Dr Gemma Kelly at Walter and Eliza Hall Institute:"If we disable this protein called MCL-1 then the cancer cells die."
Researchers have discovered that by disabling a protein found in lymphoma cells they can limit the cancer's growth and ultimately make it disappear.
The finding has implications for the development of new drugs to treat not only lymphoma but also other types of blood cancers such as leukaemias and hard tumour cancers, including some lung cancers.
Up to 70 per cent of human cancers have unusually high levels of a protein known as MYC. The protein causes cancerous changes in cells by forcing them into abnormally rapid growth.
''What we've found is that these MYC-driven cancers are exquisitely dependent on a protein called MCL-1 for their continued survival,'' said molecular biologist and lymphoma researcher Gemma Kelly. ''So if we disable this protein called MCL-1 then the cancer cells die.''
The finding by researchers at Melbourne's Walter and Eliza Hall Institute is published in the journal Genes and Development on Wednesday. The research team showed that when denied the protein MCL-1, the cancer cell death was rapid.
''It's dramatic,'' Dr Kelly said. ''It occurs within 24 to 72 hours.''
Dr Kelly said cancerous cells also proved more sensitive to a reduction in MCL-1 protein levels than healthy cells, suggesting the side effects associated with a treatment using this approach would be tolerable.
The research team from the institute's molecular genetics of cancer division, including Marco Herold and Andreas Strasser, used cell samples taken from patients diagnosed with Burkitt lymphoma. These cells were then used to grow more cells in culture for research to assess how to stop MCL-1 from functioning.
The information allows researchers to identify novel targets, which would aid the development of new cancer drugs.
Professor Strasser said in many cases, even a 50 per cent reduction in the levels of MCL-1 would kill the majority of cancer cells allowing a patient to go into long-term remission. ''It means that the targeting of MCL-1 might really be possible without causing too many side effects in normal tissue,'' he said.
The research builds on more than three decades of work at the Walter and Eliza Hall Institute into how the MYC protein drives cancer development and how the survival of normal and cancerous cells is regulated.