Episode 4
The One with the Curse in the Gift
ANANKE (Ἀνάγκη)
In ancient Greek myth, Ἀνάγκη was not merely a goddess — she was Necessity itself. Born before even the gods, she embodied the unbreakable forces of fate, time, and natural law. No one, not even Zeus, could defy her. We name this book Ananke because cancer, too, is not a curse, but a consequence — the price of complexity, of life daring to grow. In every act of creation lies a seed of destruction. That is the law of Ἀνάγκη — eternal, inevitable, and silently unfolding in us all.
WHY IS CANCER EVERYWHERE ?
"Nothing in biology makes sense except in the light of evolution"
- Theodosius Dobzhansky
"Even the most beautiful body carries inside it the seeds of its own destruction.”
— Susan Sontag
“To have a body is to suffer. To be alive is to decay.”
— Alan Watts
PREFACE
There is a kind of silence that precedes all great betrayals.
Not the silence of peace, but the pause in a room before a voice says something
it cannot take back.
That silence lived at the beginning.
Before the spine, before blood, before even skin, there was
only one cell. Then, came a choice: to become many.
That choice — to divide not in defiance, but in faith — was
the first miracle.
Cells began to share, to synchronize, to die for each another. They gave up
their right to grow wild, to be immortal, to be alone.
They became tissues. Then organs. Then organ systems.
Multicellularity was not a war won. It was a truce held
together by trust.
However, the truth is evolution, brutal and brilliant, never
gifts anything without consequence.
And inside this great togetherness, it left a loophole.
A shadow.
“The risk of cellular rebellion is the price we pay for
being made of many parts.”
— Mel Greaves, Cancer: The Evolutionary Legacy (2000)
That rebellion — small, selfish, molecular — is what we now
call cancer.
It is not foreign. It is not punishment.
It is not, despite how we speak of it, evil.
Cancer is a cell remembering what it was before the pact. A
lone wolf.
A cell unbinding itself from the body’s collective promise.
A cell that whispers: What if I didn’t stop growing? What if I lived
forever? What if I didn’t die when I was supposed to?
What is scary is that sometimes that cell survives.
We speak of cancer as something we ought to fight.
But what if it’s something we carry? Something written into us from the moment
our ancestors decided to build something bigger than themselves?
Something inevitable — not because we are weak, but because we are alive.
This story has no villain. It has no hero.
There is no monstrous thing hiding in the dark. There isn’t a magical someone
to counter it.
There is no black and white. Everything is grey.
There is beauty. There is biology. There is success. There
is failure.
This is a book written in fragments.
Some chapters are carved into fossilized bone.
Others live inside the bloodstream of a Tasmanian devil.
Some were discovered in Petri dishes. Others whispered by genes in sleep. It
is, simply, the record of a truth we rarely say out loud: Cancer is not the
exception. It is the cost of being made of many.
CHAPTER I
The
Covenant of Many
In the beginning, life was selfish.
Each cell, floating in the broth of a young Earth, was
concerned about just one thing: survival. There was no teamwork, no sacrifice,
no way to feel the weight of failure. Each cell grew for itself, consumed for
itself, and died without any ceremony. However, in this chaotic, ancient ocean,
something extraordinary happened—not once, but many times, across species and
eons.
A cell divided not only to replicate, but to build an army.
It did not stay separate. It lingered. It connected to its
sibling. And together, they began to share.
What followed was not an explosion of power but an act of
surrender.
To become many, each cell had to give up something sacred: autonomy. They had
to obey signals from outside themselves. They had to accept death, sometimes on
schedule. They had to agree to grow only when needed and rest when asked. Most
of all, they had to remember they were no longer alone. They were a part of a
whole.
This was the ancient pact of multicellularity and it was, by
all evolutionary accounts, a miracle.
But miracles, as we learn over and over, come at a cost.
To cooperate is to make yourself vulnerable. To follow the
rules means those rules can be broken. Buried deep in that pact — unspoken but
understood — was a dangerous clause:
If even one cell forgets, the whole will suffer.
“The risk of cellular rebellion is the price we pay for
being made of many parts.”
— Greaves, 2000
This rebellion is not new. It has haunted life for as long
as life has dared to grow beyond one.
It is just that today we call it cancer.
