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24 January 2017

Scottish researchers say they have identified how a faulty gene leads to lymphoma becoming to resistant to steroid drugs such as dexamethasone.

Their work centres on the RUNX1 gene and the scientists say their work suggests that finding ways to target the gene could improve treatment with these drugs.

The study showed the gene altered the balance of sphingolipids. When it was abnormally expressed, levels of ceramides, which promote cell death, were reduced. At the same time a lipid that stimulates cell growth and survival, sphingosine-1-phosphate, was enhanced.

This would interfere with the action of dexamethasone, which induces sphingolipids in lymphoma cells to promote cell death.

Professor James Neil, of Glasgow University, and colleagues, have reported their findings in the Journal of Cellular Biochemistry.

Professor Neil said: “Abnormal RUNX1 expression made lymphoma cells more resistant to treatment with dexamethasone, suggesting that drugs that can switch off the gene may be able to reverse treatment resistance in patients.

"An exciting possibility would be to see if new RUNX1-inhibiting drugs could be used in combination with steroids to reduce treatment resistance – something that we are looking forward to testing in the lab.”

Dr Alasdair Rankin, director of research at the charity Bloodwise, which backed the research, said: "This early research, carried out in lymphoma cells, has identified how faulty RUNX1 can contribute to resistance to steroid treatment.

"The next steps will be to see if targeting RUNX1 could help prevent cancer cells becoming resistant to steroid treatment, before drugs can be developed to help patients.”

Source: Runx1 orchestrates sphingolipid metabolism and glucocorticoid resistance in lymphomagenesis Journal of Cellular Biochemistry 10 January 2017; doi:10.1002/jcb.25802
Link: http://onlinelibrary.wiley.com/doi/10.1002/jcb.25802/full



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