Chronic myeloid leukaemia (CML)

Chronic myeloid leukaemia (CML)

Leukaemia is a type of blood cancer that usually affects white blood cells and bone marrow. White blood cells are an important part of your immune system that fight infection, and bone marrow is where blood cells like these are made.

There are many different types of leukaemia. Some types develop faster, and are known as acute leukaemia. 

Other leukaemias develop more slowly and are called chronic leukaemias. These include chronic lymphocytic leukaemia (CLL), chronic myeloid leukaemia (CML), chronic myelomonocytic leukaemia (CMML), hairy cell leukaemia (HCL) and large granulocytic leukaemia (LGLL).

But each type of leukaemia acts differently, and will need to be treated differently. 

Survival rates for people diagnosed with CML have been transformed with the development of tyrosine kinase inhibitors (TKI) – drugs that block the faulty protein at the heart of CML and keep the leukaemia in check.

Most people living with this blood cancer can now take a single pill and control their disease. But they aren’t cured, and some people can’t tolerate the side effects of their treatment, or become resistant to it, or find that their CML has come back. 

Our research is looking at new ways to eradicate CML completely, offering the chance of a real cure. And we want to find ways to improve the quality of life of people with CML who are taking these drugs.

 

Destroying the foundation of CML

Despite their success, TKIs cannot kill the ‘master’ CML cells, so-called ‘cancer stem cells’, which may make up only a tiny proportion of the total population of cancer cells, but produce a steady stream of new CML cells. This is why current treatments for CML are not a cure.

Searching for a cure for CML

Lead researcher - Dr David Vetrie, University of Glasgow
Leukaemia Chronic myeloid leukaemia (CML)
Crosstalk between PRC2 and BCL6 in regulating CML stem cell survival: From epigenomics to novel therapeutic approaches
Dr Vetrie is studying how two proteins called EZH2 and BCL6 work together in leukaemic stem cells. This project will help to understand the biology behind the function of these two proteins, and allow researchers to design better ways to treat and eventually cure CML.

Overcoming drug resistance and improving cure rates

Lead researcher - Professor Tessa Holyoake, University of Glasgow
Leukaemia Chronic myeloid leukaemia (CML)
Targeting p53, c-Myc and PRC2 regulatory hubs: A systematic and stratified approach to deliver new therapeutics for CML
Professor Holyoake and her team are finding ways to predict which people with CML will do well on TKIs, and those that will require alternative approaches. The team are investigating how networks of proteins in leukaemia stem cells work together to aid cancer cell survival, and how they may be targeted with new drugs. This research hopes to significantly improve CML cure rate, and provide new forms of treatment for people with drug resistance and advanced phase disease.

Improving the lives of people living with CML

Tyrosine kinase inhibitor (TKI) drugs have improved the outcome for people with CML dramatically. Most people can take a daily single pill to control their CML and can live a normal life. 

But although TKIs can control the disease, people with CML have to stay on their treatment for life, and may experience substantial side effects to their medication. 

We have provided some support for a trial called DESTINY, that wants to find out if people who are doing well on their TKI can safely reduce their dose, or even come off it altogether. However, the study is not complete and reducing or stopping treatment will not be right for everyone, so it’s really important that people with CML talk to their doctor before considering any change to their medication.

We are also supporting a trial that specifically wants to improve the outlook for people who are doing less well, and have progressed to the blast phase of CML. For this group of people, treatment with current TKIs becomes limited because they have already received all the available drugs in succession during the chronic phase. 

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