Both of my grandfathers died from cancer—one before I was born, the other when I was only three. For decades after, I’d fortunately been spared from thinking much about cancer. That changed a few summers ago, when my best friend from college texted me with some alarming personal news: Stage 3 breast cancer. At age 31.

Caught wholly unprepared, I quickly Googled what “Stage 3” meant.

Oncologists classify tumors in four distinct stages. Stage 1 is relatively easy to treat: When a tumor forms, it’s often a small and localized mass of cells. Issues arise in Stage 2, when the tumor grows in size and encroaches on surrounding tissues, potentially gaining invasive properties. In Stage 3, a startling development can occur, termed “neoangiogenesis,” where the tumor generates its own network of blood vessels to supply its cells with the energy and nutrients they need to persist and divide with great ferocity. In Stage 4, “metastasis,” the tumor gains the ability to move about the body and colonize other tissues. This devastating final stage renders the cancer incredibly difficult to defeat.

Okay, I thought. Stage 3 sounds bad, but it could be worse.

Stage 3 is considered an “advanced” form of breast cancer, but nowadays the 5-year survival rate is 87%, thanks to modern treatments. Chemotherapy and radiation target and kill cancer cells. Hormone therapy interferes with the tumor’s ability to grow. Immunotherapy supercharges the body’s natural defenses against cancer or allows other drugs to work better in combination. And precision surgery can physically remove malicious masses from the body. Despite these medical marvels, approximately one in six people die of some kind of cancer, with some 600,000 Americans dying last year alone.

A broader cure for cancer is the elusive holy grail of oncology, a field that attracted $242 billion in 2024 and produced over a million research papers in the past decade—none of which I had read before 2025.

As a space scientist, I toil in a distant corner of academia. But, to my surprise, one oncology study caught my eye last year. That paper, published in the journal Evolution, Medicine, and Public Health by a team of biologists led by Frédéric Thomas, suggested that understanding tumors through a recently developed evolutionary framework could yield innovative cancer therapies.

My jaw dropped as I devoured the paper. The radical evolutionary framework these biologists leveraged was…mine.

Skyward Inspiration

In my astrobiology lab, I work on developing ways to search for signs of extraterrestrial life. My research spans modernizing life-detection techniques for solar system exploration to understanding how biospheres might appear on planets orbiting distant stars. 

Every night, I’d drift off dreaming of finally finding life on another world. Every morning, I’d rise to confront the sobering reality that we don’t even know what life is. It’s this grand philosophical problem that draws me to astrobiology.

All life on Earth—from the bacteria in your gut to the most magnificent blue whale—is unified by common chemistry: a shared language of nucleic acid polymers, proteins, sugars, and lipids inherited from a last universal common ancestor that lived some four billion years ago. 

But there’s no guarantee that life on another planet—life that emerged and evolved in a different environmental context—would share Earthly life’s chemistry and physiology. Sculpted by an otherworldly habitat and joggled by the randomness of evolution, extraterrestrial life might not employ DNA as its genetic polymer, might not choose ATP as its molecular energy currency, might not even use water as its solvent. If alien life differs markedly from familiar life, our traditional life-detection techniques might fail to recognize it.

When I arrived at Carnegie Science in Washington, D.C., as a postdoctoral fellow in 2021, I was intent on finding new ways to search for extraterrestrial life with this puzzle in mind. What signals could we scour the heavens for if not water, DNA, or little green men? 

I remember my very first conversation with my mentor at Carnegie, Bob Hazen. Over lunch at a D.C. Indian restaurant, Bob and I immediately agreed that information could be a unifying concept in our quest for life, both as we know it and as we don’t. In other words, life anywhere in the universe would be rich in information, accrued through billions of years of evolution.

Over the next two years, he and I, along with a team of colleagues with diverse expertise in science and philosophy, put together a proposal for a new view of information and evolution. As we worked, a startling revelation took root: It became abundantly clear that information isn’t limited to biology, and evolution isn’t confined to biology either.

In the mid-19th century, British naturalist Charles Darwin explained biological evolution as organisms inheriting variable traits. They pass traits from one generation to the next when the variations help that organism survive or reproduce. 

But that’s just one way for things to get more complex over time. Looking out into the wider universe, we also see patterning, ordering, and diversification in systems that are not alive. In other words, Darwinian evolution may be just one example of a much more general phenomenon. Isotopes and minerals also evolve. So does language and technology. Anything can be an evolving system, so long as it:

  1. Contains many interacting components
  2. Explores different configurations of those components
  3. Selects the most functional configuration. 

Evolution is a dance between creativity and selection. Systems must both generate new possibilities and winnow possibilities to those that “work.”

At the most basic level, things are selected for their ability to persist in three different ways:

  1. Static persistence—entities resisting decay, like a stable isotope or a weathering-resistant mineral. Here, “function” means simply to be.
  2. Dynamic persistence—systems maintaining themselves, like a hot star burning fuel for billions of years. Here, “function” is to continue.
  3. Novelty generation—the ability to discover new ways of persisting, as in biology inventing flight and sight. Here, “function” is the capacity to change.

