oncogene
An oncogene is like a stuck accelerator pedal on a car. The normal version of the gene tells a cell when it is fine to grow and divide; when that gene is altered so it stays switched on, the cell keeps pushing forward and divides far too much. The result is a powerful push toward uncontrolled growth.
Oncogenes arise from normal genes called proto-oncogenes, which have everyday jobs in signaling, cell division, and survival. A mutation, an extra copy of the gene, or a chromosome rearrangement can convert a proto-oncogene into an oncogene that is overactive or active at the wrong time. Familiar examples include RAS, MYC, and the fusion gene behind the Philadelphia chromosome.
Oncogenes typically act in a dominant fashion at the cell level: a change in just one of the gene's two copies can be enough to drive abnormal growth. This is the opposite of tumor-suppressor genes, where both copies usually must be lost. Because oncogenes are switched on, many cancer drugs aim to block their overactive products.
In chronic myeloid leukemia, the BCR-ABL fusion gene created by the Philadelphia chromosome acts as an oncogene, producing a constantly active growth signal.
A chromosome rearrangement can build an oncogene.
Oncogenes are gain-of-function changes: the altered gene does too much. Contrast this with tumor-suppressor genes, where the damaging change is loss-of-function.