When the orchestra stops playing: investigating the elements of cancer development

 “If we fill a room with people and ask them if they know anyone who has had cancer, most of them will raise their hands,” explains Júlia Urgel, a PhD student in the Cancer Biology Laboratory of the Department of Medicine and Life Sciences at Pompeu Fabra University.

Cancer is nothing more than “an excessive growth of cells that have lost their identity and function,” says Etna Abad, a PhD student in the same laboratory. A situation of cellular chaos that is often due to the cell losing essential proteins to suppress the appearance of tumors, such as p53.

In Etna’s words, “p53 is like the conductor of an orchestra. It helps the cell to manage and regulate the cell cycle, the use of nutrients, division, death, and so on.

If it stops working, it starts giving wrong indications and all these mechanisms fail.” “So much so that in 50% of cancer cases, p53 is mutated. And for now, we have no effective therapies to treat these cases,” adds Julia. In her lab, they all study the role of p53 in one way or another. While Etna studies whether a protein regulated by p53, which is a tumor suppressor in lymphomas, is also important for other types of cancer, such as lung cancer; Julia studies cell metabolism, i.e. how the cell obtains energy and how it picks up the pieces to build everything it needs to function properly. That’s because cancer cells have a somewhat different metabolism. So, she tries to find those genes that are essential for a cancer cell to survive. And although they both work in the lab and are away from patients, they admit that they always have the therapy in mind. But first, they need to understand how cancer cells work and see what differentiates them from the healthy ones. Understanding how different proteins “talk” to each other in order to finally design a specific, targeted therapy.