Cancer, however, is not an invasion. It is a memory. A cell
remembering what it once was: alone, unchecked, immortal.
To understand cancer — truly, painfully understand it — we
must go back. Not to the hospital room, not to the biopsy, not even to the
mutation. But to the moment cooperation was born.
Multicellularity is more than a biological arrangement. It
is a system of laws, an evolutionary governance. Cells must obey limits on
proliferation. They must undergo apoptosis — programmed cell death — when
damaged. They must communicate, share resources, and maintain the integrity of
their surroundings. These principles were the foundation of organisms, from
jellyfishes to giraffes.
“Multicellularity involves cooperation among cells and
suppression of unregulated proliferation, but these systems can fail.”
— Aktipis et al., 2015
And they do fail. Constantly.
To prevent collapse, evolution armed us with molecular
guards such as p53, RB and many more.
However, these systems are not perfect. They are ancient.
They are good enough to keep most of us alive for a few decades, sometimes more
— and that, evolutionally speaking, is a win.
Simply put, perfection in biology is just way too expensive.
Redundancy uses energy. Surveillance slows reproduction. Evolution left us with systems that work most
of the time.
Until they don’t.
Every time a cell divides, it copies three billion base
pairs of DNA and every copy comes with a chance for error. Most are harmless.
Many are repaired. It’s the one that slips through that can turn one’s life
upside down.
Tomasetti and Vogelstein, in their 2015 Science
paper, showed that the risk of cancer in a given tissue is closely tied to the
number of stem cell divisions in that tissue. More divisions mean more rolls of
the dice and more rolls of the dice means more chances of something going
terribly wrong: a mutation that allows it to grow without stopping, without
listening, without dying.
“Variation in cancer risk among tissues can be explained by
the number of stem cell divisions.”
— Tomasetti & Vogelstein, 2015
This is how it begins — not with a scream, but a
duplication.
What makes this betrayal so profound is not its violence,
but its subtlety.
A cell does not announce its treason. It simply stops
listening. It silences p53. It bypasses RB. It rewires its metabolism, avoids
immune detection, recruits blood vessels to feed its hunger. And it keeps going.
It is no longer part of the whole. It is itself again.
As Steven Frank writes in Dynamics of Cancer, cancer
is not the opposite of life. It is life — accelerated, unchecked, stripped of
restraint. It is evolution itself only turned inward.
“Cancer is the result of natural selection operating within
the ecosystem of the body.”
— Frank, 2007
That is perhaps the most difficult truth: cancer is not a
flaw in the system. It is the system itself, only misapplied. It is what
happens when the very tools of survival — mutation, adaptation, competition —
are unleashed inside a single body.
It is evolution’s shadow.
When a single cell forgets the covenant, it begins again.
Alone. And from that forgetting, tumours rise. They are not invaders. They are
architects of their own dark architecture — using the same bricks, the same
blueprints, just repurposed.
We call it cancer. But that name comes late.
The act came first.
Chapter II
The
First Betrayal
It did not begin with a war cry. There were no flames of
inflammation, no swollen wound, no obvious enemy. It began with a single
change—a letter misspelled in the vast lexicon of life. One among billions, so
small it might never have been noticed but ever since that molecular tremor,
the body would never again be whole.
A single cell, entrusted with the delicate balance of growth
and rest, made a decision it was never meant to make. It chose itself. It chose
to stop following the ‘rules.
This is where cancer begins—not in violence, but in the
betrayal of restraint.
The Tyranny of Precision
At the heart of every cell lies the genome, a three-billion-letter-long
code. This code is copied every time a cell divides—written and rewritten with
perfect speed, over a lifetime, trillions upon trillions of times. However,
this repetition is not graceful. It is astonishingly error-prone. Hence, evolution
is clever but cost-conscious. It has built a system of guardians to patrol this
chaotic archive.
Among them, the most sacred is p53—the so-called
“guardian of the genome.” When DNA is damaged, p53 awakens. It pauses cell
division and calls upon enzymes to repair. If the damage proves irreparable, it
utters the final command: death. This is not cruelty. It is a sacrifice. A
single cell removed to preserve the integrity of the whole.
Standing beside p53 is RB, the gatekeeper of the cell
cycle. At the threshold between rest and replication, RB holds the line. Only
when the signals are true and the DNA intact does it release the cell to
divide. These two proteins form a cornerstone of cellular law. They are judges.
