Researchers from a leading Australian university have made a significant breakthrough in overcoming drug resistance in certain cancer treatments.
Scientists from the University of South Australia and SA Pathology’s Centre for Cancer Biology have discovered a way to suppress a specific protein that promotes resistance to drugs commonly used to treat a rare, but devastating type of blood cancer.
Acute myeloid leukaemia (AML) affects blood and bone marrow. It’s not technically a single disease, rather AML is the name given to a group of leukaemias that develop in the myeloid cell line in the bone marrow. Myeloid cells are red blood cells, platelets and all white blood cells excluding lymphocytes.
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AML can occur at any age but is far more prevalent in those aged 60 and over. The condition is rare, and accounts for just 0.8 per cent of all cancers diagnosed in Australia. The disease recently claimed the life of professional golfer Jarrod Lyle.
Apart from traditional chemotherapy, AML is often treated with a drug known as Venetoclax, but many patients report that after initially responding well to the treatment, over time the AML cells become resistant to the drug.
In a study published in the journal Blood, the research team demonstrated that by altering lipid metabolism in the body, they could artificially inhibit a protein that was responsible for the resistance.
“This process makes AML cells exquisitely sensitive to Venetoclax, while leaving the normal white blood cells unaffected,” says Dr Jason Powell, one of the co-authors of the study.
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The debilitating condition can cause a number of potential symptoms including: anaemia, persistent fatigue, dizziness, shortness of breath, frequent or repeated infections, slow healing from wounds, unexplained bruising, swollen lymph nodes and bone pain.
Up until now, the prognosis for AML sufferers was grim, with fewer than 30 per cent of patients surviving five years after diagnosis.
“Each year in Australia, around 900 people are diagnosed with AML, a cancer of the blood and bone marrow characterised by an overproduction of cancerous white blood cells called leukaemic blasts,” says Professor Stuart Pitson, another study co-author.
“These cells crowd out normal white blood cells, which then can’t do their usual infection-fighting work, thereby increasing the risk of infections, low oxygen levels and bleeding.”
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It’s hoped the discovery will open the door to new drugs and therapies being developed to treat AML and potentially improve survival rates.
“For most people with AML, the chances of long-term survival are no better now than they were last century,” Assoc Prof Ross says SA Pathology haematologist Dr David Ross says.
“Now, we have a chance to remedy that. New treatments that prevent Venetoclax resistance have the potential to prolong survival, or even increase the chances of a cure in a disease for which improved outcomes are desperately needed.”
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