By silencing a mechanism that allows cancer cells to reject anti-cancer drugs, a new breakthrough out of MIT and Harvard could dramatically increase the efficacy of treatment.

In addition to disabling a tumor’s defenses and delivering anti-cancer drugs, the new nanodevice fluoresces can help scientists monitor treatment.

In the war against cancer, scientists often have to act like battlefield commanders, devising creative attack strategies to bring the disease to its knees. A new tactic developed by researchers from MIT, Harvard Medical school and Queen Mary University of London involves a super-small device that disarms cancer cells so tumor-shrinking drugs can be delivered.

The device, known as a “nanobeacon,” consists of a gold nanoparticle covered with strands of DNA. Before the nanobeacon is activated inside a cell, the DNA strands are folded back on themselves like hairpins. When they arrive at the right spot inside a cancer cell, however, the strands open up, releasing anti-cancer drugs and binding to messenger RNA (mRNA), “the snippet of genetic material that carries DNA’s instructions to the rest of the cell,” according to an MIT news report about the research published Monday in Proceedings of the National Academy of Sciences.

Specifically, the nanobeacons latch onto the strand of mRNA responsible for making a protein known as MRP-1. When overexpressed, this protein, found in all cancer cells to varying degrees, can act like a pump that eliminates treatment drugs, rendering them ineffective. When the nanobeacons connect with the RNA, however, this mechanism is disabled. In effect, the drug-resistant gene inside the cancer cell is shut down cold.

Additionally, Artzi adds that the nanobeacons can be engineered to interact with other genes inside cancer cells — not just those responsible for producing drug-resistance proteins. In fact, the researchers are now experimenting with using the method to shut down a gene that causes gastric tumors to spread to the lungs.