Cancer is form of cellular revolt, and a new theory finds that insight to be full of potential. Cancer is a disease as old as recorded history, and yet modern science still hasn’t managed to cure it.
There’s certainly a huge incentive to find a cure. Cancer has been a leading cause of death worldwide for decades. In the United States and other industrialized nations, cancer is second only to heart disease in regard to fatalities, claiming about 600,000 lives a year.
In pursuit of a cure, President Richard Nixon famously declared a “war on cancer” in 1971 with the National Cancer Act. Billions of taxpayer dollars have gone into fighting the disease every year since. Just for 2024 alone, the proposed budget of the National Cancer Institute is $7.8 billion.
But finding the magic bullet that will finally put an end to this brutal war has taken much longer than anticipated. Throughout the ’70s and ’80s, the annual cancer death rate only grew. Annual cancer fatalities did finally see some decline in the 1990s, but not because of new cures. Instead, the credit goes to public health efforts to cut cigarette smoking.
So what exactly have we learned in the more than 50 years since this war began, and why do we still lack better weapons to fight it? Dr. Jason Fung MD examines these questions in his book “The Cancer Code, a Revolutionary Understanding of a Medical Mystery.”
Fung says that while the miracle medicines we’ve eagerly awaited have been slow to materialize, we have gained many insights into how the disease forms and the ways in which we can prevent it.
Fung is a Toronto-based nephrologist best known for his work in treating diabetes with diet. His interest in cancer began as he was examining its connection to obesity. Large cohort studies find that individuals with severe obesity present an elevated risk of some types of cancer by up to seven times.
In 2016, after reviewing more than a thousand studies, the International Agency for Research on Cancer concluded that 13 different cancers are clearly obesity-related. “Obesity has been linked to cancer in a very strong relationship,” Fung said.
According to the National Cancer Institute, individuals who have a higher body mass index (BMI) at the time that their cancers are diagnosed, or who have survived cancer, have a higher risk of developing a second, unrelated cancer.
Of course, lots of environmental influences have also been linked to cancer formation, such as exposure to asbestos, radiation, and dioxin chemicals, just to name a few. The World Health Organization (WHO) maintains an ever-growing list of carcinogens and their cancer-causing potential.
Carcinogens of all varieties are certainly something to be mindful of. However, many of the items found on this list don’t have the effect that you might imagine. In fact, a majority of cancers can be traced back to our own daily habits.
“When they rank the population attribution risk, smoking is the highest one, at about 30 to 35 percent. A lot of the other things we think about, like chemicals and so on, are very, very small in terms of how much it contributes to a population’s risk of cancer—it’s like one or two percent,” Fung said. “There’s another massive one, about 30 to 35 percent, which is diet.”
According to the WHO website, about one-third of deaths from cancer are due to tobacco use and a high BMI, as well as alcohol consumption, low fruit and vegetable intake, and lack of physical activity. This information tells us what can trigger cancer. But big mysteries still remain. “Why does this happen? And why does it happen to so many people?” Fung asks.
Cancer is characterized by mutating cells, and these mutations can emerge anywhere in the body and allow cancer cells to develop the ability to grow beyond what the body would normally allow.
With benign cancers, a large mass may form, but it isn’t life-threatening. However, when malignant cancer develops, it invades and destroys normal, healthy tissue. In order to save a patient from a malignant mass of mutated cells, doctors rely on heavy artillery in the form of surgery, chemotherapy, and radiation.
“These are all treatments that are inherently toxic to all cells, but they kill cancer cells a bit faster than they kill regular cells. So they tend to have a lot of side effects,” Fung said. Various forms of this cancer-killing approach have been around for about a century and remain the predominant methods of treatment. Yet over the course of this killing spree, researchers have repeatedly reported that safer, more sophisticated treatments lie just around the corner.
This premise and promise came with the discovery of DNA, as researchers began to look at the genetics of cancer to better understand the nature of the disease. They found genes that controlled growth (oncogenes) and discovered mutations of these genes that resulted in excessive growth. They also discovered genes that slow down growth, called tumor-suppressor genes, as well as mutations that reduce tumor-suppressing abilities.
These observations gave rise to what is known as the somatic mutation theory, and for years, doctors and drug companies believed that this theory would lead to an efficient, high-tech approach to cancer medicine. If cancer’s growth is merely the result of mutating genes, then why not simply focus on the undesirable mutations? Fung says that the first few drugs to spawn from this strategy were remarkably successful and suggested that a cancer-free future might not be far off. One of these drugs, called Imatinib, targeted a type of leukemia and effectively cured the disease. Instead of aiming to kill cancer cells through surgery, chemotherapy, or radiation, Imatinib was designed to fix the genetic mutation that caused the disease.
