Cancer is one of the most frightening diseases in the world today; it’s deadly and often extremely hard to cure. As such, doctors and researchers have spent enormous amounts of time and money trying to figure out exactly what cancer is, how it works, and how to cure it. The Cancer Code by Jason Fung is an overview of scientists’ major discoveries about cancer, starting from ancient times and continuing to the present day. Published in 2020, it’s one of the most up-to-date and comprehensive books on this topic.
Fung breaks down the history of cancer research into three paradigms, which this guide will refer to as Models for simplicity's sake. These Models are different ways scientists of the time understood cancer: why it occurred, how it progressed, and how it could be treated. Fung explores each of the three Models, their strengths and shortcomings, and their implications for treating cancer. In doing so, he also explains why curing cancer was nearly impossible until the last century or so, and why new discoveries provide hope for more reliable and safer treatment options in the future.
(Shortform note: In The Cancer Code, Fung explores each Model separately in a more-or-less chronological order. This is effective because it provides a clear and logical timeline of cancer research.)
Fung is a nephrologist specializing in nutrition science and metabolic diseases. As such, he brings a unique perspective to the fight against cancer. He puts special emphasis on how cancer uses our natural bodily functions to grow and spread, as well as how we can adjust our lifestyles to reduce our chances of developing it.
In this guide, our commentary will expand on some of Fung’s key ideas, offer counterpoints to others, and suggest some other books for further reading on this complex topic. We’ll also examine the current effectiveness of a number of cancer treatment methods and what recent discoveries might imply about future treatment options.
In order to treat cancer, scientists first had to answer the question: What is cancer? In other words, they needed to figure out what was going wrong with patients’ bodies so that they could determine how to fix the problems.
Fung says that scientists’ earliest understanding of cancer—dating at least back to Ancient Egypt—was simply a description of its symptoms, most notably the tumors that form in patients’ bodies. As such, many scientists developed an understanding of cancer as an abnormal growth that would eventually kill its victim. Others believed that cancer was caused by an imbalance of black “bile” in the body.
(Shortform note: Both this book and Siddhartha Mukherjee’s The Emperor of All Maladies discuss the Ancient Greek belief, dating to around 130 AD, that cancer was caused by an imbalance of black bile (which we now know doesn’t exist). However, Mukherjee adds that the theory—though wrong—was extraordinary for its time because it recognized that cancer was a systemic problem rather than a localized growth. Once the “black bile” theory was disproven, it would be nearly two thousand years before modern doctors rediscovered that fact.)
Working from this very early and incomplete model, it seemed like cancer should be treated by destroying or removing the tumors. However, as Fung points out, a simple description of cancer’s symptoms didn’t address how or why those tumors formed, so doctors’ attempts at treatment almost invariably failed. Indeed, up until the last 100 years or so, medical texts all agreed that cancer was incurable.
(Shortform note: Hippocrates, an ancient Greek physician who’s often called the father of modern medicine, was one such doctor who wrote about the futility of trying to cure cancer. Instead, he urged doctors to offer comfort to their patients—perhaps one of the earliest examples of hospice care. Until quite recently, with enormously improved knowledge and modern treatment options, relieving symptoms and keeping patients comfortable was the best doctors could do when faced with cancer.)
This early understanding of cancer merely as a harmful tumor was woefully incomplete. Thanks to decades of dedicated research, we now have a much better understanding of what cancer is and how it works.
Fung tells us that cancer is not a single disease, but rather a type of disease. Almost every cell in the body has the potential to turn cancerous, and each cancer will be different depending on where it’s located and what type of cells are affected. However, all cancers have some things in common:
Rapid, endless cell division. Cancer cells divide quickly and ignore the chemical signals that normally cause that process to stop. Furthermore, while there is normally a limit to how many times a particular cell can divide, cancer cells can keep doing so forever. This is because cells contain structures called telomeres at the ends of their chromosomes; normally, telomeres shorten each time a cell divides, and the cell undergoes apoptosis (cell death) once the telomeres become too short. However, cancer cells use an enzyme called telomerase to rebuild them, meaning the malignant cells are functionally immortal.
