MANY T cell leukaemia patients could be treated by a drug which suppresses the BCL-2 protein, according to researchers from KU Leuven, Leuven, Belgium. In their study, the team were able to pinpoint a specific ribosome defect which causes an overproduction of BCL-2, which in turn enables the survival of cancer cells in many of these patients.
Previous research has revealed that defects in ribosomes, the protein builders of the cell, plays a role in various types of cancer. In this new study, for the first time the impact of a ribosome defect on T cell leukaemia has been described. This defect is present in 10% of paediatric T cell leukaemia patients and leads to a substantial increase in the production of BCL-2, known as the ‘survival protein’. BCL-2 is able to prevent cell death, and when it is created in particularly large quantities, can enable cancer cells to escape treatment.
Survival of Cancer Cells
“Cancer cells take advantage of the BCL-2 protein: it helps them to survive under difficult circumstances, including chemotherapy,” explained Prof Kim De Keersmaecker, KU Leuven.
Suppression of T Cell Leukaemia
The researchers then tested a BCL-2 suppressing drug in mice with T cell leukaemia and the specific ribosome defect; this drug is already used to treat chronic lymphocytic leukaemia. They found that this treatment successfully suppressed T cell leukaemia in the mice.
The findings provide hope that such a treatment could be used in T cell leukaemia patients with this ribosome defect in the future, although the authors acknowledged that more research is needed before a specific treatment can be developed.
“This hasn’t been tested on human beings yet,” elucidated Prof De Keersmaecker. “Patients with leukaemia often get a drug cocktail, while our study only tested the BCL-2 inhibitor. That’s why our follow-up study will focus on a cocktail of this BCL-2 inhibitor and other drugs. For patients with the ribosome defect analysed in our study, this avenue is definitely worth examining in greater detail.”
James Coker, Reporter
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