There is the typical way in which diseases can sneak up on their victims. The scarring that is the hallmark of fibrosis can go undetected for years before patients show any symptoms.
Studying cancer cells that survive chemotherapy treatment, scientists from Roche AG subsidiary Genentech Inc. have implicated a member of the human epidermal growth factor receptor, or HER, family in such treatment resistance.
Stem cells are supposed to be the fountain of youth for other tissues. But stem cells themselves age, too, meaning that sooner or later, the fountain of youth could use some rejuvenation itself.
"For much of the 1900s, we studied neurons" to understand brain function, Philip Haydon told BioWorld Today. "And the reasons were purely technical. . . . We could listen to neurons, and we could talk to them." Neurons communicate electrically, and electrical recording and stimulation techniques made them amenable to studying. But in terms of what goes on in the brain, looking only at neurons is bound to deliver a minority report.
Autophagy, Beth Levine told BioWorld Today, "can very simply be understood as a cellular housekeeping mechanism." But that simplicity is deceptive. Autophagy's housekeeping, it turns out, sits at a crossroads that gives it a role in many diseases.
Researchers have created a mouse with a reporter gene that appears to light up at the earliest stages of tumor development, regardless of the tissue type in which the tumor is developing.
Mutations in the genes for BRCA1 and BRCA2 were the first mutations identified that could predict an increased risk of cancer for their carriers. Some of them remain the strongest predictors of such increased risk – carriers of certain mutations have a 75 percent lifetime risk of developing breast or ovarian cancer.
