Jan 9, 2026, 11:19 AM ET

Cancer is One of the Universe's Fundamental Phenomena | Athena Aktipis, Arizona State University

Cancer is fundamentally a breakdown of multicellular cooperation, where individual cells defect from the organism's interests to maximize their own replication.
Five foundational pillars of multicellular cooperation collapse in cancer:
- Inhibition of proliferation (cells divide when they shouldn't).
- Control of cell death mechanisms (cells avoid apoptosis).
- Mechanisms for resource transfer (cells monopolize resources).
- Division of labor (cells fail to differentiate and specialize).
- Maintenance of the extracellular environment (cells pollute their surroundings).
This framework aligns with the "Hallmarks of Cancer," though the evolutionary perspective adds "breakdown in differentiation" as a critical missing hallmark.
Evolutionary pressures within the human body are intense due to short cell generation times (days) compared to organismal generations (decades), allowing cancer to evolve rapidly like a bacterial infection.

Multicellularity was achieved through multi-level selection, shifting the unit of selection from individual cells to the group (organism).
Organisms employ three levels of monitoring to suppress cellular cheating:
- Cellular Intrinsic: Internal sensors (e.g., TP53 gene) detect DNA damage or physiological errors, halting the cell cycle or triggering apoptosis.
- Neighborhood Level: Cells communicate survival and growth signals, allowing the local environment to isolate or eliminate suspicious cells.
- Systemic Level: The immune system acts as a backup to detect and remove rogue cells or pathogens throughout the body.
The immune system's primary evolutionary driver may have been the prevention of contagious cancer (transmissible tumors) rather than internal cancer, as early multicellular life faced massive risks from cells invading from other individuals.
Contagious cancer is exceptionally rare in most species due to high genetic diversity and robust immune barriers; known exceptions include Tasmanian devils (low genetic diversity, spread via biting) and dogs (transmissible venereal tumor).

Peto's Paradox: Large, long-lived species like elephants do not have higher cancer rates than small species like mice, despite having vastly more cells and more opportunities for mutations.
Evolutionary Life History Theory explains this via trade-offs:
- Slow Life History (Elephants): Invest heavily in somatic maintenance, DNA repair, and multiple copies of tumor suppressor genes (elephants have 20 copies of TP53) to ensure survival long enough to reproduce.
- Fast Life History (Mice): Prioritize rapid reproduction and growth, accepting higher cancer risk because extrinsic mortality (predation) is high, making long-term somatic maintenance evolutionarily irrelevant.
Trade-offs for increased cancer suppression include slower wound healing and reduced tissue regeneration capacity, as rapid proliferation increases the risk of malignant transformation.

Cancer cells exhibit "division of labor" and cooperation, such as some cells specializing in producing growth factors while others specialize in immune evasion or reproduction (cancer stem cells).
This cooperation creates a meta-population dynamic where:
- Cooperation allows tumors to grow and metastasize.
- "Hyper-cheaters" can emerge within the tumor, exploiting the resources produced by cooperating cells, potentially leading to tumor collapse or instability.
- Metastasis likely represents an evolved trait selected over many generations for the ability to collectively extract resources and move, rather than random mutation.
Resource patchiness within a tumor drives the evolution of motility; cells in low-resource zones are selected for traits that facilitate movement to new niches.

Adaptive Therapy: Instead of eradicating tumors with maximum dosage (which selects for resistant cells), treatment is calibrated to maintain a population of sensitive cells that compete with and suppress resistant cells.
- Treatment is paused when the tumor shrinks, allowing sensitive cells to rebound.
- Treatment resumes when the tumor grows, targeting the proliferating resistant cells.
- Clinical trials suggest this approach can extend patient survival in late-stage cancers (e.g., prostate, breast) by preventing the fixation of resistance.
Feeding the Tumor: Maintaining steady resource availability may reduce the selective pressure for cancer cells to evolve motility and metastasis.
Mutation Rate Suppression: NSAIDs (e.g., aspirin) may reduce cancer progression by lowering the mutation rate and inflammation, which otherwise create permissive environments for cheating cells.

Human societal defects (e.g., tax evasion, corruption) structurally mirror cellular cheating: individuals defecting from group norms to gain private resources, undermining the collective surplus.
Restorative Justice: Analogous to adaptive therapy, this approach focuses on reintegrating offenders and managing "crime" rather than seeking total eradication, which often leads to escalation.
Memes as Pathogens: Some ideas spread by exploiting human cognitive vulnerabilities without benefiting the host, similar to how cancer exploits cellular machinery, though they do not strictly "cheat" on a pre-existing rule set in the same way.
Planetary Scale: Human environmental degradation can be viewed as a "cancerous" behavior where local cheating (resource extraction) threatens the survival of the global system.

Parent-Offspring Conflict: Maternal and paternal genes within a fetus have misaligned interests due to asymmetry in relatedness.
- Paternal genes favor extracting maximum resources from the mother to maximize the current offspring's fitness, even at the cost of the mother's future reproductive potential.
- Maternal genes favor balancing resource allocation across current and future offspring.
This conflict manifests via genomic imprinting (epigenetic tags), where paternal genes promote growth and maternal genes restrict it.
Escalation of this conflict can lead to pathological outcomes like preeclampsia, where the fetus's drive for resources triggers a maternal immune response that raises blood pressure, potentially endangering both.

Current existential risks include nuclear war, future pandemics, and the misuse of AI to amplify human nefarious intent (e.g., AI-enabled disinformation).
Risk Perception: Common belief that disasters cause immediate societal collapse (chaos, violence) is largely a myth; empirical evidence shows that acute disasters often trigger spontaneous, need-based cooperation.
Preparation Strategies:
- Individual: Stockpile 72 hours of food/water using shelf-stable items already part of one's diet (e.g., couscous) to avoid waste and ensure readiness.
- Community: Build "Z-teams" (support networks) based on need-based transfers rather than market insurance, which fails when risks are systemic (everyone hits at once).
Zombified Media: A project using the "zombie apocalypse" frame as a playful, interdisciplinary tool to teach risk management, cooperation theory, and scientific literacy to diverse audiences.