Do cancer cells work “collectively” to survive?
Professor Peter Friedl and his team are studying how a shared cell survival system could be behind both cancer cell spread and treatment resistance. This could reveal brand new ways to stop cancer in its tracks.
Hope for the future
Once melanoma and other cancers have spread (metastasised), they can no longer be treated with surgery – instead, a system-wide approach to treatment is needed. Unfortunately, metastatic cancers are difficult to treat, and even the latest drugs are only able to extend a patient’s life by a few months.
Professor Peter Friedl believes that it may be possible to target both the spread of cancer cells and how they resist treatment at the same time, and that this could be a promising path to new treatments. Professor Friedl and other cancer researchers have started to uncover how cancer cells may communicate, possibly working “collectively”, to spread around the body and avoid the effects of treatments. Uncovering this knowledge could help find ways to make treatments like chemotherapy more effective for more cancer patients.
Melanoma is a serious type of skin cancer that appears as a mole or dark patch on the skin.
Melanoma starts in melanocytes, a type of cell in the skin and eyes that produces pigment. Melanocytes are found in the deepest layer of the epidermis, which is itself the outermost layer of the skin. If DNA in a melanocyte becomes damaged, for example because of too much UV exposure, it can begin growing out of control.
Melanoma is the 5th most common cancer in the UK – almost 20,000 people were diagnosed in 2020.
Cancer cells are often thought about as “lonely riders”, says Professor Friedl, but in fact they may be able to form a kind of multi-cell ecosystem that benefits the cells by helping them spread and avoid being killed. These two survival systems, cancer spread and treatment resistance, are usually studied independently – as separate survival methods performed in different ways.
If successful, this project could be the first in the world to bridge the gap between cancer metastasis and treatment resistance, and show that communication between cells that helps them act “collectively” is behind both behaviours. By uncovering how cells communicate to do this, Professor Friedl believes they could reveal brand new ways to target cancer cells – disrupt the systems cancer cells use to act “collectively”, and you could both slow their spread and expose them to the effects of treatments.
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