“By the 1990s, we’re starting to get these treatments, and people were just incredibly excited. There was huge enthusiasm,” Fung said. The problem was that the mutations behind most cancers were far more complex than the leukemia that Imatinib targeted. The Cancer Genome Atlas project, for example—which sequenced the genes of several thousand cancer specimens to see what kind of mutations were found to occur—uncovered a vast universe of possibilities that one or two wonder drugs would never be able to reach.
A project to catalog all the known mutations found in various types of cancer in 2018 revealed about 6 million. As these dizzying details emerged, the once-high hopes of a gene-based cure to extinguish every cancer began to fade. According to Fung, somatic mutation theory advanced our understanding of cancer, but not in the ways scientists had anticipated. Instead of allowing us to decode and tweak a few problematic genes, it unearthed an untenable plethora of possibilities that could develop into cancer. The theory collapsed under the weight of all these variables and failed to deliver more than a few effective treatments for a few rare genetic cancers. “The number of genetically targeted drugs that make a difference in cancer you could probably count on one hand, because you can target one mutation, but you can’t target 70 mutations or 100 mutations,” Fung said. “So it was a dark period in oncology where the progress, which was so optimistic at the beginning, just sort of fell right down by the wayside.”
Following the dashed dreams of somatic gene theory—which had been the prevailing ideology in cancer research for more than 50 years—a new understanding has arisen. “That started to happen from about 2010,” Fung said.“It’s leading once again to huge optimism that we’ll be able to figure it out.”
This emerging ideology builds on the genetic knowledge gained from the past but also adds a more plausible understanding of why these mutations develop. While the somatic gene theory viewed cancer as a handful of random genetic accidents that somehow manage to outsmart our immune defenses, this new approach sees cancer as a means of cellular survival. “It’s not random. That’s the thing that was always very strange about the somatic mutation theory is that it was just bad luck,” Fung said. “So this opens up this huge array of possibilities of what you can do with cancer once you move past this genetic paradigm. It explains a lot about cancer.”
The developing picture of cancer comes from observations that show that cells, which originate from our own multicellular organism, begin to develop traits of a single-celled organism. They replicate endlessly and compete with neighboring cells for resources. “A liver cell is going to try and play nice with all the rest of your cells. It’s going to stay where it’s supposed to stay in the liver, and it’s going to help the lung. It’s going to help your heart, and so on,” Fung said. “A liver cancer cell acts completely different. It will grow. It will invade other things. It’s going to grab resources from other cells. It’s going to invade the lung. It’s going to do everything it can to destroy the other cells. But that’s because it’s acting as a single-celled organism, as opposed to the cooperation mandate of a multicellular organism.”
It’s the exposure of any chronic, sublethal cellular damage that’s responsible for this breakdown of multicellular cooperation, be it tobacco smoke, asbestos, or radiation. Fung compares the change from healthy cells to cancer cells to the shift that happens when a once-great human civilization crumbles. Imagine that normal cells behave much like people do in a stable human society. They live and die in predictable cycles and, in a way, benefit the body as a whole.
In the post-apocalyptic world of cancer, however, it becomes a world of every cell for itself. Once civilization breaks down, due to prolonged exposure to one cancer-causing agent or a multitude of carcinogens, sickened cells strike out on their own. They no longer follow the rules of polite society and begin acting independently, rejecting civilization in a selfish focus on their individual interests.
When this switch occurs, our immune systems come to see these cancerous cells as a separate species. “We have the immune system to patrol against these invasive species like bacteria and viruses and so on, and it will try and kill cancer cells, because it sees it as a foreign cell,” Fung said.
While the somatic gene theory imagined cancer as a kind of fluke, it failed to explain why so many people developed it. Flukes are rare, but cancer isn’t. “In fact, cancer is a very, very common occurrence,” Fung said. “It’s basically these small pockets of rebellion that are all over the body, and the immune system is there like a police force trying to stamp it out. Sometimes it’s able to hide and sometimes it gets killed, because it gets flushed out into the open.”
The knowledge that stems from this new paradigm will inevitably influence how we treat cancer going forward. Fung mentions new treatments in this vein that are currently in development, such as methods that may boost our immune systems. But he notes that the first step must always be to stop the influence that may be responsible for the body developing cancer.
“The thing is to look at the environmental causes and try to get rid of them. The most successful thing we’ve ever done, of course, is the stop smoking campaign. That’s really probably saved more lives than anything else,” Fung said. “If you recognize that obesity is related to cancer, which is already well established now, then, again, public health measures should really try to combat that.”
Any opinions, views and beliefs represented in this article are personal and belong solely to the author/s and do not necessarily reflect the opinion, views and beliefs of the organisation and employees of New Image™ International
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