There is no vital force that separates biology from chemistry and physics; life is just another mechanism for exploring the possibilities of persistence in the cosmos’ cauldron of creativity.

Cancers as Evolving Systems

Bob Hazen and I published our paper on a unifying theory for evolution in October 2023. Since then, it’s been cited over 200 times by soil scientists, neuroscientists, and AI researchers. But none of these new directions surprised me more than the oncology paper. 

Like all biological systems, tumors are dynamically persistent entities. They are open systems that must incessantly consume raw materials and export waste. However, while tumors are made up of human cells, they don’t evolve like Darwin theorized that finches or tortoises evolve. They do not have progeny to which they pass on inheritable traits. 

Cancers contain many different types of cancerous cells. Tumors are often highly differentiated collections of malicious cells. In the same way that one collection of athletes can outcompete another, one configuration of cancer cells can persist better than another group inside our bodies. Some tumors inhibit the body’s immune system; others engineer their local environment like farmers to support their growth. Thomas et al. recognized that a tumor’s ability to try many different configurations under the selective forces of our body’s defenses makes cancer an evolving system.

Thomas’ team reframes the stages of tumor progression as a series of functional innovations that enhance the cancer’s persistence against the body’s defenses. 

Thomas et al "Leveraging selection for function in tumor evolution: System-level cancer therapies" https://doi.org/10.1093/emph/eoaf022

Initially, cancer cells persist because they can counteract competition from neighboring cells in their tissue of origin. Then, small collectives of cells gain the function of invading surrounding tissues. Another leap occurs when larger conglomerates gain the function of forming its own vascular network, bolstering persistence by consistently replenishing a feedstock for the tumor’s metabolism. Finally, the tumor acquires the ability to spread to other parts of the body, making it a devastatingly persistent, distributed entity. 

Remarkably, understanding cancer through the lens of persistence suggests a radical new approach for treatment. Traditional cancer therapies aim to eradicate the tumor by killing or removing as many cancerous cells as possible. That may sound like a good idea, but carpet-bombing cancer can cause collateral damage to healthy tissues. More importantly, a blitzkrieg strategy ignores the fact that cancers—especially late-stage cancers—are functional systems that have evolved to persist, grow, and metastasize despite the body’s best efforts to defeat it. Simply aiming to remove as many malignant cells as possible may not be the most effective strategy: If the cancer is not completely eradicated, the tumor might regenerate itself, and those cells that survive the first rounds of treatment are often much more resistant to subsequent treatments. The last word a once-successful cancer patient wants to hear is “recurrence.” 

Instead, the team argues that cancer therapies should focus on disrupting a tumor’s ability to gain new functions. The goal should not be to eliminate every last cancer cell, but to suppress the key elements that are responsible for cancer progression, such as its ability to form blood vessels or evade immune response.

Even if the tumor does not completely disappear, it will have been set back to a less aggressive stage of development. As it regenerates its functional network from scratch, the hope is that it will fall down an evolutionary trajectory toward a less malignant version of itself.

Careful surveillance of the cancer’s functional state can allow for more intricate strategies. Thomas’ group advocates for a clever tactic they call an “evolutionary double blind,” trapping tumors in situations where adaptations that make them resistant to one treatment render them susceptible to another. 

Targeting a tumor’s support systems does not require new drugs, just a new mindset. The biologists hope that an “intentional therapeutic logic that integrates knowledge of tumor organization and evolution” will combat cancer more effectively than classic therapies while using less-invasive versions of existing procedures. They write that such a shift in strategy has the potential to “transform cancer from a fatal to a manageable chronic disease.”

Perhaps the future of cancer isn’t dying from it…but becoming able to live with it.

Left: Crescent Nebula (NASA); Right: Lysosome clusters (National Institutes of Health)

My friend from college is on the mend. Her bouts of chemo and radiation are over. Her surgery is complete. All signs indicate that she’ll be a part of the 87% who bounce back from Stage 3 breast cancer. For her, today’s medicine was enough.

But for millions of others, it won’t be. Cancer continues to take more lives each year than car accidents, armed conflicts, and all infectious diseases combined. Because of cancer, I’ll never hug one of my grandfathers again, and I’ll never have the chance to meet the other.

I once thought my research—my celestial rabbit holes—couldn’t be further from the quotidian concerns of human wellbeing. But in recent years I’ve discovered that’s not true. Asking “Are we alone?” invites us to reflect upon what life shares in common with other complex, persistent phenomena.

Selection for function exists at every level, from the atomic to the planetary, from cells to cities to cancer. We may each be interested in studying our own little corner of the universe, but nature isn’t fractured by our disciplinary boundaries. That there’s even the slightest chance that anything I’ve ever done as an astrobiologist could have a positive impact on someone’s health is a startling reminder that the world is connected in beautiful ways.

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