They are sentinels. They are peacekeepers in a world of microscopic ambition.
Yet none of them were built to last every attack.
These systems evolved not for immortality, but for
reproductive sufficiency. They are strong, but not unbreakable. Efficient, but
not infallible. When they fail, it is not because the body has done something
wrong. It is because the body was never designed for perfection.
The Breaking of the Watchmen
In countless cancers, this covenant is broken first through
p53. The gene that encodes it—TP53—is among the most frequently mutated
in all of oncology. The mutation may be a subtle substitution, a missing exon,
a silencing methyl group. It may render p53 helpless, or worse: turn it rogue.
With p53 silenced, the cell’s first line of introspection
vanishes. Errors proceed without pause. There is unchecked accumulation of
damaged DNA. The cell, no longer
required to answer for its flaws, begins to replicate anyway.
However, freedom from scrutiny is not enough to spark a
revolution. The cell must also be told to grow. And so often, in tandem,
arrives a mutation in Ras—a small GTPase protein responsible for
transmitting growth signals from the membrane to the nucleus. When Ras is
mutated, it becomes permanently active, a tyrant whispering “divide” into the
cell’s ear, even in the absence of any external command.
This combination—mutated Ras, silenced p53—is among the most
dangerous in all of biology. The brakes are cut. The gas is pressed. The body,
once governed by restraint and reciprocity, now hosts a cell that listens to
nothing but its own corrupted signal.
The Rise of a Clone
From this one cell, a lineage emerges. Not by explosion, but
by persistence. One becomes two. Two become four. Four become forty. Each
generation, carrying the same silent mutations, grows with increasing
indifference to the rules that once bound them.
The clone expands, not yet a tumour, but no longer benign.
It is indeed a quiet uprising.
It begins to rewire metabolism, shifting toward glycolysis
even in the presence of oxygen—a phenomenon known as the Warburg effect. It
suppresses apoptotic pathways, builds tolerance to hypoxia, and begins to
express proteins that deceive the immune system. Eventually, it coaxes nearby
blood vessels to grow toward it, nourishing its expansion. The transformation
is not sudden. It is architectural.
Cancer is often described as a failure. But in this moment,
it is something closer to a dark brilliance—a cell that retools every survival
strategy to serve only itself.
The Ecology of Betrayal
What we witness here is not chaos, but evolution. As the
evolutionary biologist Steven Frank has argued, cancer is a process of natural
selection within the ecology of the body. The fittest cell is not the one that
serves the organism, but the one that survives and replicates within its
immediate environment—even if that means destroying the host in the process.
This is the quiet truth: evolution does not care for
morality. It cares only for persistence. Recall Darwin’s “survival of the
fittest”.
In this light, cancer is not foreign. It is the shadow of
evolution itself—adaptation turned inward, growth stripped of consequence,
survival made self-serving. The very mechanisms that built us—mutation,
replication, selection—are the same that undo us.
And so, the first betrayal is not an act of evil. It is a
reversion to a more ancient code. A memory, perhaps, of the unicellular
ancestors from whom all life once came. In becoming multicellular, we asked
each cell to sacrifice its autonomy but the capacity for autonomy never left.
It only lay dormant.
Until now.
The Human Cost of a Molecular Rebellion
It is tempting to speak of cancer in metaphors of war. However,
the cell that begins this journey is not a soldier, nor a monster. It is, in a
sense, innocent. It is not choosing destruction. It is simply choosing itself over
the body, over the rules, over the quiet harmony of cooperation.
Sadly, it is in that very choice that lies the tragedy because
this cell is not alone; it brings others with it. It builds a colony. A tissue.
A tumour.
What began as a single act of defection becomes an empire.
This is the betrayal that echoes through every patient’s
story. It is not a betrayal of the body by the outside world. It is a betrayal
from within. The rules are broken not by an invader, but by one of our own, by
a cell that was once like the rest, once obedient.
There is no villain here—only process. Mutation.
Miscommunication. An imperfect design, pushed past its limits.
And yet, though there is no villain, there is still grief. Betrayal
is the price we pay for the privilege of being made of many. For daring to
grow, to specialize, to think. For living long enough to remember.