(Shortform note: Telomerase is one reason why cancer grows so uncontrollably, but it also provides a promising target for cancer therapy. Healthy cells don’t use telomerase—so, if doctors found a way to stop telomerase from working, the cancer cells would rapidly divide until they die while normal cells would be unaffected. However, as of writing this guide, telomerase-targeted therapy is still being studied for effectiveness and safety, and therefore isn’t ready for use on patients yet.)
Metastasis and invasion. Cancerous cells break away from the primary tumor and travel throughout the body, creating secondary tumors in other locations. Fung says that this process, called “metastasis,” is what separates benign tumors from malignant ones and what makes cancer so dangerous. A benign tumor can grow to enormous size without causing much harm to the patient, but a metastatic tumor—one that sheds cells into different types of tissue where those cells don’t belong—is deadly.
(Shortform note: Cancer cells seem to possess a near-limitless ability to invade other tissues. For example, The Immortal Life of Henrietta Lacks describes how cells cultured from a particular strain of cancerous tissue attached to tissue samples taken from other people, and even from other species. Any sample contaminated in this way eventually became overrun by those cancerous cells.)
Co-opting nutrients and energy. Cancerous tumors induce nearby blood vessels to grow throughout the tumor, a process called angiogenesis, thereby providing the malignant cells with oxygen and other nutrients. Also, cancer cells usually use a fast but inefficient method of producing energy, meaning that they use up much more glucose (sugar) than ordinary cells.
(Shortform note: Because tumors need constant blood flow to grow and spread, one method of treating cancer involves using angiogenesis inhibitors to starve the tumor of nutrients and thereby stifle its growth. However, since angiogenesis inhibitors don’t directly kill cancer cells, they often have to be given over a long period of time and in conjunction with other treatments to fully cure cancer.)
In short, cancer is a type of disease where your own cells parasitize your body. Malignant cells grow, divide, and spread, fueling themselves by consuming enormous amounts of energy and nutrients, all while evading your natural defenses.
Early doctors’ concept of cancer as simply a harmful tumor wasn’t enough for them to truly understand or treat it. Fung tells us that it took until the 1900s—when scientists began exploring the field of genetics in earnest—to develop a more accurate model of cancer.
This new model, which we’re calling Model 2, described cancer not merely as a growth but also as the result of harmful mutations in a cell’s DNA. Those mutations caused normal processes, such as energy production and cell division, to run wild.
In short, Model 1 described cancer’s symptoms, while Model 2 described its mechanisms: the biological processes behind the disease. By learning how malignant cells functioned, scientists believed that they would be able to develop treatments that disrupted those functions, thereby curing the disease.
What Are Mutations?
In simple terms, a mutation is a change to a cell’s DNA (its genetic information). DNA carries instructions for building various proteins; those proteins go on to perform countless different functions, including transporting nutrients, protecting the body from infection, and providing the structural framework for new cells. Because DNA is like a blueprint for proteins, changes to the DNA—in other words, mutations—can change how those proteins are built and how they function.
Mutations are actually quite common and, in most cases, are harmless. However, some mutations give rise to proteins that don’t function correctly, which have harmful effects on the people carrying those mutations. Common examples of genetic disorders caused by mutations include Down syndrome, cystic fibrosis, sickle cell anemia, and—as Fung says here—cancer.
Fung says that Model 2 is based on the idea of somatic mutations: changes in the DNA of somatic cells, which are any cells other than gametes (sperm and eggs). The fact that these mutations don’t affect gametes is important because it means cancer can’t be inherited—for example, a person with lung cancer won’t produce a child with lung cancer.
German biologist Theodor Boveri developed an early version of this theory in his book The Origin of Malignant Tumors, published in 1914. In this book, Boveri observed that the human body must have mechanisms both to promote cell growth and to restrict it. Without such mechanisms, numerous normal processes would be impossible—for example, growing from a child to an adult and having that growth stop once you reach maturity. Therefore, Boveri reasoned, mutations to the genes that control cell growth could cause malignant tumors to form.
Cancer researchers in the 1970s discovered several genes like those Boveri had hypothesized, and many more have been found since. Cancer almost always involves mutations to these growth-promoting genes (now called oncogenes) and growth-restricting genes (called tumor suppressor genes). In short, malignant tumors form because mutated oncogenes promote growth too much, and mutated tumor suppressor genes are unable to prevent that growth.
