Training your cells how to spot a cancerous spy
One of the problems with trying to fight cancer is that cancerous cells are really the person’s own cells that have gone rogue, growing out of control. Trying to identify the cancerous cells is like looking for spies in your own group, and our immune system is pretty bad at it. We on the outside may be able to tell who the spies are, but our own body can’t. So how do you fight cancer?
Two ways. One useful approach is to use drugs we have designed that will try and target the cancerous cells. The problem here is that often the drugs kill other cells as well: cells we don’t really want to be killing.
Another way is to teach your body who the spies are. This is what researchers from the University of Pennsylvania have done, to great effect, for a handful of leukemia patients. The results were published yesterday in the journal Science Translational Medicine and in the New England Journal of Medicine.
What they did was this: they remove some of the patient’s own T-cells: the kind that can’t tell good cells from bad ones. They infect these cells with a retrovirus they created that will introduce a new gene into the DNA of the cells, making them produce a new protein receptor on the surface of the cell. This receptor, now on the surface of the T-cells, will let the cells identify any other cell expressing a protein called CD19, a protein that only leukemia cells and B cells have. The T-cells will kill only (except for the B cells) the cancerous cells, a vast improvement over most drugs. They turned the patient’s novice T-cells into an elite Navy SEAL targeted attack squadron.
The researchers did something else clever too. They realized that they couldn’t train enough T-cells on their own, so they taught the T-cells how to call for backup. They introduced another signal into the cells, so that whenever the T-cell binds to a CD19 cell (cancerous one), the T-cell will release chemicals calling for more of itself to be produced.
The results have been astounding, reducing a two pound tumor to zero in just a few weeks. Totally awesome.
This is very exciting news for cancer therapy. So could it also work for other diseases like HIV? I don’t think so, and here is why. Cancer is not infectious like HIV and it evolves very very slowly. If we designed such a therapy for HIV, it would not be long until the fast-evolving HIV simply stopped expressing CD19 (or a similar protein) on its surface, thus evading detection like antibacterial-resistant bacteria. And because HIV is transmissible (unlike cancer), this new HIV could then spread to other patients. So while this is great news for cancer patients of the future, a different approach will be needed for other important diseases.