Acute lymphoblastic leukaemia (ALL)

Acute lymphoblastic leukaemia (ALL)

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. These include acute lymphoblastic leukaemia (ALL), acute myeloid leukaemia (AML), acute premyelocytic leukaemia (APL), and B or T-cell acute lympoblastic leukaemia.

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

Acute lymphoblastic leukaemia (ALL) is an acute form of leukaemia, or cancer of the white blood cells found in the bone marrow. ALL happens when white blood cells don’t mature properly and grow too fast, and end up building up in the bone marrow, crowding out healthy blood cells. ALL develops more quickly than some other blood cancers, so quick diagnosis and treatment are really important.

There are different types of ALL. The most common are B cell ALL, T cell ALL, and Philadelphia positive ALL. These are all types of ALL that affect children as well as adults, but childhood and adult ALL are different. In this section we have included only research that is relevant to adults, so for information on childhood leukaemia research please go here for ALL projects, and here for AML.

We are supporting a number of ALL research projects that are looking into what causes leukaemia, and how treatment resistance emerges and what we can do to reverse it. We also have an exciting project that is looking at a new targeted treatment that is called ‘oncolytic virus therapy’.

Finding innovative ways to treat leukaemia

Treating ALL currently entails a number of powerful chemotherapy drugs. While these drugs are initially effective in reducing the number of ALL cells, this robust but often toxic approach only achieves long-term survival in half of the adults with ALL. And if a person relapses after chemotherapy, the chances of survival are extremely low. 

Chemotherapy kills cells that are in the process of splitting into two new cells. Because cancer cells divide much more often than most normal cells, chemotherapy is much more likely to kill them. But chemotherapy often damages healthy cells in the body too. This can leave people with long-term health issues such as heart disease and strokes, infections, fertility problems, and tragically, even the increased risk of a second cancer appearing later on in life. 

We want to develop better and less harmful treatments for people with ALL. 

One promising treatment approach is to use ‘oncolytic virus therapy’ to treat cancer. This is where viruses are engineered to seek out and destroy cancer cells, leaving healthy cells unharmed.

Turning the measles virus into a leukaemia killer

Lead researcher - Professor Adele Fielding, University College London
Leukaemia Acute lymphoblastic leukaemia (ALL)
Combining CD20 targeted, oncolytic measles virus with rituximab and corticosteroids in the treatment of acute lymphoblastic leukaemia
Professor Fielding and her team are genetically ‘reprogramming’ measles viruses to selectively infect and kill ALL cells from adults, leaving normal cells unharmed. To avoid the patients’ natural immunity that might clear the measles virus therapy, the researchers are investigating how to best combine the modified measles virus with two drugs: one that weakens certain immune responses, and one that might make the ALL cells more recognisable to the virus.

Tackling treatment resistance

Although many people with ALL respond to initial treatment, disease relapse occurs frequently. 

Leukaemia cells often stop responding to therapies because they develop new genetic faults that help the remaining leukaemia cells to find new ways to survive and grow, potentially leading to a hard-to-treat cancer coming back. 

Another mechanism of treatment resistance is that there are a small population of ‘sleeping’ leukaemic cells, which can resist chemotherapy treatment and cause late cancer recurrence. 

Our researchers are looking at how leukaemic cells evade the effects of treatment, and what can be done to overcome this resistance.

Tackling chemotherapy resistance in T-cell ALL

Lead researcher - Dr Marc Mansour, University College London
Leukaemia Acute lymphoblastic leukaemia (ALL) T-cell acute lymphoblastic leukaemia (T-ALL)
Overcoming chemoresistance and discovering novel therapeutics for high risk T-cell acute lymphoblastic leukaemia
The team want to find out what genes are responsible for chemotherapy resistance. They will also test drugs in the lab to find those that selectively kill cells that are missing the EZH2 gene. Researchers hope they can develop drugs that are targeted to leukaemia cells in people with high risk T-cell ALL, that will have fewer side effects than current chemotherapies.

Understanding what drives leukaemia

Our genes pick up mistakes that occur when cells divide. These mistakes are called faults or mutations and happen throughout our lives. They are caused by the natural processes in our cells, and by various other factors.

Oncogenes are genes that, under normal circumstances, play a role in telling cells to start multiplying and dividing. Normally, in adults, this would not happen very often. And in cancer, oncogenes are often permanently switched on, so the cell multiplies out of control. 

Healthy cells sense the presence of cancer genes as they lead to significant changes in the normal metabolism of the cell known as ‘cancer stress’. As a response, healthy cells undergo suicide or terminally arrest cell division, a mechanism considered as an immediate barrier to prevent cancer. Unfortunately, some cells pass this barrier leading to leukaemia and lymphoma. 

We have a research project that is looking at how cells ignore the warning signs of cancer stress, that could lead to a new treatment for leukaemia.

Characterising the genetic changes that arise from DNA damage in leukaemia and lymphoma

Lead researcher - Dr Niklas Feldhahn, Imperial College London
Leukaemia
Oncogene-induced stress as driver of B cell lymphomagenesis
Dr Feldhahn wants to understand how cells ignore cancer stress by identifying the changes in the DNA that confer cancer gene tolerance. Researchers will be looking at changes in the BCR-ABL1, MYC and RAS genes, that are frequently mutated in either ALL, CML or Burkitt’s lymphoma. The team want to develop strategies to reverse these changes in cancer cells, which could be a new and promising strategy for the future treatment of leukaemia and lymphoma.

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