How Cancer Works

Every day, cells throughout your body make mistakes. DNA gets damaged during normal division, chemicals from pollution slip past defenses, and replication errors slip through. Most of the time, your cells catch these problems and self-destruct or get repaired. But occasionally, a single cell accumulates the right combination of errors, stops listening to the body’s signals, and begins a journey that ends in cancer.

The short answer

Cancer is a disease of uncontrolled cell division caused by mutations in specific genes that regulate growth, death, and repair. These mutations allow cells to ignore signals that normally tell them to stop dividing, live longer than they should, or invade surrounding tissue. What we call cancer is actually hundreds of distinct diseases, each with different causes, behaviors, and treatments.

The full picture

The difference between normal cells and cancer cells

Your body replaces roughly 330 billion cells every day. Most of these are routine replacements: skin cells die and flake off, gut lining refreshes itself, blood cells turn over. This process is orderly because cells follow strict rules. They divide only when told to, they die when damaged, and they stay in their designated tissues.

A cancer cell ignores these rules. It divides when it shouldn’t, ignores signals to stop, and refuses to die when it becomes damaged. More disturbingly, cancer cells can migrate to other parts of the body, a process called metastasis, and establish new tumors in organs far from where the cancer started.

The transformation from normal to cancerous doesn’t happen all at once. Researchers now understand that cells accumulate mutations over years, sometimes decades, before they become malignant. This is why cancer risk increases dramatically with age. A 30-year-old has a roughly 1 in 200 chance of developing cancer in the next decade. By age 60, that jumps to about 1 in 10, according to National Cancer Institute data.

The genes that matter

Not all genetic mutations cause cancer. Your genome contains specific genes, often called oncogenes and tumor suppressor genes, that determine whether a cell behaves itself.

Oncogenes are genes that promote cell growth. When functioning normally, they act like gas pedals: they help cells divide when the body needs new cells. But when mutated, they become stuck in the “on” position. The cell keeps dividing even when it shouldn’t. The RAS gene family, one of the most commonly mutated oncogenes in human cancers, is permanently “on” in about 30% of all tumors.

Tumor suppressor genes act as brakes. They slow or stop cell division, repair DNA damage, and trigger cell death when problems become too severe to fix. The p53 gene, sometimes called the “guardian of the genome,” is the most important tumor suppressor. It detects DNA damage and either pauses division for repairs or ordered cell death if the damage is too severe. Roughly 50% of all cancers involve a mutated or disabled p53 gene, research shows.

How mutations accumulate

Mutations happen through several mechanisms. Some are inherited: about 5% to 10% of all cancers come from mutations passed down from parents, like the BRCA1 and BRCA2 genes that dramatically increase breast and ovarian cancer risk.

Environmental factors cause others. Tobacco smoke contains over 70 known carcinogens that directly damage lung cell DNA. Ultraviolet radiation from sunlight causes specific mutations in skin cells that lead to melanoma. Processed meat was classified as a carcinogen by the World Health Organization in 2015, linked to colorectal cancer through compounds formed during processing.

But the most common source of mutations is simply the noise of normal cell division. Each time a cell divides, it must copy 3 billion base pairs of DNA. Errors happen. Most get caught and fixed by proofreading enzymes, but some slip through. Over a lifetime, these random replication errors accumulate. A 2017 study published in Science estimated that about 66% of the mutations in some cancer types come from random replication errors, not inherited traits or environmental exposure.

The hallmarks of cancer

In 2000, researchers Douglas Hanahan and Robert Weinberg published a landmark paper identifying six “hallmarks” that define cancer cells. This framework, published in Cell, has become foundational in oncology research.

The first hallmark is sustained proliferative signaling: cancer cells make their own growth signals or become insensitive to signals that would normally stop them. The second is evading growth suppressors, like the disabled p53 we discussed. The third is resisting cell death, where cancer cells ignore signals that would trigger programmed cell death.

The fourth hallmark is enabling replicative immortality. Normal cells can divide only about 50 times before they enter a permanent growth arrest called senescence. Cancer cells find ways to maintain their telomeres, the protective caps on chromosomes, allowing them to divide indefinitely. The HeLa cell line, taken from Henrietta Lacks in 1951, is still alive and dividing in laboratories worldwide.

