Lung cancer cell. Image Credit: Anne Weston, Francis Crick Institute (CC BY 4.0)
Cancers arise when harmful changes happen in the genetic information of certain cells. These ‘mutations’ are different from person to person, but overall, they disrupt healthy cells in similar ways. In particular, cancer cells tend to lose features that help cells work together in the body. Researchers have suggested that cancers may emerge when cells stop being able to cooperate with each other as part of an organism.
Our bodies still rely on old genes that were present in our earliest, single-cell ancestors. However, we also have newer genes that evolved when the organisms in our lineage started to have more than one cell. A complex network of signals exists to ensure that both sets of genes work together smoothly, and previous studies have suggested that cancers may appear when this delicate balance is disrupted.
To address this question, Trigos et al. have now used a computational approach to analyse different types of tumours from over 9,000 patients. This showed that, in cancer, many mutations disrupt the genes that coordinate old and new genes. These mutations were usually small, punctual changes in the genetic sequence. However, large modifications, such as an entire gene being deleted or repeated, took place more often in the old or the new genes themselves. Therefore, different classes of mutations have specific roles when disrupting how old and new genes work in cancer.
While certain genes highlighted during this analysis were already known to be associated with cancer, others were not – including genes present during the evolution of the earliest animals on Earth. Looking more closely into how these genes can cause disease may help us better understand and fight cancer.
