Oncogene

In every cell of the body lies a long blueprint, the DNA. Sections of this blueprint are called genes, and each gene contains the instructions for a particular building block of the cell. Some of these genes control when a cell should divide and multiply. If such a control gene is altered by a copying error, it can permanently send the signal “divide.” A gene in this faulty, constantly active state is called an oncogene. The harmless original form, which simply regulates normal growth, is called a proto-oncogene.

The stuck-accelerator defect behind many types of cancer

Cancer arises when cells multiply even though the body doesn’t need them to. Oncogenes are one of the most common triggers for this. A helpful image: the proto-oncogene is the accelerator pedal of cell division. An oncogene is an accelerator pedal that is jammed and can no longer be released.

There is a second type of cancer gene that must be distinguished from this. Tumor suppressor genes slow down cell division—they are the brakes. In their case, it is the failure that is dangerous, not overactivity. A tumor often only develops once both the accelerator and the brakes are defective at the same time. That’s why a single mutation is usually not enough.

This matters in practice because a jammed accelerator can be specifically blocked. A drug can inhibit the product of an oncogene. Rebuilding a missing brake, on the other hand, is much harder. This is precisely why oncogenes are the favorite targets of modern cancer drugs.

How a harmless gene gets out of control

There are several ways in which a proto-oncogene can become an oncogene. The simplest is a point mutation: a single letter in the genetic code is copied incorrectly. The resulting protein then has a slightly altered shape and can no longer switch itself off. In the well-known gene KRAS, a single swapped building block is already enough.

A second route is amplification. Instead of two copies of a gene, the cell suddenly has twenty. Each copy functions normally, but together they generate a far too strong growth signal. This happens, for example, with the gene HER2 in certain forms of breast cancer.

A third route arises when chromosomes break and fuse back together incorrectly. In the process, two gene fragments that actually have nothing to do with each other can merge. The best-known example is the so-called Philadelphia chromosome in a form of blood cancer. Important to know: such changes almost always arise only during the course of life, in individual body cells. They are then not passed on to children.

Oncogenes in medicine and in business news

Anyone who receives a cancer diagnosis today often has the tumor genetically tested. A lab reads out which oncogenes are active in the tumor cells. The therapy is then derived from this finding. This is called targeted therapy, because the drug matches precisely the defect that was found.

A famous example is imatinib, a drug against chronic myeloid leukemia. It blocks the protein that arises from the fused gene. Before its introduction, this disease was usually fatal; today, most affected people live with it for many years. Cases like this explain why pharmaceutical companies pour billions into this field.

That’s why the term also turns up in financial news. When a biotech company announces that its drug candidate targets a particular oncogene, investors react to it. Increasingly, artificial intelligence is helping to find new oncogenes and matching drug candidates within huge genome datasets. One common misconception shouldn’t get lost here: an oncogene is not a guarantee of cancer, but one risk factor among several.