Researchers show how leukemia cells 'hide' from treatment
In a first-of-its-kind study collaboration, new research has uncovered that chronic lymphocytic leukemia (CLL) cells may switch between different survival signals, helping explain why treatments work well for some patients but stop working for others. These findings could ultimately help pave the way for more personalized treatment.
A groundbreaking study has revealed that chronic lymphocytic leukemia (CLL) cells may switch between two distinct survival signals, potentially explaining why some patients respond well to certain treatments while others develop resistance to them. Researchers from the University of Sussex, led by Professor Simon Mitchell, developed computer models to predict how CLL cells from different patients would respond to survival signals.
The research, published in the journal Blood, could pave the way for more personalized treatment approaches. CLL is the most common adult leukemia, and while Bruton's tyrosine kinase inhibitors (BTKi) have improved outcomes, responses can vary. Some patients eventually develop resistance to treatment, but mutations are not always the cause.
The study found that CLL cells can use a second pathway, called Toll-like receptor 9 (TLR9), to evade treatment when the usual B-cell receptor (BCR) pathway is blocked. This new understanding could help scientists and clinicians better predict treatment responses, identify patients who may need additional drugs, and avoid ineffective treatments, potentially reducing side effects and hospital stays.
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