Researchers have found a potential new weapon in the fight against melanoma which could help treat late-stage cancers that are resistant to existing drugs.
The method involves knocking out one of the survival pathways of cancer cells, and was developed by researchers from the Babraham Institute, pharmaceutical company AstraZeneca and the Cancer Research UK Cambridge Centre.
Researchers say it is effective at triggering tumour cell death and delaying treatment resistance in the deadliest form of skin cancer.
Lead researcher Mathew Sale from the Babraham Institute said the study demonstrated melanoma cells were "addicted" to a protein, MCL1, for survival - but only when they are treated with existing drugs.
Dr Sale said treatments that target the MCL1 protein in conjunction with existing drugs can be more effective than existing drugs alone.
"By targeting both vulnerabilities at the same time we can kill melanoma cells, causing greater inhibition of tumour growth over a longer time period," he said.
Cancer cells can rely on various "survival proteins" to stay alive despite the effect of treatment.
So far researchers have not been able to isolate which of these proteins are used by melanoma cells, but the study published in Nature Communications found that melanoma cells rely on the MCL1 protein.
MCL1 is critical for the cells to survive when exposed to standard drugs that inhibit other proteins, such as trametinib or vemurafenib.
Researchers used an MCL1 antagonist in the lab and showed that by blocking MCL1, the agent disabled the back-up survival system in melanoma cells.
Combining it with a treatment like vemurafenib had a double effect against cancer cells, eliminating them more effectively.
The drug combination also worked by reducing, or sometimes eliminating, melanoma tumours derived from patients and grown in mice.
Group leader at the Babraham Institute Simon Cook said the study was based on more than a decade of research.
"This study stems from 15 years of basic research in which we have sought to understand the normal signals that control whether a cell lives or dies," he said.
"... Thanks to a long-standing partnership with AstraZeneca and the Cancer Research UK Cambridge Centre we were able to translate this basic research to understand and potentially better treat melanoma."
Australian Associated Press