Cancer does not come from the outside. It is born in the
very miracle of what we are.
Chapter III
The
Bones That Remember
The earth remembers what we forget. Its stones bear witness
to secrets our bodies no longer hold. Long before microscopes, hospitals, or
the word “cancer” even came into existence, the world had already known it. It
had watched cells grow wild and wars erupt beneath the skin of creatures long
since turned to dust.
Cancer, as it turns out, is not a modern affliction. It is
not a failure of industrial food or synthetic chemicals. It is far, far older
than medicine. Older than humans. Older than the very species that gave rise to
us.
Cancer is ancient and it is the bones that remember.
In the Shadows of Time
In 2016, paleopathologists announced something astonishing:
a 240-million-year-old fossil of a stemmed bony fish (Osteichthyes)
showed signs of osteosarcoma—a malignant bone tumour—on its spine. It was, and
remains, one of the oldest known cancers in the vertebrate fossil record. Later
that year, a team working in South Africa published evidence of metastatic
cancer in the fossilized vertebrae of a Homo naledi specimen, dated to
nearly 1.7 million years ago.
But even that is not where the story begins.
In a hadrosaur—a duck-billed dinosaur that lived 77 million
years ago—researchers identified signs of hemangiosarcoma, a vascular tumour,
in its tail vertebrae. These dinosaurs roamed the Cretaceous (a geological
period that lasted from about 145 to 66 million years ago) when flowering
plants were just evolving. Even then, cancer had already arrived.
It is tempting to call these cases rare but that would be a
misreading. Fossilization is an extraordinary filter. Soft tissues rot; only
the densest structures endure. For cancer to leave its mark on bone, it must be
aggressive, chronic, and untreated. However, what we find in the fossil record
is not the whole truth. It is simply the loudest survivors of a quieter
epidemic.
The Universality of Malignancy
If cancer has been with us since the Triassic (over 230
million years ago), then it is not bound to our habits or diet or environment.
It is something deeper—something shared.
In a 2015 review published in Nature Reviews Cancer,
Athena Aktipis and colleagues mapped the evidence of cancer across the tree of
life. Their conclusion was clear: “Cancer is a disease of multicellularity.
Wherever complex organisms evolve, so does cancer.” They documented tumours in:
- Reptiles
(e.g., snakes with lymphoma)
- Birds
(avian leukosis virus causing cancers in poultry)
- Dogs
(osteosarcomas and mammary carcinomas)
- Whales
(intestinal tumours, despite vast body size)
- Elephants
(despite having dozens of copies of p53, even they are not immune)
- Clams
and mussels (in which transmissible leukaemia-like diseases have been
documented)
What unites these species is not their lifestyle, but life
itself. The moment cells agree to cooperate—to grow, to specialize, to refrain
from unlimited division—they also create the conditions for betrayal. And
betrayal is what cancer is.
Peto’s Paradox: Giants Who Should Die But Don’t
There is a question that haunts evolutionary oncology: if
every cell has a chance of becoming cancerous, why don’t large animals—whales,
elephants, giraffes—get more cancer than small ones?
This is Peto’s Paradox, named after epidemiologist
Richard Peto, who observed in the 1970s that cancer incidence doesn’t scale
with body size or lifespan. A mouse and an elephant have vastly different
numbers of cells and lifespans, but their lifetime cancer risk is remarkably
similar.
The resolution to this paradox lies in evolution’s subtle
ingenuity.
In a 2015 eLife study, Joshua Schiffman and
colleagues reported that elephants have at least 20 copies of the TP53
gene, compared to just one in humans. These extra copies produce a highly
responsive DNA damage system, triggering apoptosis far more aggressively in
damaged cells. In effect, elephants have sacrificed regenerative potential in
exchange for cancer suppression.
Naked mole rats, meanwhile, produce a high-molecular-mass
hyaluronan (a large sugar molecule in the extracellular matrix that regulates
cell growth, movement, and tissue structure) that prevents cells from crowding,
triggering early contact inhibition—a powerful anti-tumour mechanism. It's as
if their cells are trained to say “enough” before the crowd even gathers.
Bats, long-lived and metabolically intense, show unique
adaptations in immune surveillance and DNA repair.
