Close up of researcher working with samples in a lab

Research projects

Seeking a possible new target for lymphoma treatment

Researcher

Professor Bruno Amati

Project period

Jan 2024 - Dec 2026

Country

Research Institute

European Institute of Oncology (IEO)

Cancer types

Lymphoma

Award amount

£234,000

Project aim

Professor Bruno Amati and his team are investigating new ways to target a type of fast-growing lymphoma that can be particularly difficult to treat.

Hope for the future

Diffuse large B cell lymphoma is a type of blood cancer that affects our white blood cells. Approximately 5,000 people are diagnosed with this lymphoma in the UK every year. It can be quite aggressive, and although many cases can be successfully treated, others are harder to clear and sadly, can sometimes come back.

Professor Amati has a bright idea about a new way to treat diffuse large B cell lymphoma. The team are focusing on a particular molecular mechanism that some aggressive types of lymphoma cell seem to rely on heavily to survive and grow. They think this mechanism, called ‘nonsense-mediated decay’, could be the key to finding a new way to target the disease. If their hunch proves to be right, this could be the first step towards a new treatment option for patients.

Meet the scientist

Professor Amati has always been interested in "oncogenes" - those genes that have been shown to be super-activated and to drive disease progression in cancer. What did these genes actually do in cells? And how did they contribute to normal development and disease? He always had plenty of questions, and the answers seemed to be lurking around the corner... a pretty irresistible attraction for a young biologist! He has worked on this topic for over three decades now, around the world - in Switzerland, the UK, the USA and now Italy - helping to find the answers.

The science

All cells need special mechanisms to help regulate how they survive and grow, and nonsense-mediated decay is one of these mechanisms. It acts as a sort of ‘quality control’ for the genetic material in our cell, and helps to make sure that faulty genetic molecules are destroyed before they can cause any harm.

During earlier experiments, Professor Amati and his team gathered some exciting data suggesting that nonsense-mediated decay may actually be incredibly important for some types of lymphoma cells.

This finding was unexpected, and at first the team were surprised. Now, thanks to funding from our Curestarters, the researchers can build on their exciting new finding and investigate in greater depth exactly how and why some lymphoma cancer cells rely on nonsense-mediated decay. The team then hope to search for new drugs which could interfere with this process.

If successful, their work should help to build up a detailed picture of a possible new vulnerability in B cell lymphoma. It will hopefully lead the way to future lymphoma cures, and possibly even cures for other cancers with similar vulnerabilities.

Professor Bruno Amati

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