Today's topic is the cure for cancer, something a grail in medicine. It will be challenging to produce, but I think that the difficulty is presently overestimated by much of the public and those in the mainstream of the research community. The reasons for this are understandable: the past half century of cancer research is a story of continually discovered ever greater complexity in cancer biology. It is the sheer exuberant variation in cancer - between types, between tissues, between individuals, and even between tumors in an individual - that makes it such a daunting foe. Every cancer is an evolving mess of broken cells with its own character and biochemical quirks.
We stand now in the early stages of a revolution in biotechnology, however, and the rapidly expanding capabilities that brings to the research community are beginning to reveal that, for all their variety, cancers do have at least some shared characteristics and shared vulnerabilities. It is the commonalities in cancer, things that are emerging now and would have been exceedingly expensive to discover and exploit even a mere twenty years past, that will act as a foundation for the coming generation of effective cancer therapies. In that spirit, I offer you three and a half ways to cure cancer, outlined very briefly below:
1) WILT, whole-body interdiction of lengthening of telomeres
WILT is my least favorite cure for cancer, but it is nonetheless hard to argue that it isn't in fact the ultimate cure for cancer. Cancers absolutely depend upon ways to lengthen telomeres, the protective caps at the end of chromosomes that shorten with each cell division, putting a limit on the life span of ordinary cells. A cell with little left of its telomeres stops dividing, destroys itself, or becomes senescent - and thus not much use as a cancer cell. Telomeres are lengthened by the activities of the telomerase enzyme and the mechanisms imaginatively known as alternative lengthening of telomeres (ALT), both of which are abused by all cancers in order to create unfettered growth.
Disable telomerase and the genes for ALT in a human, and the result will most likely be a human who cannot suffer cancer. There is a reason this is my least favorite approach however, and that is that your stem cell populations require the ability to lengthen telomeres in order to continue to maintain your tissues over the long term. A person who underwent a hypothetical WILT treatment would need stem cell transplants or a similar way to refresh all of the different stem cell populations of the body - and there are many - every decade at least. WILT means exchanging the threat of cancer for an arguably greater dependency on medical technology.
Research into WILT is currently funded to a modest degree by the SENS Research Foundation under the OncoSENS program, with a focus on establishing a a sufficient understanding of ALT to determine the best and most comprehensive way to disrupt its mechanisms.
2) LIFT/GIFT, leukocyte/granulocyte transfusions
Somewhere out there, someone possesses immune cells (the white blood cells called leukocytes or granulocytes) that can kill your cancer. You might consider this approach to immune therapy as being analogous to first generation stem cell therapies that are presently available in many parts of the world: take someone else's immune cells, grow them in culture, and then transplant large numbers of them into your body, where they work to destroy cancer. This methodology has been shown to produce exceedingly impressive results in mice, such as entire lineages of cancer-resistance mice, but it isn't known why exactly it works so well - which makes it hard to proceed to clinical applications in the US, where a full scientific understanding of the mechanisms involved is generally required.
A couple of startups are presently working in this area, such as ImmunePath (probably) and Munogenics, with little funding and slow progress, so far as I'm aware. There is also a small ongoing clinical trial in Florida that looks like it'll wrap up later this year.
This is exactly the sort of application of cell therapies that should do well in the medical tourism arena, and indeed is appearing as an option in some overseas clinics. It is easy enough to implement that any group that can presently carry out stem cell transplants should also be able to manage immune cell transplants. More publicity, signs of progress in obtaining human results, and greater funding for trials would go a long way towards speeding the spread of this therapy and this determining whether the results in mice continue to translate well into humans.
3) Targeted cell killing technology, plus the search for commonalities in cancer
Modular targeted cell killing technology platforms with a slot for a sensing system are well in hand in the lab, and are a big part of why the next generation of cancer therapies will be far more effective and far less traumatic than chemotherapy. A great variety of such systems are presently under development: nanoparticles such as gold rods that can be heated by radiation; nanoparticles such as dendrimers that carry motes of chemotherapy drugs; nanoparticles that carry an RNA interference payload; engineered viruses; engineered bacteria; trained immune cells; and so forth.
The commonality here is that all of these systems are designed to destroy specific cells with minimal damage to surrounding cells - all that is needed are mechanisms to ensure that these cell-killers only target cancer cells. This largely means discovering suitable markers on a cell surface: specific proteins that differentiate cancer cells by the degree to which they are present, and which are sufficiently general to appear in a sizable population of patients or many types of cancer.
The big uncertainty here is whether or not researchers will find targets shared by many cancers that are sufficiently discriminating to allow enough preferential targeting of cancer cells. It's possible to layer multiple poorly discriminating targets to get a highly discriminating system, however, and there are promising signs of late on this front. You might look at trials involving therapies targeting CD47, for example, which appears on most cancers per the latest research.
If there are enough markers like CD47 out there, then it should be possible to build a comparatively small suite of general cancer therapies that will kill 80% of cancers at any stage, metastatic or not, with minimal side effects. At this point in the development of medicine even twenty different loads for the same basic system to effectively tackle 80% of all cancers looks like a very good thing - and very plausible too, if the process of discovering cancer commonalities keeps going the way it is. All that is needed is one kill mechanism and a delivery platform modular enough to accept the different sensor mechanisms while still being manufacturable at low cost, such as through the use of dendrimers or viruses.
3.5) The mechanisms used by naked or blind mole rats
Naked mole rats don't get cancer, and it appears the same is true of blind mole rats, but for different reasons. Present understanding of the evolved mechanisms by which these animals manage to stay cancer-free for the several decades of their life spans, even while living in an environment that produces a tremendous amount of cellular damage, is advanced enough to have a sensible discussion on how to recreate it in humans.
This really only counts as half a potential cancer cure, however. It does seem to grant cancer immunity, or as near to it as counts, but it is a big question mark as to how hard it will be to safely have our cells start to behave in the same way as those of a mole-rat - even only temporarily. In the case of naked mole rats, the mechanism in question involves the genes p16 and p27, which suggests that it's something that could be accomplished via gene therapy, but much remains to be done in order to find out how much work there is here.
So this is certainly as intrusive a proposal as WILT, i.e. we're talking about altering human metabolism and genetic programming, but far less is known regarding how best to move forward with this strategy. Still, it is probably the case that more researchers are working on it than are in the case of WILT - the cancer community is large and well funded, and the study of mole rats is well recognized these days.