Whales—especially the bowhead, which can live over 200
years—carry expanded repertoires of tumour suppressor genes, including
duplications in PCNA, ERCC1, and REV1, involved in DNA
repair.
In each case, evolution found a different answer to the same
problem: how to grow without collapsing. Peto’s Paradox teaches us that cancer
is not simply a matter of having more cells or more time. It is a question of
how well evolution has prepared the body’s internal defences. These species do
not defy cancer by chance—they survive by innovation.
When Cancer Becomes a Legacy
Yet, for all these defences, cancer still finds a way. In
dogs, we see spontaneous bone tumours remarkably similar to human osteosarcoma.
In Tasmanian devils, a facial cancer spreads not through inheritance, but
through direct cellular transmission.
There are marine bivalves in which leukaemia passes through
seawater, and wolves whose lung tumours mirror patterns seen in human smokers.
Each case is not an outlier, but a thread in a larger matrix.
Cancer does not belong to humans. It does not belong to one species or one
century. It belongs to life—life that dares to divide, to grow, to age.
What the Fossils Teach Us
It is one thing to understand cancer as a modern disease. It
is another to recognize it as a phenomenon carved into stone.
When we find signs of metastasis in ancient bones, we are
not simply studying pathology. We are looking at evolution’s long war with its
own invention. We are seeing, in the fossilized skeletons of extinct species,
the same cellular defect that afflicts our loved ones today.
This continuity is sobering. But it is also, in a strange
way, unifying.
The same disease that haunts our hospitals today once grew
inside the bones of dinosaurs. The tumours that defy our chemotherapies once
challenged the immune systems of ancient fish. We are not alone in this, nor
are we exceptional.
A Memory Older Than Memory
And so, the earth remembers what we try to forget: that
life, when it becomes complex, also becomes fragile.
Cancer is not an aberration. It is an ancient companion.
Our bones are newer. Our medicine, younger still. But the
story we are living—the struggle to grow without losing control—has been
written before. In the fossilized tail of a hadrosaur. In the pelvis of an
early hominin. In the bone marrow of a wolf.
The bones remember and now, so must we.
When Cancer Becomes Contagious
There are cancers in this world that do not die with their
host. They live on—hitchhiking between bodies, slipping past immune sentinels,
wearing new skins like disguises. They are not diseases. They are immortal
clonal lineages.
Cancer, in rare but terrifying cases, becomes contagious.
The Body as Border
For most of evolutionary history, the immune system has
guarded the self. It is not merely a defence against infection. It is a
definition. T-cells and antigen-presenting cells continuously ask: Is this
me? Any cell that answers incorrectly is destroyed.
But cancer can learn to lie. Tumour cells often downregulate
MHC class I molecules (cell surface proteins that help the immune system
recognize and destroy infected or abnormal cells), cloak themselves in
immune-suppressive cytokines, or recruit regulatory T-cells to silence the alarm.
In humans, this escape lets cancer flourish within.
However, in some species, that escape goes further. A cell
no longer merely avoids destruction—it migrates. It becomes a parasite. A
cancer not of that host, but of another.
And thus, the border dissolves.
Devils in the Dark: The Tasmanian Plague
In 1996, on the island of Tasmania, scientists noticed
facial tumours spreading rapidly among Tasmanian devils. The tumours grew with
grotesque speed, distorting the face and mouth, eventually killing the animal
through starvation or metastasis.
At first, it seemed a typical epidemic. But deeper genetic
analysis revealed something astonishing.
Every tumour in every afflicted devil was genetically identical.
Not similar. IDENTICAL.
They were not tumours generated by each animal. They were
the same cancer, passed from one devil to another through bites during
mating or combat. A single Schwann cell—a nerve sheath cell from one long-dead
devil—had given rise to a cancer that lived on in hundreds, then thousands, of
others.
That cell no longer belonged to any individual. It had
become its own organism.
This disease is known as DFTD—Devil Facial Tumour
Disease—and it is one of only a few known clonally transmissible cancers
in mammals.
But it is not alone.
The Ancient Lover: CTVT
Long before the devils, there was the dog.
Canine Transmissible Venereal Tumour (CTVT) is a
cancer passed between dogs during mating. It is not species-wide. It is not
regional. It is global, and it is ancient.
Genetic analyses have traced every case of CTVT to a single
origin: a dog that lived over 11,000 years ago, likely in Central Asia.
