oncogene
/ ON-koh-jeen /
Think of a car with a gas pedal that has become stuck to the floor. No matter what the driver wants, the engine keeps roaring and the car keeps accelerating. An oncogene is the cell's stuck gas pedal: a gene that, once it goes wrong, pushes the cell to keep growing and dividing whether or not it has been told to. It is one of the main drivers that turn a normal cell into a cancer cell.
More precisely, an oncogene is a mutated or overactive version of a normal gene whose proper job is to encourage cell growth and division at the right times. The normal, well-behaved version is called a proto-oncogene; when a mutation, an extra copy, or a faulty fusion makes it permanently 'on,' it becomes an oncogene. The protein it makes might be a growth signal, a receptor that catches such signals, or an internal relay in the chain that tells the nucleus to divide. Importantly, oncogenes act in a dominant way: a single overactive copy is usually enough to push a cell toward unrestrained growth, like one stuck pedal being enough to speed the car.
Oncogenes matter because they are direct, well-understood targets for treatment. Famous examples include RAS (mutated in many cancers), MYC, and HER2 (overactive in some breast cancers, treated with drugs that block it). A common confusion is to think oncogenes are 'alien' genes inserted into us; they are not. They are our own ordinary growth genes that have been damaged or overexpressed. Their counterpart, the brake-failing tumor suppressor gene, must usually also fail for cancer to develop — a stuck accelerator is most dangerous when the brakes are broken too.
About one in five breast cancers makes far too much of the HER2 receptor, an oncogene product that keeps shouting 'grow' at the cell. The drug trastuzumab (Herceptin) latches onto HER2 and muffles that signal, which is why doctors test tumors for HER2 before choosing treatment.
An overactive oncogene (HER2) is a target drugs can switch off.
An oncogene is not a foreign gene; it is your own normal growth gene gone overactive, and a single faulty copy can be enough (it acts dominantly).