We haven’t been able to cure cancer yet, but a group of researchers from London’s Francis Crick Institute says they’ve made an exciting discovery about how mutated cells develop in the lungs. The group presented its findings for review at a September conference hosted by the European Society for Medical Oncology. It claims to have cracked the code on how the disease grows in the body over time and is then “triggered” in a way that activates cancer cells years or even decades after they were first present.
Researchers initially wanted to examine potential links between air pollution and lung cancer rates. According to the Institute’s Professor Charles Swanton, their findings fundamentally redefine how we view the disease and could usher in a “new era” of cancer research. “It actually rethinks our understanding of how tumors are initiated,” said Swanton.
The study explores an emergent theory on cell mutation that runs counter to traditional belief. Conventional wisdom suggests that as a normal cell divides, it accumulates more and more mutations to its genetic code. Eventually, a point is reached where the code becomes too mutated, and cancer begins to form as a result.
This “new” theory, which was hypothesized as early as 1947 by a scientist named Isaac Berenblum, suggests that while mutation of the cell’s genetic code over time does indeed happen, the cells themselves do not begin to mutate into cancer unless triggered by an outer substance.
This research looks to build on that idea, investigating why these cells are eventually triggered and the types of substances or behaviors that set these reactions off. Researchers reviewed lung biopsy data for more than 400,000 individuals of varying age groups from England, South Korea, and Taiwan. The intent was to break them down based on the presence of a common form of air pollution called particulate matter 2.5 (PM 2.5). They found that individuals who lived in areas with a higher concentration of higher air pollution levels were more susceptible to developing lung cancer over their lifetimes.
It all has to do with how PM 2.5 is detected in the lungs. Researchers say the particulate is enough to trigger a chemical alarm, which occurs by releasing something called interleukin-1-beta into the lungs.
That substance activates the lung’s cells all at once, at which point any cells with sufficiently mutated DNA begin to multiply rapidly. PM 2.5 exposure is not a guarantee of eventual lung cancer — the particulate is everywhere there is air pollution. However, it is sufficient for setting off a chain reaction in one in every 600,000 cells in a healthy 50-year-old’s lungs.
The group’s findings have several implications for the world’s cancer fight. The data provides possible additional evidence of a defined link between air pollution exposure and lung cancer development in healthy, non-smoking humans, as highlighted in a 2021 study from the National Cancer Institute, part of the National Institutes of Health. Both studies strengthen arguments for increased national and international efforts to maintain better air quality standards.
The study also gives the medical community further hope for developing a mass-produced drug to prevent lung cancer. Similar to how specific communities take potassium iodide supplements in the event of a nearby nuclear emergency to limit exposure to certain radiations, there is the potential for the interleukin-1-beta chemical to be used as protection.
In the meantime, experts have begun wondering whether the findings could lead to similar developments with other forms of exposure-related cancers. “This mechanism may be important in other cancers with carcinogens other than air pollution,” said Richard Smith, chair of the UK Health Alliance on Climate Change.