The tumour that formed in that dog’s genitals never died. It lives still—in
street dogs in India, in sled dogs in Alaska, in feral packs across Africa.
That dog is long gone but its cancer survives, one cell at a
time.
CTVT is the oldest known living cancer. It is, biologically
speaking, a kind of immortal body—a clone that has outlived every
civilization it ever walked through.
It has adapted remarkably: slowing its aggressiveness,
evolving a complex relationship with the host’s immune system, even expressing
canine-like genes to blend in. It does not kill quickly because it has
learned—like any successful parasite—that its own survival depends on its
host’s.
When the Line Between “I” and “Other” Vanishes
These cancers unsettle because they violate something
sacred: that illness belongs to us. That our suffering ends with us.
In these
transmissible tumours, the self becomes a vector, and the cancer becomes
its own lineage—no longer defined by the individual but by the cell itself. It
is not dog cancer. It is a dog that is cancer. It is not a devil’s tumour.
It is a devil reborn endlessly as malignancy.
The immune system, so good at detecting foreign threats,
fails when the threat masquerades as kin. In devils, genetic bottlenecks
have made their immune diversity shallow—so cells from others often pass as
“self.” In dogs, CTVT has evolved mechanisms to suppress immune recognition
entirely.
These are not metaphors. These are biological facts. This is
the TRUTH.
Echoes Across the Tree of Life
Transmissible cancers are not limited to devils and dogs. In
marine environments, bivalves such as soft-shell clams, cockles, and mussels
have shown leukaemia-like transmissible cancers. In these cases, tumour cells
drift through the water, invading the haemolymph of nearby animals.
In 2021, researchers found that transmissible cancer cells
had jumped between clam species, meaning not just horizontal
transmission, but cross-species parasitism.
In humans, true transmissible cancer is vanishingly rare—but
not impossible. A few case reports exist: a surgeon accidentally implanting tumour
cells in a cut; organ transplant recipients developing cancers from donor
cells; and, most chilling, a 2015 report in The New England Journal of
Medicine of a man infected by cancer cells from a tapeworm.
Even in us, the door is not locked—only guarded.
The Self That Refuses to Die
What are we to make of a cell that lives longer than its
species? That carries with it the full genetic record of a long-dead animal,
but no memory of its body?
We are used to thinking of cancer as an error but it is an adaptation.
These are cells that have solved death by becoming something else.
They do not belong to any one organism anymore. They belong
to themselves.
And yet, they came from us.
This is perhaps the most haunting truth of all: that the
very machinery meant to knit us together—replication, repair, identity—can be
retooled into something that survives not with us, but instead of us.
We thought cancer ended with the body.
But in these creatures, cancer has found a way to endure—by
shedding the idea of self, and becoming a lineage of its own.
The disease has become the organism. And the organism, a
legacy.
It is no longer merely a betrayal.
It is a rebirth.
CHAPTER V
The
Fault in Our Flesh
“The longer we live, the more our cells forget.
Each division is a chance to misstep. Each scar a silent gamble.”
They say wisdom comes with age. So does cancer.
We often imagine the human body as a fortress built strong,
reinforced with youth, governed by rules. The truth is, the body is not a
fortress. It is a living negotiation. It repairs itself not by perfection, but
by faith—that cells will remember how to divide, how to heal, how to stop. Yet
with every cycle, memory fades. The code stutters. And in the quiet of ordinary
replication, something ancient begins to stir.
Cancer does not always arrive like thunder. Sometimes, it
begins in the soft forgetting.
The Arithmetic of Risk
Every human body begins as a single cell. From that one,
comes all: neurons, muscle, marrow. By adulthood, trillions of cells form the
tissues of a single body. Every day, billions of them divide—replacing blood,
lining the gut, healing wounds.
Before each division, cells must duplicate the entire human
genome: three billion letters of DNA. This copying is astonishingly accurate,
but not perfect.
According to Tomasetti and Vogelstein (Science, 2015),
much of the variation in cancer risk between tissues can be explained by a
single factor: how often that tissue’s stem cells divide. The colon, for
example, is constantly regenerating and carries a higher lifetime cancer risk
than, say, the brain.
Each division is a chance for something to go wrong. Each
scar a silent gamble.