Genetic Risk Factors for Cancer
In saying that the vast majority of cancer results from somatic mutations, this theory understates the impact that genetics can have on cancer rates. Fung touches on this topic, saying that genetics account for approximately 5% of all cancers, but that’s on the low end of usual estimates.
Other sources indicate that germline mutations—changes to the DNA of sperm and egg cells, which will be passed on to offspring—could account for as many as 20% of all cancers. More common estimates put the number somewhere in the 5 to 10% range, depending on the specific mutations and cancer types being studied.
Knowing what genetic risk factors you carry is important because it allows you to more effectively manage those risks. For example, smoking is (of course) harmful no matter what genes you have, but if you’ve got a family history of lung cancer then it could be especially dangerous for you.
A key point of the somatic mutation theory is that cancer can’t be directly passed down to offspring (although various genes do make certain types of cancer more likely). But if bad genes don’t cause cancer, what does? Fung tells us that cancer is almost always the result of environmental factors called carcinogens—literally, “tumor creators.”
The list of known carcinogens is enormous and constantly growing. Some of the best-known carcinogens include tobacco, asbestos, and radiation (such as x-rays or UV radiation from the sun). Others include soot and wood dust, certain drugs, and even some pathogens such as the Rous sarcoma virus and human papillomavirus (HPV). The common thread between all of these carcinogens is that they damage or destroy cells. Sometimes the body fixes that damage incorrectly, causing slight changes in the genetic material—in other words, mutations.
(Shortform note: Despite carcinogens being so common and numerous, determining whether any given substance is carcinogenic is a difficult process. Biologists can test carcinogens directly on tissue samples in the laboratory, but they generally use very high doses of the substance to make the results more obvious. This means that lower levels of exposure might not be harmful at all—for example, we know that soot and smoke can cause cancer, but that doesn’t mean that sitting around a campfire is dangerous. Another method is for epidemiologists to look for areas with unusually high rates of a particular cancer, then look for unique environmental factors that could be causing it. Numerous different agencies are needed to research possible carcinogens and to review the results of such research.)
Many of these mutations are harmless, and your body’s natural defenses usually identify and destroy any mutations that arise. However, over time and with repeated damage to the cells, it becomes more likely that at least one of those mutated cells will turn cancerous. In short, every time the body has to repair itself (for any reason), there’s a very small chance that those repairs will produce malignant cells.
(Shortform note: Since the odds of any given cell turning malignant are so low, it might seem strange that cancer is as common as it is today. However—as Fung says in a later chapter—even under normal conditions, the human body produces around ten billion new cells every day. Damage from carcinogens further increases that number. Therefore, cancer is what statistician Nassim Nicholas Taleb would call a Black Swan: an event that, while extremely rare and impossible to predict, is very likely to happen eventually. Furthermore, Black Swans tend to have enormous effects when they do arise—like how most mutations have minimal impact on a person’s health, but cancer’s specific mutations lead to a devastating and fatal disease.)
The good news, according to Fung, is that knowledge of carcinogens is the best weapon we have in the fight against cancer, as well as the easiest one to use. After all, it hardly matters what specific cancer-causing mutations UV radiation produces, or how to treat the disease those mutations cause, if we just wear sunscreen to make sure that damage doesn’t happen in the first place.
(Shortform note: Fung’s insistence that preventing cancer is more effective than curing it isn’t just hypothetical; there are many studies showing how cancer rates decrease when carcinogens are more strictly controlled. For example, rates of lung cancer in the US decreased sharply after tobacco companies were forced to stop airing commercials on television, and mesothelioma rates saw a similar decline with increased regulations on asbestos. Of course, it’s common sense that reduced exposure to carcinogens results in lower rates of cancer, but it’s reassuring to see hard data bearing out that logic.)
Fung says that Model 2, while technically accurate, still fails to explain what cancer really is. It’s like trying to understand how a tree grows by cataloging every leaf on it—we’d learn a lot about individual leaves, but very little about how and why the tree itself grows. More to the point of cancer research, we wouldn’t learn anything about how to stop or reverse the tree’s growth.
Indeed, despite scientists mapping hundreds of cancer genomes, finding countless cancer-related mutations, and promising personalized treatment that targeted each patient’s specific form of cancer, a 2018 study found that less than five percent of cancer patients benefited from treatments targeting specific mutations. In other words, decades of research and billions of dollars in funding had failed to produce results.
