Eureka Live: Beating the Big C
Cancer treatment research has made some remarkable breakthroughs in recent years, and with the focus on targeted cancer therapies, will continue to do so over the next ten years.
This month’s Eureka Live event at the Cheltenham Science Festival focused on how these therapies work and how they could revolutionise what it means to be diagnosed with cancer in the future.
Professor Mike Stratton, Head of the Cancer Genome Project and Director of the Wellcome Trust Sanger Institute, spoke of how far genome sequencing has come since the Human Genome sequence was announced ten years ago. Back then it took 13 years to sequence one complete genome. Now, the Cancer Genome Project aims to sequence 25,000 cancer genomes in seven years.
“With the Human Genome Project, we were like Captain Scott in Antarctica. We’d reached the end of the journey but didn’t really know what it meant. Now, we have a GPS view of the genome,” said Professor Peter Johnson, chief clinician at Cancer Research UK.
Stratton explained that cancer is caused by “driver abnormalities” in key genes – just one badly behaving cell can trigger the development of cancer. “By identifying these genes, we can make drugs to target the proteins they make. We can switch off cancer genes and switch off cancer” Genomic sequencing, he said, is a vastly better diagnostic tool then microscopic biopsy of a tumour, as it can highlight the precise target for a drug.
Johnson told of one mother who was given four extra years of life thanks to gefitinib (Iressa). The drug targeted the effects of the P53 gene mutation that caused the cancer to spread from her breast to her brain and lungs.
The next step is to make these treatments available to all suitable patients. Johnson later suggested a network of cancer centres, bringing together Cancer Research UK, The Technology Strategy Board, the Department of Health and the Medical Research Council, to make the most effective use of mapped cancer genomes sequences.
Professor Fran Balkwill, of the Centre for Cancer and Inflammation at Barts and the London Medical School, said an early cancer cell was like a delinquent child: a “cancer neighbourhood” allows cancer to spread, in the same way that a bad neighbourhood doesn’t exactly encourage good behaviour. A cancer neighbourhood, said Balkwill, consists of non-cancer cells that have the cancer gene – if we target these as well as the cancer cells, the cancer cannot move, mutate and spread. To control and destroy cancer, the immune system needs to be “woken up,” she said.
Mark Henderson, Science Editor of The Times and our chair for the evening, wondered if cancer could become a chronic, rather than life threatening, in a similar way to HIV. While Peter Johnson agreed that we “must aim high” he said we have to be “practical and feasible”. Cancer can be kept under control using targeted treatments for many years, but it often comes back.
Stratton explained that tumours evolve and acquire more mutations – 99.99 per cent of a tumour might be killed, but the survival of one single cancer cell could have additional mutations resistant to the current treatment.
The strategy is to create second and third generation targeted therapies that kill off these remaining rogue cells. With the mapping of more cancer genomes, future “dynamic” treatments can be planned in advance and the original drug switch for the second generation one before the cancer comes back.
Audience questions prompted a look at the lack of evidence for cancer-preventing claims of ‘superfoods’ and the pharmaceutical industry’s search for profits. Mike Stratton recounted how one pharmaceutical company was advised by accountants not to develop a certain drug to treat Chronic Myeloid Leukemia because there was no money in a drug that so dramatically cured patients. But they soon changed tack when they realised patients were coming out of remission and would need to take the drug for the rest of their lives.
Peter Johnson highlighted the need to narrow the relative costs of drugs – something that targeted therapies could help with. If a drug is known to have a specific effect on a certain type of mutation, it can be given to specific patients, saving the NHS from spending money on drugs that will not work for many.
The hope is that one day cancer can be targeted, remitted and in some cases completely destroyed, so that a cancer diagnosis is less of the death sentence it is often perceived as
today. The panel agreed that improving early diagnosis was important in this. Balkwill pointed out that epithelial cancers can be prevented by stopping cancer cells invading the basal cell membrane. Mapping the early genetic changes of cancers, particularly prostate, would be essential.
As Peter Johnson said “the revolution in diagnosing cancer will be the biggest medical advance of the next decade.”
Louise Crane, Special Projects Officer, Wellcome Trust