Scientists have recruited anthrax, a potentially deadly infection, to deliver cancer drugs, a new study describes, and could one day change the way we treat cancer.

Bacillus anthracis bacteria have very efficient machinery for injecting their toxic proteins into cells, and MIT researchers have learned from and utilized this delivery system to better administer cancer drugs.

"Anthrax toxin is a professional at delivering large enzymes into cells," lead researcher Bradley Pentelute said in a statement. "We wondered if we could render anthrax toxin nontoxic, and use it as a platform to deliver antibody drugs into cells."

Described in the journal ChemBioChem, Pentelute and his colleagues effectively disarmed the anthrax toxin in order to create a version that can deliver two proteins known as antibody mimics, which can kill cancer cells by disrupting specific proteins inside the cells. Most anti-cancer drugs rely on antibodies to target receptors found on cancer-cell surfaces. The problem is, it's very difficult to get proteins inside cells.

"Crossing the cell membrane is really challenging," Pentelute explained. "One of the major bottlenecks in biotechnology is that there really doesn't exist a universal technology to deliver antibodies into cells."

So the MIT team turned to nature, exploring the possibility of mimicking the anthrax toxin's system to deliver small protein molecules as vaccines.

To achieve this, the researchers had to first render the anthrax bacteria non-toxic by removing the toxic sites of two anthrax proteins, called lethal factor (LF) and edema factor (EF). The MIT team then replaced the toxic regions with antibody mimics, allowing these cargo proteins to catch a ride into cells through what is called the protective antigen (PA) channel.

This technique allowed the researchers to successfully target and kill several proteins, including Bcr-Abl, which causes chronic myeloid leukemia. They are now testing this approach to treat tumors in mice and are also working on ways to deliver the antibodies to specific types of cells.

"This work represents a prominent advance in the drug-delivery field," added Jennifer Cochran, an associate professor of bioengineering at Stanford University.