(Shortform note: As a counterpoint to Fung’s pessimism here, in The Emperor of All Maladies, physician Siddhartha Mukherjee tells us that cancer death rates in the US decreased by an unprecedented 15% between 1999 and 2005. By 2018, they had decreased by 30%. So, while attempts to develop personalized and targeted treatments mostly failed, the knowledge that researchers gained during that time had an enormous impact on the fight against cancer.)
In addition to failing as a basis for treatment, Fung says that Model 2 also fails as an explanation of cancer. The somatic mutation theory can’t explain why cancer is so common, or why there are so many different types of cancer that all share the same characteristics.
The odds of numerous specific mutations—uncontrolled growth, hiding from the immune system, leeching the body’s nutrients, and so on—all arising in a single cell are incredibly low. Therefore, random chance can’t explain why cancer is so prevalent among modern-day humans.
(Shortform note: If it’s statistically impossible for random mutations alone to cause cancer, why did it take so long for researchers to reject the somatic mutation theory? In The Structure of Scientific Revolutions, Thomas Kuhn explains that anomalies—scientific observations that the current paradigm fails to explain—are often ignored since scientists are hesitant to reject old, established knowledge. In this case, some argue that scientists have in the past ignored or misinterpreted data that contradicts the somatic mutation theory. This includes a study that found that nearly all of the same somatic mutations occur in people with and without cancer, casting doubt on the assumption that these mutations are the primary cause of the disease.)
Having dismissed both of the previous models, Fung presents a newer hypothesis. Model 3 was not proposed by a biologist, but by physicist Paul Davies, whom the National Cancer Institute reached out to in 2009 in the hope that an outsider’s viewpoint could provide some new insights about cancer.
Model 3 suggests that cancer is an atavism: an evolutionary throwback in which ancestral traits reemerge in modern organisms. In this case, Davies proposed that cancer is the re-emergence of traits from the earliest single-celled organisms, caused by evolutionary pressure from carcinogens. (We’ll explain this evolutionary pressure in more detail later.)
In short, Model 1 described what cancer is, Model 2 described how it works, and now Model 3 offers a theory about why it happens.
(Shortform note: In The Selfish Gene, biologist Richard Dawkins gives an idea of what these earliest organisms might have been like. He describes simple molecules that gained the ability to replicate themselves using resources in the environment. Eventually, those easily-available resources were depleted and the replicator molecules needed to compete with each other. As a result, they evolved traits like protective protein membranes, as well as more efficient ways to find and consume nutrients so they could continue replicating themselves. In short, they became simple—but fully functional—self-contained organisms.)
To support this idea of cancer-as-atavism, Fung points out that cancer cells act like simple organisms: They grow, feed, reproduce, and evolve. Therefore, rather than Model 2’s concept of random mutations causing cells to run wild, this hypothesis says that cancer’s behavior is actually extremely logical and focused on survival; not the survival of the host, but of the cancerous “organism.”
(Shortform note: At the beginning of The Selfish Gene, Dawkins gives a biologist’s answer to the age-old question of why life exists: to survive and reproduce. Model 3 is suggesting that’s exactly what cancerous cells are doing—surviving and reproducing by any means necessary. That’s why Fung says they behave like organisms.)
Atavism explains why cancer can be found in nearly every animal species on Earth: It’s because the traits of cancer come from our oldest common ancestors. Furthermore, there’s genetic evidence for this theory in addition to the behavioral evidence—mutations in cancerous cells are most likely to affect those genes that evolved shortly after the first multicellular organisms emerged, effectively reverting them to the genes of single-celled organisms.
(Shortform note: The human genome contains an incredible amount of what, until recently, scientists called “junk DNA”—genetic material that doesn’t seem to serve any purpose. While we’ve recently discovered that some of this DNA does serve a purpose within the body, that “junk” also includes pseudogenes, which scientists believe are essentially evolutionary leftovers. In other words, pseudogenes are broken or suppressed copies of genes that our ancestors carried. Model 3, cancer-as-atavism, could mean that some of those suppressed genes are reactivating.)
In other words, malignant cells didn’t need to evolve cancerous traits from scratch, because the genes for the traits were already in their DNA. The cells just needed to evolve (or devolve) in such a way that those genes reactivated.
