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LPT funds new childhood kidney cancer research

LPT funds new childhood kidney cancer research

Two projects 'offer real hope for kinder treatments'

We are thrilled to announce two new research projects focused on Wilms tumour, a common childhood kidney cancer.

Led by expert researchers, these projects promise to develop our understanding of the way Wilms tumour cells survive chemotherapy and of how to cure hard-to-treat cases.

University of Liverpool researcher Dr Bettina Wilm is trying to find out why Wilms tumours are able to grow back after treatment in her project, titled 'Understanding how Wilms tumour cells escape chemotherapy'. 

Cancers can grow back after treatment, known as a relapse, if some of the cancer cells weren’t killed during treatment.

One of the ways that Wilms tumour cells can do this is by becoming dormant – however these cells can later be re-activated, leading to a relapse.

Phil Brace said that funding research that gives hope to children is at the heart of The Little Princess Trust's mission.

This is thought to be caused by surviving cancer cells communicating with dormant cells after treatment ends.

Bettina wants to understand more about these processes. She said: "This research study will increase our knowledge of how cancer cells communicate with neighbouring cells.

"Of particular interest for us is how some cancer stem cells within the Wilms tumour manage to persist after chemotherapy.

"We believe that the communication of cancer cells with their neighbouring cells is important since cancer cells may be able to evade the effects of chemotherapy by becoming senescent and then re-activating at a later stage, when they then can multiply and spread."

In her new Little Princess Trust project, Bettina will be studying cancer samples from Wilms tumour patients, looking at the samples’ behaviour and genetics, and at which molecules are present in the cancer cells and how they communicate.

She hopes to find a detailed insights into the molecules that cells use to communicate within the tumour.

These processes and molecules could also identify targets for new treatments that would help prevent relapse, or help doctors predict which tumours would grow back.

Not only could Karim’s work form a new treatment for high-risk Wilms tumour, but it could also be safer and more effective for patients as each medicine can be given at a lower dose.

Meanwhile, Professor Karim Malik will be looking at a new way of attacking cancer cells in his project, titled 'Assessing a potent combination treatment to fight Wilms tumour'. 

Wilms tumour develops when cells contain too many growth-promoting proteins, such as a protein called MYCN.

Reducing the amount of MYCN in cancer cells could be a way to treat Wilms tumour, but researchers have not been able to find a way to target MYCN directly.

Karim’s team at the University of Bristol have found a protein that MYCN relies on, called PRMT5. There are already medicines available that can target this protein, and Karim has found that a combination of two of these medicines can kill Wilms tumour cells.

In this project, Karim will use cancer cells grown from patient samples and other established models of Wilms tumour to understand how proteins like PRMT5 work in Wilms tumours, what they do, and how medicines targeting them can fight this cancer.

Not only could Karim’s work form a new treatment for high-risk Wilms tumour, but it could also be safer and more effective for patients as each medicine can be given at a lower dose. 

Phil Brace, from The Little Princess Trust, said: “Funding research that can give hope to children with cancer is at the heart of our mission.

"We are delighted to have been able to fund two new Wilms tumour projects and to be supporting two excellent researchers.

"These projects are exciting because they offer real hope for kinder and more effective treatments that prevent children from relapsing. We look forward to seeing their results!”

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The MBE for voluntary groups was awarded to The Little Princess Trust by Her Majesty Queen Elizabeth.