Led by professor of oncology Ron Levy, a team at Stanford has come up with a promising new cancer treatment
Harnessing the body's natural immune defenses to take the fight to cancer, known as immunotherapy, is an especially promising area of cancer research with the potential to tackle all forms of the disease. Scientists from Stanford University are now reporting an exciting new advance in the field, discovering that a single injection of immune-stimulating agents can quickly destroy tumors in mice, and promisingly, clinical trials investigating its effects in humans are already underway.
Alongside chemotherapy, radiotherapy and surgical removal, immunotherapy has come to be heralded as the fourth pillar in cancer therapy. Though our immune system automatically kicks into gear when cancer is detected, the cancerous cells are quite adept at evading it, multiplying and then eventually overpowering it.
So immunotherapy is a way of swinging the odds back in the immune system's favor. Some of the common approaches include targeting the built-in switches that stop natural cancer-fighting proteins do their thing, boosting other proteins that ramp up the presence of cancer-fighting T cells, and removing T cells, genetically engineering them to attack tumor cells, and then returning them to the body.
All have shown promise in different ways, but all have their limitations, such as nasty side effects, high costs and/or very involved preparation and treatment times. Led by professor of oncology Ron Levy, the Stanford researchers have come up with a potentially much better way of doing things that involves delivering a potent cancer-killing mix in a single injection.
The technique sees two immune-stimulating agents injected directly into solid tumors. One of these is already approved for human use and is currently injected directly into tumors of melanoma patients, while the other has already been tested for human use in other, unrelated clinical trials.
"This treatment is 'off the shelf' and nothing has to be made for each patient," Levy tells New Atlas. "We are using very low doses of the two medications. So this should be very inexpensive compared to other treatments."
Just microgram amounts of each of these agents is injected into the tumor. One of these is a short strand of DNA called CpG oligonucleotide, which boosts an activating receptor on the surface of cancer-fighting T cells that have infiltrated the tumor in search of the enemy. The other binds to that same receptor and amplifies the T cells' response to kill the tumor.
The beauty of this approach is that it does not stop at the injection site. The team found that some of these activated T cells will leave that first tumor in search of others around the body, seeking them out and destroying them. In an experiment where laboratory mice had lymphoma tumors transplanted into two separate sites in their bodies, injecting the agents into one tumor saw the regression of not just that tumor, but also the second that hadn't been injected at all.
The team says this worked "startlingly well," and that 87 of the 90 mice treated were cured. Those that weren't had their tumors regress following a second treatment, with similar results observed in mice with breast, colon and melanoma tumors. But uncovering the exact mechanisms behind the T cells tumor-hunting behavior will take further research.
"This is a subject that we are still investigating in the animal models where we can track T cells by a variety of different methods that are not possible in humans," Levy explains.
Although the researchers are optimistic of using this approach to treat all kinds of cancer where T cells have infiltrated the tumor, Levy tells us they will start with lymphoma because "it is the cancer of the immune system and most likely to respond to this maneuver." To that end, a trial is already underway designed to investigate the effectiveness of the technique in 15 patients with low-grade lymphoma.
If that proves successful, several years down the track the team imagines injecting the agents into solid tumors before surgical removal to avoid recurring tumors through metastasis (the spread of cancerous cells throughout the body) or lingering cancer cells, or even as a way of nipping in the bud tumors that can arise through genetic mutations.
"I don't think there's a limit to the type of tumor we could potentially treat, as long as it has been infiltrated by the immune system," Levy says.
The research was published in the journal Science Translational Medicine.
Source: Stanford University