A New Model, or Corrections to An Old One?
While Fung presents Model 3 as a revolutionary new understanding of cancer, we could also see it as simply an updated version of Model 2. To illustrate this point, Thomas Kuhn’s The Structure of Scientific Revolutions says that there are two ways science progresses:
Method one: puzzle-solving. This is part of what Kuhn refers to as “normal science,” where scientists steadily build upon our existing knowledge. They may find the need to make minor corrections, but it isn’t necessary to completely overturn our current understanding of the topic.
Method two: revolution. This happens when scientists find something that the current model can’t explain, and a minor correction isn’t sufficient. For example, when astronomers found that the Earth-centric theory of the solar system couldn’t predict the movements of stars and planets—no matter how much they tweaked the theory and played with the numbers—it eventually became clear that the opposing Sun-centric theory was more accurate.
In this case, Fung presents the Atavistic Theory of cancer as a revolution, overthrowing the established Somatic Mutation Theory. In reality, the Somatic Mutation Theory wasn’t wrong, just incomplete; cancer is the result of mutations, but those mutations are less random and less extreme than scientists previously thought. That solves the puzzles of why cancer is so common and why different forms of cancer have such strong similarities.
Fung says that this model of cancer as an evolving species solves the two major shortcomings of the somatic mutation theory. First, cancer does not spring up at random—the elements of cancer are already present in our DNA, so all the cell needs to become malignant is for those genes to reactivate. This provides a much more satisfactory answer to cancer’s prevalence than random chance could.
Second, Model 3 reveals that genetically-targeted treatments are mostly ineffective because of cancer’s genetic variation. After turning cancerous, cells continue to divide and mutate extremely quickly, meaning that even cancerous cells within a single patient can have countless different genetic traits. So, while a targeted treatment will kill many of the malignant cells, it’s very likely that some will be resistant to it. Even worse, those surviving cells will continue to reproduce, meaning that cancer can evolve to resist any given treatment.
Therefore, to cure a patient and avoid relapse, doctors must either find and target the root mutation—the original genetic change that all the cancer cells share—or use a battery of different treatments to ensure that every malignant cell is destroyed.
Counterpoint: Model 3 Isn’t Totally New
To pose a partial counterpoint to Fung, doctors have known for decades that not all cancer cells respond to treatment the same way and that multiple treatment methods are much more effective than any single targeted treatment.
In The Emperor of All Maladies, Mukherjee describes a number of advancements in treatment that took place in the 1950s and early 1960s. Doctors found that using cocktails of multiple chemotherapy drugs worked significantly better than any single drug and that using radiation therapy in conjunction with chemotherapy further increased the treatment’s effectiveness. They also found that, for a patient to be truly cured without relapsing, every trace of cancer had to be wiped from that patient’s body.
So while doctors might not have been thinking of cancer as its own species, they certainly knew that it had genetic variation, as well as the ability to reproduce and adapt, and they treated the disease accordingly.
Using this new model of cancer as a separate species, Fung describes how the disease progresses in three phases:
We mentioned before that there are countless known carcinogens, and that carcinogens cause damage that the body sometimes repairs incorrectly. However, Fung says that viewing cancer as an evolving species provides a more complete explanation of how carcinogens work: carcinogens create evolutionary pressure at the cellular level.
Every known carcinogen causes some kind of damage—the sun damages your skin, tobacco smoke damages your lungs, and so on. The damage isn’t serious enough to kill every cell the carcinogen reaches, but it does kill some of them, leaving the surviving cells to reproduce. The cells most likely to survive are those with the traits of cancer: rapid reproduction, the ability to ignore signals that trigger cell death, the ability to co-opt the body’s resources for their own survival, and so on.
In short, cells evolve cancerous traits because they’re very effective survival mechanisms.
Evolution: Survival of the “Good Enough”
If we consider cancer as an independently evolving species, it might seem strange that it would evolve in such a way as to kill its host (and therefore itself). However, evolution isn’t intelligent and it doesn’t plan ahead; it simply means organisms that are able to survive and reproduce in their current environment will do so.
While evolution is commonly framed as survival of the fittest, some biologists argue that it would be more appropriate to call it survival of the adequate. In other words, evolution doesn’t try to create some hypothetical perfect organism (for instance, a cell that could survive carcinogens without turning malignant); it’s the process by which “good enough” organisms create more “good enough” organisms.
