Cells normally follow rules
The adult body contains many trillions of cells, and most of them are continually replaced or maintained. Whether a cell divides, rests, specializes or dies is governed by signals from its surroundings and by internal checks. Together these form the system of cell growth control. Growth factors tell cells when to divide, checkpoints in the cell cycle pause division if DNA is damaged, and a process of programmed cell death, called apoptosis, removes cells that are damaged beyond repair.
Cancer is what can happen when these controls fail in a cell lineage, and the cells keep dividing when they should not.
Cancer is a genetic disease of cells
In most cases, cancer begins with changes in DNA within a single cell. These changes may be small mutations, or larger rearrangements and gains or losses of chromosome pieces. They can arise from random errors when DNA is copied, from exposure to harmful agents such as tobacco smoke or ultraviolet radiation, from certain infections, or from inherited variants that raise risk. In most cancers the changes are acquired during life rather than inherited.
Two broad types of genes are especially important:
- Proto-oncogenes normally promote growth in tightly regulated ways. When mutated into oncogenes, they can act like a stuck accelerator pedal.
- Tumor suppressor genes normally slow division, repair DNA or trigger cell death. When they lose function, it is like losing the brakes.
A single mutation is rarely enough. Cells have layered safeguards, and most cancers seem to require several changes accumulating over years, which is one reason risk generally increases with age. The immune system also removes some abnormal cells, though cancer cells can evolve ways to evade it.
An evolutionary process inside the body
A useful way to see it is as natural selection within a population of cells. A mutation that lets a cell divide slightly faster or survive better gives its descendants an advantage. Further mutations add to this, and over time the dominant group of cells becomes more abnormal. Within a single tumor, different cells often carry different mutations, which helps explain why cancers can become resistant to treatment. The same logic of selection applies in the evolution of antibiotic resistance in bacteria, though the mechanisms differ.
Shared features of cancer cells
Researchers have described a set of capabilities that many cancers acquire, in various combinations. Cancer cells often:
- Keep dividing without the usual growth signals
- Ignore signals that say stop
- Resist programmed cell death
- Divide an unusually large number of times
- Encourage new blood vessels to grow into the tumor
- Invade nearby tissue and spread to distant sites, which is called metastasis
- Alter their energy use and avoid the immune system
Not every cancer has every feature, and the mix differs from one tumor to another.
Tumors, benign and malignant
A mass of abnormal cells is called a tumor. A benign tumor tends to stay in place and usually does not invade surrounding tissue, though it can still cause problems depending on its location. A malignant tumor can invade and spread. Most deaths from cancer are linked to metastasis rather than to the original tumor alone. Some cancers, such as those of the blood, do not form solid masses.
Why “cancer” is many diseases
Cancers are named and classified by where they start and what type of cell they come from. Different types vary in their causes, behavior, speed of growth and response to treatment. Even tumors in the same organ can differ at the molecular level. That is why current work in cancer research increasingly looks at the specific genetic changes in each tumor, an approach connected to personalized medicine.
Risk, causes and a note on statistics
Many factors are linked to risk, including age, tobacco use, certain infections, alcohol, radiation, family history and some inherited gene variants. In many cases, the cause for an individual person is unknown, and chance plays a role in which mutations occur. Researchers often debate how much of cancer risk is due to chance and how much to avoidable exposures, and the answer differs by cancer type.
When reading news about cancer risk, it helps to remember that a change in relative risk can mean a very small change in absolute risk, and that correlation and causation are not the same. Careful habits for reading statistics are worth having here.
What this article is and is not
This is a biology primer, written to explain concepts, and does not offer guidance on detection, symptoms or treatment, which depend heavily on cancer type and individual circumstances. Anyone with health concerns should consult a qualified medical professional.