This does not make cancer inevitable. It makes it statistically
plausible—a consequence not of flaw, but of arithmetic.
The Stem Cell Paradox
Stem cells are miracles of renewal. They persist quietly in
adult tissues—dividing only when needed, regenerating organs after injury,
replacing cells lost to time. Yet their very power makes them dangerous.
Stem cells must self-renew. They must resist death. They
must proliferate on demand. These are also the traits of cancer.
In Frank’s “Dynamics of Cancer” (2007) and later
works by DeGregori (2013), researchers argued that stemness is both
life-giving and oncogenic. Tissues with the greatest regenerative capacity
are often the most cancer-prone, not in spite of their power—but because of it.
The irony is brutal. What helps us heal when we are young
can kill us when we grow old.
Aging and the Shifting Ground
With age, tissues change—not just in appearance, but in
environment. The microecology of the body becomes less supportive of normal
cells. Inflammation increases. DNA repair falters. The immune system weakens.
These changes alter the selective pressures that shape which cells
thrive.
As DeGregori (Nature Reviews Genetics, 2013) showed, aging
does not just increase mutations—it changes the fitness landscape. A
mutation that would have been harmless or eliminated in youth can begin to
dominate in the altered biology of old age.
In other words: the body, over time, becomes more hospitable
to malignancy.
It is not just that more mutations accumulate. It is that
their meaning changes. The same mutation can be ignored at 25, tolerated
at 50, and dangerous at 70—not because it changed, but because we did.
DNA Repair: Faithful, but Finite
Cells are equipped with remarkable DNA repair systems: base
excision repair, mismatch repair, homologous recombination, and more. Tumour
suppressor genes such as p53, BRCA1, and ATM coordinate
this defence, scanning for damage, pausing the cycle, and triggering apoptosis
when needed.
But repair has limits. The systems are probabilistic, not
infallible. Evolution does not build perfect machines; it builds systems that
are good enough for reproductive success.
Repair slows with age. Fidelity drops. Cells begin to accept
imperfections as normal. The line between regeneration and mutation gets
blurred.
The Trade-offs Made by Evolution
We often ask why evolution did not design cancer-proof
bodies. The answer lies in evolution’s priorities. Natural selection
optimizes for early-life reproductive fitness, not long-term stability.
If a gene helps an organism survive to reproduce—even if it causes cancer at
60—it will not be selected against.
This is known as antagonistic pleiotropy—a gene that
has both helpful and harmful effects at different life stages.
Growth factors, sex hormones, stem cell activity—these are
essential in development. Later in life, however, they may fuel malignancy.
Evolution, having done its job, is no longer watching.
The Aging Genome: A Landscape of Errors
By the time a person turns 60, their cells may carry hundreds
to thousands of mutations. Most are harmless. Some are drivers.
Studies in recent years have revealed that even “healthy”
tissues of older individuals—oesophagus, skin, colon—carry clonal expansions
with known cancer-associated mutations (e.g., in TP53, NOTCH1,
DNMT3A).
These are not yet cancers. They are timebombs—dormant
for now, but poised.
The longer we live, the more our cells forget how not to
become cancer.
So Why Do We Still Survive?
Given all this—constant mutation, aging defences, fragile
balances—why does cancer not strike everyone?
Because the body, for most of life, works. Tumour suppressor
pathways still respond. Immune surveillance still functions. Apoptosis still
holds the line. For many, the system defers collapse long enough to allow full,
rich lives.
Yet even in health, the risk never disappears. It merely
waits.
In the End
This is the fault in our flesh: that to be alive is to risk
imperfection. That to heal is to divide. That to grow is to mutate.
Cancer is not an aberration of the living. It is an echo
of living itself.
We are born with the seeds of renewal and the seeds of ruin
side by side.
That they grow at all is a miracle. That they grow together
is the human condition.
Chapter VI
The
Answer
Why Is Cancer Everywhere?
Because complexity creates fragility.
Because evolution writes in trade-offs.
Because life — true, living life — must risk being undone.
Cancer is not the enemy of life. It is its byproduct.
To ask why cancer is everywhere is to ask why we are
made of many cells, why we grow, why we age, why we heal, and why we eventually
falter. The answer is not written in a single gene or pathway, but in the
entire arc of multicellular existence.