In short, carcinogens create an environment where cells with cancerous traits have significant advantages over cells without those traits. The fact that those malignant cells might kill their host years down the line is irrelevant—they’re able to survive and reproduce, and therefore, they do so.
Growth factors are naturally-occurring chemicals and proteins that, as the name suggests, stimulate cell growth and cell division. Every multicellular organism needs growth factors; however, since rapid cell growth is the primary hallmark of cancer, growth factors create an ideal environment for cancerous cells to flourish. More cells also mean more mutations—more genetic diversity—which helps to prepare the cancerous “species” for the next step in its evolution.
The body’s growth factors are controlled by nutrient sensors that detect the presence or absence of various nutrients in the body. When nutrients are plentiful, the growth factors activate; when nutrients are scarce, the growth factors deactivate so the body can focus on conserving energy and culling damaged cells.
(Shortform note: Interestingly, while Fung says Model 3 proves that genetically-targeted cancer treatments won’t work, others believe that discoveries about how cancer grows and feeds could provide exactly the sort of genetic targets researchers have been looking for. Specifically, if cancer cells all use the same kinds of nutrient sensors and growth factors, then developing a way to disrupt that process—for example, with a drug that binds to a nutrient sensor and blocks it—could allow doctors to “starve” the cancer and kill it, hopefully with minimal side effects to the patient.)
According to Fung, growth factors and nutrient sensors explain why cancer is so much more prevalent in Western countries: Our diets contain a lot of processed foods with easily-accessible nutrients, meaning those growth factors are almost always active. As a result, our bodies create cells more rapidly and destroy mutated cells more slowly than usual.
With this in mind, Fung suggests that reducing our consumption of processed foods and intermittent fasting can help to prevent cancer by reducing growth factor activity. He puts particular emphasis on controlling our insulin levels; eating a lot of simple sugars causes the body to produce a lot of insulin, which acts as a growth factor and increases the likelihood of cancer.
(Shortform note: Fung is a nephrologist—a kidney doctor—with a particular interest in dietary health and metabolic diseases such as type 2 diabetes. Therefore, not surprisingly, he spends a great deal of time discussing the possible connections between diet and cancer. However, except for certain types of meat, there’s little scientific evidence that any particular dietary factors increase the risk of cancer. Currently, the only commonly accepted connection between diet and cancer is that obesity is associated with increased cancer risk.)
As a cancerous tumor grows, it also metastasizes. This means that the tumor sheds cells into the blood, where they are carried to different parts of the body. Those cells invade tissue in other places and give rise to new, secondary tumors.
However, Fung says that the process of metastasis is more complicated than many people think. The cells shed by the primary tumor face enormous evolutionary pressures: First of all, the immune system will find and destroy most of these cells while they’re still in the blood. Then, those few that can evade the immune system are still unlikely to survive—for example, a cancer cell that evolved in the liver wouldn’t be well suited to grow in the stomach.
Therefore, rather than simply spreading out from the primary tumor, metastasis can be a circular process. Malignant cells—further evolved from the evolutionary pressures they faced while traveling through the body—sometimes return to that first tumor and reattach to it in a process called tumor self-seeding. Now, these new cells must compete with the original cancer for resources; only the cells that reproduce most quickly and invade other tissues most effectively will survive.
Over numerous cycles, this process eventually gives rise to cells that are strong and aggressive enough to survive in other parts of the body, and those are the cells that go on to form secondary tumors. In other words, cancer doesn’t just fight against the body’s defenses; it’s in constant competition with itself to produce the hardiest and most virulent organisms possible.
Treatment Implications of Self-Seeding
As it turns out, cancer cells don’t return to the original tumor simply by chance; one study observed that tumors send out chemical signals encouraging circulating cancer cells to reseed it. That same study found that—as Fung says—self-seeding increases how quickly cancer grows and how effectively it performs other functions like angiogenesis.
As with every new discovery about how cancer grows and develops, doctors are hopeful that the discovery of self-seeding will provide new opportunities for targeted treatments, allowing them to fight cancer more effectively and with fewer harmful side effects. By preventing self-seeding, it may be possible to slow or even stop cancer’s growth and spread throughout a patient. It should also prevent local tumors from reappearing after surgical removal, as commonly happens with breast cancer.
