The ability of immune system cells to identify and kill cells of a particular type of cancer varies enormously from person to person, even with medical interventions designed to point the immune system in the right direction. This is demonstrated in the variability of some forms of cancer vaccine:
When a tumor is surgically removed, proteins are collected, cultured and introduced in a Petri dish to dendritic cells taken from the patient's blood. The new, "educated" dendritic cells are then injected into the patient where they are intended to recognize and destroy lingering tumor cells. Patients receive three vaccinations at two-week intervals. A fourth vaccination is given six weeks after the third.
This study centered on the immune responses of 32 patients enrolled in a Phase II clinical trial. Seventeen patients had a significant positive response after three vaccinations; 15 showed no such responsiveness.
Forty-one percent of vaccine responders, compared to seven percent of non-responders, survived at least two years.
It is this variability that led to the work of Zheng Cui in transferring cancer fighting immune cells between mice, which you might recall from past SENS conferences:
the simple transfusion of the cancer-fighting immune cells from the resistant mice effectively transfered the same remarkable protection to the normal mice. And even more excitingly, the treatment didn't just prevent cancers from forming, but actually fought off existing cancer: when researchers transfused the anti-cancer white blood cells into normal mice with existing skin tumors, the tumors regressed completely in a matter of weeks. Moreover, a single dose of the cancer-fighting immune cells gave the normal animals a cancer immunity that often lasted for the rest of their lives.
A recent article looks at Cui's work and attitudes towards getting the job done - if you have something that demonstrably works, getting it to the clinic should run in parallel with figuring out how it works. That's a tough sell these days, however, yet another consequence of rabid over-regulation of medical research and development.
First, we had cancer-resistant mice and asked, 'What can we learn from it?' The reason it’s resistant is because it has very different white cells. So then that immediately prompted the concept of therapy, because you can easily transfer white cells. You can extract them as a therapeutic agent and give them to another mouse. It’s a therapy. It’s much better than to find the gene. If you find the gene, then you have to understand the mechanism, and you have to find a way to put the gene into the cell, into all the cells you want to, and that would not work very easily. The technology as we speak right now is not really mature for that area. You might have to wait another 10, 20 years before that technology catches up with the concept. However, what we found is a cell as a therapeutic agent, so why not go ahead and see how it works. It worked really well in mice, so the next question, very obviously, is can we find a similar cancer resistance for humans as a donor for a therapeutic agent. And the answer is yes, we did find quite a few of them
A lot of people don’t like this because they said I have not a single idea of how it works. And I said, "Why should I?" If I can already go into therapy, why should I spend so much time now to find out how it works? That dispute was with the establishment, that’s why this trial has not been funded.