Upending decades-old dogma, researchers say enzymes long categorized as promoting cancer are, in fact, tumor suppressors and that current clinical efforts to develop inhibitor-based drugs should instead focus on restoring the enzymes' activities.

Protein Kinase C (PKC) is a group of enzymes that act as catalysts for a host of cellular functions, among which are cancer-relevant activities, such as cell survival, proliferation, apoptosis, and migration. The discovery that they are receptors for tumor-producing phorbol esters, plant-derived compounds that bind to and activate PKC, created a dogma that activation of PKCs by phorbol esters promoted carcinogen-induced tumorigenesis.

A team of scientists based at Brown University has found that reducing expression of a fundamentally important gene called Myc significantly increased the healthy lifespan of laboratory mice, the first such finding regarding this gene in a mammalian species.

Myc is found in the genomes of all animals, ranging from ancestral single-celled organisms to humans. It is a major topic of biomedical research and has been shown to be a central regulator of cell proliferation, growth, and death. It is of such widespread and fundamental importance that animals cannot live without it. But in humans and mice, too much expression of the protein that Myc encodes has been closely linked to cancer, making it a well-known but elusive target of drug developers.

A group of white blood cells known as B cells play a key role in the human immune response but need a protein-targeting signal called mannose 6-phosphate (M6P) in order to proliferate, differentiate, and present immune cell-activating antigens, according to a study in The Journal of Cell Biology.

Immune cells slice up antigens in organelles called lysosomes and attach the fragments to complexes that display them on the cell surface in order for these peptides to bind and activate other immune cells. To ensure that they can cut up the antigens, cells steer newly made enzymes to lysosomes by tagging them with M6P molecules.

A team of researchers has identified the genetic mutation responsible for glycogen storage disease type IIIa in Inuit in northern Quebec, Canada, in a study published in CMAJ (Canadian Medical Association Journal). The paper identifies a mutation in the gene encoding the glycogen debranching enzyme (AGL), which had previously been undetected in a decade of investigation by the same authors.

Wildfires send hot flames and smoke high into the air, including black carbon emissions associated with climate change and risk to human health. Unless the United States adapts sensible forest management policies, which means fewer instances of the Department of the Interior and environmental lobbyists conspiring to manipulate science reports, carbon emissions from wildfires in the contiguous U.S. could increase by 50 percent by 2050 and double by 2100.

Some media, such as the New York Daily News and NBC, have reported that the Asian H5N1 strain of highly pathogenic avian influenza has now entered the United States. This is incorrect and they were told it was not the same strain by the United States Geological Survey and then suggested it was anyway.

There was avian flu that was recently found, in a green-winged teal in Washington state, but it is a different strain and is not known to harm humans nor has it been found in domestic poultry.