Having theoretical gaps is not the same thing at all as being pre-theoretical, but I agree with you that there are definitely big gaps in our knowledge. I'm not confident that Jason knows what the "commonly assumed" role of transposons is among cancer biologists, I think he either needs to be more precise in his language here or quote a more reliable source for the views of this expert community or preferably both.

The germ theory of disease is, most essentially, the theory that infectious diseases are caused by invasion of the patient's body by a pathogen. It is defined by the type of thing that is the root cause of the disease - in this case, a non-human cell, virus, or even a malformed protein.

The direct equivalent in cancer is the theory that the cancer is made from a human's own cells growing out of control. That's a universally accepted fact and it has been for a long time. Again, I know that you know this, so I'm just really unclear about why you're proposing that we don't have the equivalent of germ theory for cancer.

But let's elaborate, because I am in biomedical engineering and it might be that I'm acquiring a little bit of expert syndrome, assuming that facts that are obvious to anyone in the field are equally obvious to those who are not.

You are correct in saying that the difficulty with cancer is fundamentally one of targeting! The nastiest cancer cells have evolved a range of capabilities:

• They look like healthy cells, so the immune system doesn't want to destroy them
• They produce signaling proteins that tell the immune system to calm down, which we call an "antiinflammatory microenvironment"
• They evolve resistance to chemotherapies, so that a drug and dose that would kill the cancer will also prove so lethal to healthy human cells that there's no benefit to administering it anymore 
• They spread to new locations throughout the body. Since drugs don't always work equally well in all tissues, they might find a safe haven when they metastasize
• They rearchitect tissue in ways that are compatible with their own growth and survival
• They weaken the patient's physical health and physically infiltrate crucial tissue, making it riskier to operate

Figuring out a way to either get a drug to the physical location of the cancer cells but not to the healthy cells, or finding a drug that will selectively damage cancer cells but not healthy cells, is a huge challenge. Since cancer cells are not only alive and capable of evolution, but thrive off the same bodily conditions that normal cells survive best on, it's much harder to destroy them than it is to destroy bacteria (a challenge which is also becoming harder with the evolution of antibiotic resistance).

Fortunately, we are in the midst of figuring out a range of solutions to overcome these targeting challenges. Here are some examples, several of which we're actively doing in my own lab:

• Cancer creates an acidic pH nearby, and we can devise drug delivery systems that are activated by low pH
• We can take out patient immune cells, equip them with genetically engineered detectors for the patient's specific cancer, and then re-introduce them into the host
• We can drive a pro-inflammatory state at the cancer site so that the host immune cells can eliminate the cancer instead of getting shut down when they're nearby
• We can destroy all the cancer cells with really severe treatments that would normally kill the patient, but save and reintroduce the cells needed to allow the host to regenerate and survive after the treatment
• Some cancers are caused by infectious diseases, and we can vaccinate against those
• We can do genetic testing for things like breast cancer-promoting genes, and women can choose to have a preventative masectomy to reduce their risk from these genes. That's just one well-known example, other non-vital organs can be removed from both men and women as needed if they are at risk of developing cancer. 
• We can carefully break down the architecture of the cancer to figure out how it grows and develops, then carefully interrupt crucial links in that process in ways specific to individual cancers
• We can identify and eliminate mutation-causing carcinogens from our environment
• We can engineer synthetic or cell-based replacement organs, so that if excising the cancer would normally require destroying a critical organ, we can just take it out and then replace it with a new organ that doesn't have any cancer cells in it
• We can create sensors for cancer that detect it at an earlier stage when it's easier to treat
• We can look for things besides just cell division that the cancer needs to do more than normal, like growing new blood vessels, and inhibit those activities
• We have an ever-expanding list of ways to target cell growth and division, which cancers do more than normal human cells (but which human cells also do, which is why you lose your fast-growing hair during chemo).

This is by no means an exhaustive list, cancer isn't even my research topic, this is just stuff I've picked up from my labmates who work directly on cancer research.

The reason we have so many different strategies for tackling cancer, all tractable, is that we understand cancer really in quite a lot of detail, such that even though it's a really difficult collection of illnesses to treat due to being made of our own cells running amok, we are still able to deal with many cancers rather successfully.

There are other diseases of old age for which I'd be much more comfortable with the statement that we have no established, consensus basic understanding of how the disease works. Alzheimer's is one. Aging itself is by no means pre-theoretical, we have many decades of evolutionary theory to explain it in principle and nowadays a lot of specific biological mechanisms to flesh out the picture, so to speak.

Cancer is a case where the reason we haven't cured it, despite decades of intense research, is that it's a really tough problem and we've only developed the kinds of sophisticated tools that might let us bring the hammer down on it in the last couple decades. As you know, FDA trials take a long time, and so it takes a long time to move from basic research to the clinic.

You can see our progress though at the CDC, which shows a steadily decreasing death rate from cancer over the last quarter century.

And remember that not all of the deaths that do occur are failures of medicine. Some are because patients do the unhealthy stuff we know gives them cancer anyway, despite warnings, or they're not proactive about checkups, or they don't have access to care, or they refuse or can't afford treatment.

Meanwhile, we are continuing to build up our technology stack, finding ways to do things like safer and more robust gene therapy. Remember that CRISPR for all its hype is like a decade old discovery, so drugs that exploit the refinements we've made to it since then (which are considerable) have really only had a few years maybe to get tested in preclinical models.

Whatever medications are coming out today are the biomedical equivalent of ancient light from distant stars, showing us the picture of what biomedicine was capable of 15 years ago. In a regime of explosive exponential growth in technology, particularly biotech, there's going to be a huge gap between the insane stuff we can engineer in the lab today and what patients are able to take advantage of in the hospital. That might look like some sort of stagnation, but it's not, it's just the nature of the beast when human lives are on the line if you fuck up the technology and the rules aren't built from the ground up with math the way they are on computers. Personally, I'm thrilled with the biomedical universe and it feels like it's moving insanely fast, but I understand why it might not look that way if you're not working in the field as a professional because of the time delay between discovery and drug.

Now all we need is the nanobots…