The fifth hallmark is inducing angiogenesis, the creation of new blood vessels. Tumors need oxygen and nutrients to grow beyond a tiny size. Cancer cells release signals that recruit blood vessels to feed the growing tumor.

The sixth hallmark is activating invasion and metastasis. This is what makes cancer deadly. Local tumors can often be surgically removed. But when cells break away, travel through the bloodstream, and establish new tumors in distant organs, treatment becomes dramatically harder.

How cancer spreads

Metastasis is responsible for about 90% of cancer deaths. The process begins when some cells within a tumor acquire mutations that allow them to break through the surrounding tissue structure and enter the bloodstream or lymphatic system.

These circulating tumor cells can travel anywhere in the body. They must survive in the bloodstream, exit through vessel walls, and then colonize a new organ. This is remarkably difficult, which is why most circulating tumor cells die. But the ones that succeed can form new tumors in the liver, lungs, bones, brain, or other tissues.

The new tumors often prefer specific organs. Prostate cancer typically spreads to bones. Breast cancer commonly reaches the brain, liver, and lungs. This isn’t random; it’s determined by the chemical environment and blood vessel structure of different organs that either support or hinder tumor cell survival.

Why it matters

Cancer killed nearly 10 million people worldwide in 2020, making it a leading cause of death globally, according to the WHO. In the United States, about 2 million new cancer cases are diagnosed each year, per SEER data.

But survival rates have improved dramatically. The five-year survival rate for breast cancer has risen from 75% in the 1970s to over 90% today. Childhood leukemia, once almost universally fatal, now has a five-year survival rate above 90% thanks to advances in chemotherapy and targeted therapies. The key to these improvements lies in understanding the biology: treatments that target specific mutations work better than chemotherapy that poisons all rapidly dividing cells.

Precision oncology, where doctors sequence a tumor’s DNA and select drugs that target the specific mutations present, represents the current frontier. Drugs like imatinib, which targets the BCR-ABL fusion gene in chronic myeloid leukemia, have transformed what was a fatal diagnosis into a manageable chronic condition for most patients.

Common misconceptions

“Cancer is one disease.”

This is perhaps the most damaging misconception. Lung cancer, breast cancer, and leukemia have almost nothing in common biologically, except that they all involve uncontrolled cell growth. They arise from different tissues, involve different mutations, and respond to different treatments. What works for one type might do nothing for another. This is why “cancer cure” is misleading; we’re likely to cure many cancers separately rather than finding a single solution.

“Sugar feeds cancer.”

This one is scientifically inaccurate, though it contains a kernel of truth. All cells, including cancer cells, use glucose for energy. But this doesn’t mean eating sugar causes cancer or that cutting sugar will cure it. Your body tightly regulates blood sugar levels, and tumor cells don’t somehow “steal” sugar from healthy cells in any meaningful way. This myth can lead patients to pursue dangerous diets while avoiding treatments that actually work.

“If someone survives cancer, they’re cancer-free forever.”

Many cancers can return years or even decades after successful treatment. These recurrences happen when a small number of cancer cells survived treatment and eventually re-grew. This is why survivors need ongoing monitoring, sometimes for life. Some cancers, like certain types of breast cancer, have meaningful recurrence risks 20 years after initial treatment.

Key terms

Mutation: A change in the DNA sequence that can alter how a cell functions.

Oncogene: A mutated gene that promotes uncontrolled cell growth.

Tumor suppressor gene: A gene that normally prevents cells from dividing too rapidly or becoming cancerous.

Metastasis: The spread of cancer cells from their original location to distant organs.

Malignant: Cancerous tumors that can invade nearby tissue and spread to other parts of the body.

Benign: Non-cancerous tumors that don’t spread to other organs.

Carcinogen: Any substance or exposure that can cause cancer.

Chemotherapy: Drug treatment that kills rapidly dividing cells throughout the body.

Targeted therapy: Cancer drugs designed to attack specific mutations or pathways in cancer cells.