Life began as single cells. They lived, divided, and competed.
Then, around 600 million years ago, something extraordinary happened. Cells
began to cooperate. They formed tissues, organs, and bodies. They gave up
individual immortality for a new kind of existence — collective, specialized,
fragile.
But cooperation requires restraint. Growth must be
regulated. Division must be timed. Death must be chosen. These are not easy
asks. They require surveillance, sacrifice, and silence. Every cell must agree
to be less than it could be — to serve a body rather than be one.
Cancer is what happens when one cell remembers itself.
When it peels away from the script. When it says no to silence.
Cancer is everywhere because the architecture of life
allows it.
- Fragility
of Complexity:
Multicellular organisms rely on strict communication between cells. Break those rules, and the whole system teeters. The more complex the body, the more potential points of failure. The more you can build, the more you can break. - Evolutionary
Trade-offs:
Nature does not optimize for perfection. It balances short-term survival with long-term risk. The very genes that promote healing and regeneration in youth may promote cancer in old age. This is not a flaw. This is a strategy. - Time
and Division:
With every birthday, your cells divide. With every division, errors accumulate. The longer you live, the more your tissues replicate, mutate, and adapt. Cancer is not always due to toxins or trauma. Sometimes, it is just math.
The Mirror of Mortality
To live is to risk falling apart. To grow is to risk growing
too much. To heal is to risk healing in the wrong way. Cancer is not a
punishment. It is not malevolent. It is not other.
It is a mirror. It reflects the costs of our design.
It is a reminder that the very gifts that define us — regeneration,
resilience, memory — are built on systems that can be bent, twisted, and
sometimes, turned against us.
So why is cancer everywhere?
Because life itself creates the possibility for its
undoing.
Epilogue
We
Who Still Divide
Cancer has accompanied multicellular life for hundreds of
millions of years. It is not a modern aberration, nor merely a product of
environmental error. It is embedded in the evolutionary design of complex organisms,
a risk that arises not in spite of biology, but because of it. The act of
living — of dividing, repairing, aging — carries within it the latent
possibility of malignancy.
Yet while we may never completely eliminate cancer from the
story of life, we are no longer powerless before it.
Across disciplines and species, we are beginning to
understand cancer not simply as a disease to be eradicated, but as a biological
phenomenon to be deciphered. From the tumour-resistant mechanisms of elephants
to the clonal survival strategies of transmissible cancers in dogs and devils,
nature itself offers a catalogue of defences that evolution has tested and
refined. These insights are reshaping how we think about prevention, detection,
and treatment.
In recent years, medicine has begun to move away from the
metaphor of war toward a model of ecological adaptation. Therapies are now
being designed not only to destroy tumours, but to manage them — to control
their evolution, reduce their fitness, and extend life by working with, rather
than against, the body’s complex systems. Adaptive therapy, immunotherapy, and
precision medicine are no longer theoretical. They are emerging as practical
strategies grounded in evolutionary biology and informed by centuries of
observation.
Moreover, the promise of early detection through tools such
as liquid biopsies and advanced imaging technologies means that many cancers
can be intercepted before they acquire the full arsenal of mutations that make
them dangerous. With each passing year, our capacity to read and interpret the
molecular language of cancer improves.
We are also learning from our failures — from the resurgence
of resistant clones, from the limits of chemotherapy, from the unpredictable
nature of tumour heterogeneity. Each setback forces us to ask better questions,
to refine our models, and to build more humane, biologically informed
approaches to care.
While it is unlikely that cancer will ever be fully
eradicated, there is growing reason to believe that it can be made more
predictable, more preventable, and more liveable. The future of oncology is not
a singular cure, but a constellation of strategies — scientific, clinical, and
social — that together form a new relationship with this ancient disease.
In this relationship, knowledge becomes power. Understanding
becomes strategy. And survival becomes possible not only through intervention,
but through anticipation.
To live is to divide. To divide is to risk. That risk will
never disappear entirely. Yet within that risk lies a deep and hard-won hope —
that even if we cannot outrun cancer, we may learn to outwit it.
And in doing so, we may come to see ourselves not as victims
of our biology, but as its navigators. We may come to see the human body not as
a battlefield, but as an evolving system — flawed, adaptive, and still filled
with possibilities.
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