A Cancer Researcher Discusses the State of Cancer Research

Risk of cancer is very important in aging; as we become older we accumulate mutations in nuclear DNA at an accelerating rate. Sooner or later the right combination occurs to create a cancerous cell, set to divide without limit, its safeguard mechanisms broken. If that cell is not caught and destroyed by the immune system then its progeny form a tumor and mutate further at an increased pace. The tumor eventually grows large enough to disrupt a nearby vital organ or spreads copies of itself to a place where that can happen, and that is the end of the story for you. Cancer can happen at any age, but it is predominantly an age-related disease because the odds are based on the level and pace of DNA damage.

Any future rejuvenation toolkit has to incorporate a robust cure for cancer. Some combination of mature next generation targeted therapies and advanced detection for early stage, more easily cured cancers should be good enough when we're talking about supporting the addition of a few decades of additional healthy life expectancy. Being able to control 95% of all cancers would probably buy that much runway for most people, provided all the other necessary components of rejuvenation were also present and available. Once we consider more time spent alive and accumulating DNA damage, something more effective will be needed. Perhaps this will prove to be along the lines of blocking all telomere lengthening mechanisms as needed, or perhaps the current genetic revolution will lead - a few decades from now - to nanomachinery or gene therapies capable of cell by cell reversion of genetic alterations to a known good base sequence.

If we believe that a robust cancer cure is good enough to cover a few decades of additional healthy life added to the present human life span, then we shouldn't be all that worried about the state of progress in cancer research. Or at least, there is little we can do as advocates for longevity science that isn't already being done a hundred times more loudly and effectively by the present cancer advocacy community. Cancer research is very well funded indeed, and largely moving in the right direction. A great deal of innovation is taking place in the laboratory, for all that the present state of regulation makes it very slow going indeed for any of that to arrive in the clinic. If, as is the case at the SENS Research Foundation, we think that more than merely robust cancer cures are needed, then there are other lines of work to support, based on the aforementioned blocking of telomere lengthening.

At the detail level, and in the mainstream of cancer research, success over the next decade or two is driven by the degree to which researchers can find and exploit commonalities in cancer. Producing a treatment that works for twenty types of cancer is much better than one that is restricted to a single type. There are so very many types of cancer that meaningful progress over the field as a whole will be overwhelmingly determined by success or failure to identify and exploit such commonalities. Not all that many people are willing to go the whole hog and work on turning off telomere lengthening, which is the one clear thing that all cancers require, but in recent years scientists have identified a number of different mechanisms that may work as therapeutic targets for fairly broad collections of cancers. It is still very early days when it comes to seeing what will work and what will not, however. The researcher quoted in the interview below is working on one such cancer commonality, but like most of the mainstream he is fairly pessimistic on whether or not these commonalities will be enough:

Will there be a cancer cure in our lifetimes?

In graduate school, Barrie Bode conducted research aimed at expanding knowledge of the biochemistry and metabolism of a normal human liver. He was particularly interested in how the liver regulated the transport and metabolism of an amino acid known as glutamine. A year after earning his Ph.D., he came across two lines of cells from a cancerous liver. On a whim, he measured the rate of glutamine import into those cancer cells - and was stunned to find it was about 10 times higher than normal. That observation changed the course of his life's work. It also led to the identification of two specific amino acid transporters that are elevated in a wide spectrum of primary human cancers and aid tumor growth. For the past two decades, Bode has been working to develop highly targeted therapies to slow the uptake of glutamine and other nutrients that feed cancer.

"I think my research group is working in one of the hot areas of cancer research - identifying unique metabolic changes in cancer and developing ways to slow, stop or exploit these changes. We're not alone in this pursuit. These are exciting times. The scientific knowledge emerging annually is staggering. And it's really revealing the complexity of these diseases that we collectively call cancer. We are light years ahead of where we were just 20 years ago and are learning new things about the biology of cancer literally each week. In fact, we're generating so much data now - including sequences of nucleic acids, sequences of expressed proteins within a tumor, the chemical signatures of metabolic systems - that there is a little bit of a bottleneck. It's not a dearth of data that's limiting medical researchers but the necessary analyses of the available and emerging data. Those analyses will ultimately reveal cancer's complex fabric and vulnerabilities.

