Our researchers are looking for answers to what starts myeloma, and if there is a way to prevent this happening. We are also supporting research to improve current treatments and quality of life for people with myeloma, and to find ways to completely eradicate the disease, offering a true cure.

In the last 20 years, we have come really far in improving treatment for people living with myeloma. But despite successful initial treatment, myeloma can come back. And there is still no permanent cure for myeloma, which affects more than 4,000 people in the UK every year.


Searching for new treatments for myeloma

People with myeloma are usually treated with chemotherapy, which can be combined with steroids and biological therapies. But despite treatment being initially successful, in some people myeloma comes back.

Our researchers are looking for new ways to treat myeloma, which could offer new hope to people living with this disease.

Search for novel drug targets for myeloma

Lead researcher - Dr Alexandra Irvine, Queen’s University Belfast
Investigation of the E3 ligase HUWE1 as a therapeutic target in Multiple Myeloma
Dr Irvine’s team have found that there is a high expression of one of the proteins that make up the proteasome in myeloma cells. They want to see if it is important in helping myeloma cells to grow and survive. The team will also test drugs to target this protein in myeloma cells. It is hoped that this research will help to find new treatment options for myeloma.

Repurposing existing drugs to treat myeloma

Chief investigator - Dr Farhat Khanim, University of Birmingham
Preclinical testing of low dose valproate and niclosamide (VaN) as novel anti-myeloma therapy
Dr Khanim and his team are looking for kinder treatments for older people with myeloma, and for those that have become resistant to current treatments, or have relapsed disease. The team has found that a combining an epilepsy medication with an anti-tapeworm drug kills myeloma cells in the lab and they now want to test this further. If successful, they plan to take this treatment into a clinical trial in older people with myeloma, and in people with hard-to-treat disease that has become resistant or has returned.

Developing CAR-T therapy for myeloma

Lead researcher - Dr Lydia Lee and Professor Kwee Yong, University College London
B-cell maturation antigen in multiple myeloma: biology and therapeutic target for chimeric antigen receptor strategy
This project is now complete. Dr Lee worked alongside Professor Yong to test a new CAR-T therapy for myeloma which targets two proteins called BCMA and TACI, found on multiple myeloma cells.  Researchers used chimeric antigen receptors (CARs) on T cells, in which surface receptors were modified into shapes that specifically bind BCMA and TACI. They also attached another protein called APRIL, which is highly attracted to binding to BCMA and TACI, creating a specific immune-based therapy called APRIL CAR.

Three pronged attack: Reducing bone disease, anaemia and sending myeloma cells back to sleep

Lead researcher - Professor Claire Edwards, University of Oxford
Targeting BMP signalling in the MGUS/MM bone microenvironment
Myeloma cells interact with the surrounding bone cells, driving forward the disease and bone damage. Drugs that block this interaction might be able to reduce bone disease and anaemia in myeloma. Now Professor Edwards wants to find out whether these drugs can also stop myeloma cells from growing, providing a potential new treatment for this disease.

Stopping myeloma before it starts

Multiple myeloma is nearly always preceded by the non-cancerous blood cell disorder termed monoclonal gammopathy of undetermined significance (MGUS). But not all people with MGUS will develop myeloma, and the reasons why only some people with MGUS progress to myeloma are poorly understood.

Researchers want to gain a deeper understanding of why some people who have MGUS develop myeloma, and are investigating ways in which we can prevent this from happening. 

We are also finding out the different patterns of gene changes that happen when MGUS changes to myeloma, and how these differ between individuals. If we can identify how each person is different, we can help doctors match the right treatment to the right person.

What role does the hormone adiponectin have in the development of myeloma?

Lead researcher - Professor Claire Edwards, University of Oxford
Regulation of tumour-suppressive adiponectin in MGUS and myeloma
Professor Edwards has identified that low levels of adiponectin – a hormone that modulates a number of metabolic processes - are associated with progression from MGUS to myeloma. She aims to find out how and why there is a decrease in adiponectin – this could help identify people with MGUS who are at greatest risk in developing myeloma.  

Finding genetic changes that lead from MGUS to myeloma

Lead researcher - Dr Surinder Sahota, University of Southampton
Defining MGUS evolution to multiple myeloma at the single cell whole exome level
Dr Sahota and his team are tracking the genetic changes that occur when MGUS turns into multiple myeloma, and how these differ between individual people. They will use this information to understand what genetic faults are driving disease progression, which may help with the development of a personalised therapy approach.

Tackling bone damage and searching for a cure

Multiple myeloma occurs in antibody-producing cells called plasma cells. Myeloma plasma cells infiltrate the bone marrow and other organs, and also activate cells called osteoclasts that break down bone. Once the myeloma causes areas of the bone to become weak, people will often experience bone pain and even fractures or breaks.

Within the myeloma cell population, there is a group of hidden, resting cells that are able to avoid the effects of chemotherapy. But these cells can become active after treatment, causing the myeloma to return.

Revealing new treatment targets in myeloma

Lead researcher - Professor Anastasios Karadimitris, Imperial College London
Transcriptional deregulation in multiple myeloma
Multiple myeloma is partly caused by genetic faults that disrupt the normal function of blood cells. However, once multiple myeloma has started, some healthy genes will also help cancer cells grow and survive. Professor Karadimitris and his team are working to identify these genes to see if they could become treatment targets. The team are also testing a new drug called I-BET762 that targets BET proteins, which activate bone destroying cells. This research will reveal new treatment targets, and may find new ways to prevent the bone destruction that occurs in multiple myeloma.

Preventing bone damage and tackling myeloma relapse

Chief investigator - Dr Andrew Chantry, University of Sheffield
Novel targets and therapeutic combinations in myeloma
Two of the most difficult problems faced by people with myeloma are the painful destruction of bone, and that despite successful treatment, the disease can come back. Dr Chantry and his team are testing a new treatment approach that will protect bone and, for the first time, repair the existing bone damage. The team will also identify the population of myeloma cells that are responsible for driving relapse, and will test new drugs to wipe out this group of cells.

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