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Fundraiser supports research into high-risk leukemia

Some patients with acute lymphocytic leukemia (ALL) have a specific gene fault that slows down or even stops cell growth when cells are under stress. That makes this form of ALL particularly hard to treat. Especially children whose disease comes back after chemotherapy have a low chance of survival. Treatments such as stem cell transplants and the relatively new CAR-T cell therapy usually do not work for these patients: new treatment methods are desperately needed.

The TP53 gene is one of the most important cancer genes: when it functions properly, it slows down the growth of cells under stress – for example with chemotherapy. But many tumors have errors in the TP53 gene, or completely lack the gene. This makes these cells less sensitive to therapy. ALL patients with these mutations, especially if their disease comes back after treatment, usually do not benefit from existing treatment. As Frank van Leeuwen says: ‘This high-risk form of leukemia is rare, but this is the group of patients that it’s all about. At the moment we cannot offer them the right treatment.’

Sid Mulder was one of the 17 children on average who are diagnosed with the high-risk form of ALL each year. He died of the disease in 2018 at the age of 17. Two years later, his parents decided they wanted to help stop the same thing from happening to other families. They started a fundraising campaign: they raised more than €6750 via social media,. Frank van Leeuwen and Natasja Dors accepted the cheque last month, on Sid’s birthday. The money will contribute to research in the Van Leeuwen group into new ways to treat TP53-ALL.


Looking for vulnerabilities
Van Leeuwen: ‘All tumors have specific addictions that you don’t see in other cells. The trick is to find out exactly what those weak spots are.’ In their research into TP53-ALL, his group examines how faults in TP53 affect leukemia cells: for example, they study how the errors change proteins in these cells. TP53 is also known to play a major role in the metabolism of cells, the way they produce energy and building blocks. According to Van Leeuwen, this makes it likely that vulnerabilities in cell metabolism can be found in TP53-ALL. By targeting these – initially in cells grown in the lab – he aims to make TP53-ALL sensitive to therapy again.

Together with Stefan Nierkens' group, Van Leeuwen is investigating whether faults in TP53 affect the production of a protein of the immune system, CD-19. That could explain why CAR-T – a relatively new treatment that reprograms the body's own defenses to specifically attack cancer cells – doesn’t work in TP53-ALL. ‘Thanks to support for our research, we can investigate why this high-risk form of ALL does not respond to existing treatments,’ explains Van Leeuwen. ‘That is the first step towards combating resistance to existing treatments, and eventually even finding new therapies.’