"I do not think there will be a cure for cancer in our lifetimes. It's still going to be a long road, but there is good news for cancer patients. Cancer is just a catchall phrase for dozens of different diseases that have the same endpoint - uncontrolled growth of tissue driven by mutated cells. Each cancer is complex and different, and even within a tissue there are distinct forms or cancer - different kinds of colon, breast, liver and brain cancers, for example, all driven by unique mutations and behaviors. Some types of cancer might be cured - that's happened already. But new pharmaceutical cures are rare. Over the next century, I'd say the chance is very remote that we will find a single 'cure for cancer.' Instead, treatments will become more refined and targeted, informed by the science and technologies that are available so that cancer can be managed much like other diseases, such as heart disease and diabetes. The plasticity, or ability to change, of cancer cells will require that these treatments be modified over time.

"There is a lot of cancer research going on, but there could be much more. The National Cancer Institute receives about 11 percent of the National Institutes of Health budget. The NIH budget likewise is about 10 percent of the national defense budget. So by deduction, we're funding cancer research at a penny for every dollar of defense."


Well, even if we don't have a robust cure for cancer soon enough, we still have cryonics as a last resort.

Posted by: Antonio at March 12th, 2015 5:36 AM

Hopefully there are at least better, more specialized cancer treatments that work far better than what we use today. Especially since while in theory cryonics might work, there has been nothing to suggest or prove that it actually will.

Posted by: Ham at March 12th, 2015 7:06 AM

There are multiple ways for cancer to develop resistance to targeted therapeutics.

Also, replicative mutations are unavoidable. They are in a sense a side-effect of evolution, which cannot proceed without them. It is probable that they play a larger role in cancer than previously believed. Calling mutations that arise during normal stem cell division in the absence of exogenous factors 'damage' is also mistaken

Posted by: rdg at March 12th, 2015 9:56 AM

"Calling mutations that arise during normal stem cell division in the absence of exogenous factors 'damage' is also mistaken"

What gives you this idea? Are you suggesting that the mutations are beneficial in a single organism? (They're not) They might be unavoidable, in much the same way that driving a car gradually puts wear on it, but that does not mean that this wear does not consist of changes that are deleterious to cell functioning: i.e. damage.

And why would exogenous factors matter? Potentially lethal mutations can be caused by any mutagen, endogenous or exogenous. Even if cellular division were perfect, the decay of totally unavoidable Potassium-40 would cause them.

Posted by: Slicer at March 12th, 2015 11:59 AM

It has already been proven (by microscopy and other means) that a cryonized brain doesn't suffer irreparable damage (that is, loss of structural information). It's true that no cryopatient have been reanimated yet, but some tissues and small organs (like a rabbit's kidney) have been sucessfully thawed to a fully functional state. So cryonics reanimation isn't physically/biologically impossible, simply we don't have the technology yet.

Posted by: Antonio at March 13th, 2015 6:38 AM

I don't know if that's been proven at all. There's no proof one way or the other if cryonics will prevent information theoretic death, or if it actually can cause it. They aren't even sure if information-theoretic death is something that actually happens. It's all speculative at this point sadly.

Posted by: Ham at March 13th, 2015 10:07 AM

Ham: Of course information-theoretic death exists. We can see it in hard drives, and it's why alphabet agencies have such firm rules for data destruction. Smashing a hard drive only generally breaks up the data, with some minor destruction. Scratching the platters destroys the scratched areas. Tossing it in a shredder should render everything unusable, but to really wipe a hard drive, your best choices are magnetism and heat.

In human brains, the main way the information gets wiped is decomposition. Cryonics prevents this.

Posted by: Slicer at March 13th, 2015 12:50 PM

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