Matt Kaiser
Posted by
Matt Kaiser

Supporting groundbreaking blood cancer research

Matt Kaiser
Posted by
Matt Kaiser
05 Aug 2013

We are delighted to have recently committed over £7million to fund some exciting and innovative blood cancer research. So I wanted to share this excitement by telling you a bit more about what will be carried out.

We need to make every penny raised by our dedicated supporters count. I’m confident that this newly funded research will take us closer to the day when our mission – to cure, prevent and improve treatment of blood cancers – is complete.

The awards fall under three broad aims that are central to our mission to beat blood cancers. These boundaries are less than black-and-white, though, as many researchers push their laboratory findings towards the clinic.

Revealing how blood cancers work

The first set of projects aim to figure out the faulty cues that cause cancer cells to go awry.

Professor Tessa Holyoake at the University of Glasgow will test whether disrupting two central master ‘watchdog’ signals – p53 and c-Myc – in chronic myeloid leukaemia (CML) cells is enough to kill all CML cancer cells and CML stem cells. In chronic lymphocytic leukaemia (CLL), Professor Graham Packham at the University of Southampton will look at how the genetic messenger that translates DNA sequence into protein is altered by the activation of a protein stuck on the surface of some immune cells – a key step in the progression of the disease.  

Dr Markus Müschen at The Institute of Cancer Research will investigate what happens in acute lymphoblastic leukaemia when two, normally separate proteins – BCR and ABL1 – fuse together and kick-start uncontrollable cell multiplication. The twist is that too much signal can lead to cell death, meaning there is a ‘goldilocks zone’ of activation where cancer can thrive. Professor Paul Farrell at Imperial College London will study defective versions of proteins in the so-called ‘RUNX’ family, which are necessary for immature blood cells to develop into mature cells.

Dr Daniel Tennant at the University of Birmingham will explore some of the changes that occur in the supporting network of cells within the bone marrow, as this can create a safe haven for abnormal white blood cells to gather, potentially leading to multiple myeloma.

And why is all this important?

By understanding these faulty protein signals, scientists can detect rogue cells earlier and design drugs to hit the root cause.

Driving smarter, faster diagnosis

We know that the earlier we pick up a cancer, the better the chances of a cure, so early diagnosis is crucial to improve survival.

Professor John Lunec at Newcastle University wants to detect leukaemic cells earlier by using the latest DNA sequencing technology to spot genetic mistakes underlying faulty ‘p53’ proteins. This is a gatekeeper signal within our cells that normally senses when DNA is too damaged for the cell to multiply.

Professor Philip Blower’s team at King’s College London will inject radioactive molecules – specially designed to home in on cancerous cells – into multiple myeloma patients. His sensitive cutting-edge imaging techniques will then provide an accurate way to detect and locate early cancers and monitor response to therapy in real-time.

Professor Duncan Baird at Cardiff University will develop a unique laboratory test to quickly and accurately segregate newly diagnosed CLL patients into those whose disease is progressing so slowly that they may never need treatment and those whose disease will progress more rapidly. He may even be able to adapt it for other blood cancer patients too. This direct translation of basic research findings into the development of technology to be used in the clinic seems particularly exciting.

Taking a different tack, Professor Richard Houlston at The Institute of Cancer Research will compare DNA from people with and without blood cancer, to find out how the small variations in the DNA inherited from our parents may raise our risk of developing leukaemia, lymphoma and myeloma. This will better predict who is at risk, potentially leading to more informed personalised treatment and screening programmes.

Inspiring new treatments & better care

Other projects will use our existing knowledge of blood cancer biology to improve treatment.

Professor Michael Overduin at the University of Birmingham will work out exactly which parts of a faulty 'PTPN11' protein’s minute 3D structure can be hit with drugs, to cripple the wayward molecule in juvenile myelomonocytic leukaemia. Also homing in on precise faults in the cell’s machinery, Drs Richard Darley and Alex Tonks at Cardiff University seek to improve acute myeloid leukaemia (AML) therapy by hitting the disease’s “Achilles’ heel”.

Current treatments that harness a patient’s own immunity to attack rogue cancer cells are promising, but they rely on large doses and previous toxic chemotherapy. Dr David Gilham at the University of Manchester will tweak the immune cells to perform better in the absence of prior treatment and examine other immune reactions that may impede anti-cancer activity.