Fung says that this new understanding of cancer—as an independent, evolving species—may represent a turning point in the fight against it. With a better understanding of how cancer operates and how the body fights against it, there is hope for more effective treatments with fewer side effects.
One promising option is immunotherapy: activating and strengthening the patient’s natural immune response. Fung points out that cancer doesn’t simply overwhelm our body’s defenses like a deadly infection does; instead, it evolves methods to hide from those defenses.
Therefore, forcibly activating the immune system and teaching it to target cancer cells—essentially, giving the patient a “cancer vaccine”—is highly effective. Furthermore, regardless of how the malignant cells continue to mutate, the immune system will still recognize them as foreign and destroy them.
(Shortform note: Immunotherapy is currently used as a cancer treatment, with mixed results. Depending on the type of cancer, immunotherapy drugs are effective in anywhere from 20% to 50% of cases. One study found that immunotherapy increased the five-year survival rate of a certain type of lung cancer from 5.5% to 15%. In short, immunotherapy can be effective, but it doesn’t seem to be the type of silver bullet that Fung implies it could be.)
Another strategy Fung discusses is adaptive therapy, developed by oncologist Robert Gatenby. Adaptive therapy uses standard chemotherapy treatments, but it aims only to keep the cancer at a manageable level instead of wiping it out entirely. This goes against the currently accepted practice of subjecting cancer patients to the strongest doses of drugs and radiation that they can withstand.
Gatenby’s reasoning is that the usual approach to chemotherapy creates extremely strong evolutionary pressure; if any malignant cells survive, they’re sure to be the ones most resistant to treatment, and those cells then pass their resistance on to a whole new generation of cancer.
Therefore, he believes that lower, less frequent doses of chemotherapy will be more reliable in the long run—there will be less pressure for the cancer cells to develop resistance to the treatment. Furthermore, drug resistance is costly in evolutionary terms; in the absence of those drugs, the cells without such resistances will be more successful. In this way, adaptive therapy seeks to turn cancer against itself by allowing the non-resistant cells to outcompete the resistant ones, then introducing another round of chemotherapy to beat them back.
While cancer is unlikely to be eliminated completely by such a strategy, Gatenby hopes that it will keep the disease stuck at an easily-managed level. This could allow more cancer patients to live longer and more normal lives than current chemotherapy methods provide.
(Shortform note: In Gatenby’s paper proposing adaptive therapy, he also said that, in some cases, he was able to achieve a stable tumor size with decreasing chemotherapy doses and increasing intervals between treatments. In other words, far from evolving resistance to chemotherapy, the cancer was actually becoming more vulnerable to it as non-resistant cells repeatedly outcompeted resistant ones. Gatenby, while acknowledging that this is a very early result and that his method needs a great deal more study, said that his results suggest adaptive therapy could eventually cure some cancers entirely—the disease would reach a point where all of the malignant cells are susceptible to chemotherapy, and would be wiped out by the next treatment.)
These methods represent a major change from previous strategies, which unknowingly played to cancer’s greatest strengths: reproduction and evolution. Currently, the favored strategy is to simply blast away at the disease with toxic drugs and radiation until nothing remains, but even this approach requires doctors to overcome cancer’s constant replication and mutation—not to mention the devastating side effects the treatment regimen has on the patient.
Fung believes that, with this new model of cancer as an evolving species, there is hope for the future of cancer treatment. He acknowledges humanity still has a long fight ahead of it, but he says we’ve started gaining ground in that fight for the first time.
(Shortform note: Even with all of these new discoveries and theories, developing treatments for cancer is a slow and expensive process. New drugs require numerous studies for effectiveness and safety before they can even be tested on humans, and even then, clinical trials must be done carefully and under strict regulations.)
The Cancer Code divides cancer research into three different Models—though each new Model doesn’t truly replace the old one so much as build upon it. Reflect on what you’ve learned about cancer from these Models and consider how you might apply that knowledge in your everyday life.
What was the most interesting or surprising thing that you learned about cancer from this guide?
Based on what you’ve learned, what’s one thing you could do to reduce your chances of developing cancer? For example, is there a particular carcinogen you could avoid?
Do you think it will ever be possible to fully cure cancer? Why or why not?