One of the worst things you can hear from you doctor is that you, or a loved one, has “triple negative” breast cancer. It stubbornly refuses to respond to the best treatments available, so doctors have to resort to chemotherapy. It strikes 16 per cent of breast cancer patients, most of them younger than 40. But we may finally have figured out how to beat it.
In the largest genetic analysis ever of these types of tumours, scientists have discovered we’ve been treating them all wrong, for years. By sequencing the DNA of 100 triple negative tumors, they’ve found that the tumours are vastly different. Which means doctors should be treating them vastly differently — but until now they were mostly treated basically the same way.
No two tumour genomes were even similar, let alone exactly the same.
“Seeing these tumours at a molecular level has taught us we’re dealing with a continuum of different types of breast cancer here, not just one,” said Steven Jones, a co-author of the study, which is published today in the journal Nature. Jones is a molecular biology and biochemistry professor who leads bioinformatics research at Simon Fraser University in British Columbia, Canada. “These findings prove the importance of personalising cancer drug treatment so that it targets the genetic make up of a particular tumour rather than presuming one therapy can treat multiple, similar-looking tumours.”
Triple negative breast cancer tumours are characterised by a lack of oestrogen, progesterone and herceptin receptors on the surface of their cells. It’s a trio of a hormone, a steroid and a protein that’s vital for a tumour’s responsiveness to drug therapies, which are designed to knock out those receptors. That means doctors throw everything they’ve got at triple negative breasts cancer: surgery, chemotherapy and radiation — a cocktail of treatments that can be almost worse than the disease itself.
But with this new knowledge that each tumour is unique, researchers hope to tailor-make treatments that will actually work based on patients’ genetic mutations, Samuel Aparicio, another co-author and researcher at the BC Cancer Research Center, told me. “This will mean sequencing patients tumours to learn their genetic makeup, initially in the context of a clinical trial of the drugs suggested by the mutations. The longer term impact is that it also provides us with a roadmap for future drug development by suggesting combinations of drugs that need to be developed.” Let’s hope that “longer term” isn’t too far off. [Nature]