Professor Mark Drayson and Dr Farhat Khanim at the University of Birmingham will study how the combination of a cholesterol-lowering drug and a female contraceptive pill can kill rogue cells in some blood cancers and whether other drugs can enhance the anti-cancer effect.

In a technically ambitious venture, Dr Elisabeth Walsby at Cardiff University will build a laboratory replica of the intricate structure of cancer cells and supporting cells. Similar to Dr Tennant’s work, this is to more thoroughly probe how CLL cells can survive in protected ‘microenvironments’ in bone marrow and lymph nodes.

Moving directly into the clinic, Professor Alan Burnett at Cardiff University is testing a suite of potential drugs in a series of innovative clinical trials to more quickly determine which ones are most suitable for and most effective in elderly AML patients.

And, finally, we were thrilled to extend our investment in a co-ordinated network of leading clinical trial centres around the UK. The initiative, having already won plaudits in the clinical community and government, will give more blood cancer patients access to life-saving treatments and set a model for establishing clinical trials in the UK.


As you can see, the projects will probe a real diversity of blood cancers. And there is a spectrum of ‘basic’ research – that is, investigation into the biology of blood cancers – and efforts to translate this knowledge into patient benefit – the ultimate goal of Leukaemia & Lymphoma Research.

Many of the lead researchers of these projects have not received LLR support before, and we’re really glad to broaden LLR’s community and welcome fresh ideas to tackle blood cancers.



Can you also tell us about the research into lymphomas? All the above is research into leukaemias.
Many thanks.


Dear Jane, you can find out about our research into Lyphomas by clicking on this link.

Thank you for your interest


Matt Kaiser

Hi Jane,

Thanks for reading. As Helen pointed out, we're doing a lot of work already in lymphomas, and the research above is just a small subset of our overall research portfolio.

Having said that, even in the work I described, there are a lot of studies related to lymphomas. Disruption of the RUNX1 protein I mentioned can cause some B cell lymphomas, so Paul Farrell's work will improve our understanding of the biology of those diseases. Part of Richard Houlston's work is to find out the inherited risk of Hodgkin lymphoma, which may help to personalise treatment and offer preventative steps. David Gilham hopes that his treatment approach will be used in B cell lymphomas, and Mark Drayson will study the effectiveness of their therapy specifically on B-cell Non-Hodgkin lymphomas

Finally, I should say there are some common mechanisms across different types of blood cancer. So other work, such as Duncan Baird's and the p53 studies, once it has been proven in one disease can filter through to benefit other blood cancers, like lymphomas.

Hope that helps!



I would be really interested, as would my family, including my brothers and adult children if you were investigating genetic links as my father has Waldenstrom's macroglobulinemia and I was diagnosed with Myeloma three years ago. Weant to understand any genetic link within the family and these diagnoses

Matt Kaiser

Hi Mandy,

Sorry to hear of your diagnosis and I hope things are going OK.

As for the inheritance of these conditions, Waldenström macroglobulinemia (WM) is known to be more common in some families. This suggests a genetic susceptibility exists, but we also know there are other risk factors like age, sex and certain infections. An estimate from the American Cancer Society suggests that about 20% of patients with WM have a close relative with WM or with a related B-cell disease.

WM is linked to multiple myeloma by a shared precursor condition called 'monoclonal gammopathy of undetermined significance' (MGUS). One review suggests that 1st degree relatives of WM patients have an increased risk of developing WM and some subtypes of non-Hodgkin lymphoma (which implies shared susceptibility genes), but not Hodgkin lymphoma or multiple myeloma. However, there does seem to be an increased risk of relatives of WM patients developing MGUS, which may be how WM and myeloma are linked.

The picture is complicated (it always is as many many genes are involved), so more work is definitely needed. The work we are funding by Richard Houlston, which I wrote about in this post, is tackling exactly these questions. He is taking a broad view across many blood cancer types and asking whether there are any regions of the genome that are associated with a higher risk of developing certain blood cancers. We've written recently about some of his findings in myeloma and we hope to see more of these groundbreaking findings very soon.