Although we’ve been to some fascinating sessions over the previous three days, ultimately we felt that this year’s NCRI final day was the most thought-provoking, with some really fascinating and challenging talks.
Here’s our round-up from the final day of the 2011 NCRI Cancer Conference, where the focus was on bowel cancer genes, personalised screening, and the cancer genome.
Personalised bowel cancer care?
Harking back to Monday’s session on stratified medicine, she gave us a guided tour of the growing understanding of the different genes that go wrong in bowel cancer, and how this will one day influence how doctors decide which treatments to give different patients.
The challenge, she said, lies in the fact that there don’t seem to be major common gene faults that allow us to tell the difference between different types of bowel cancer. This – combined with the unusual environment created by the fact that millions of cells lining the bowel are replaced every three days – means that progress in identifying new genes driving the disease is hard.
But Professor Tejpar believes they’re slowly moving towards being able to subtype the disease using molecular information, and that this will eventually change the way we approach the design of clinical trials and ultimately treatment.
Inherited risk and cancer screening
Next, Professor Ros Eeles, a Cancer Research UK-funded expert in prostate cancer genetics at the Institute of Cancer Research, hosted a standout session exploring how our knowledge of inherited genes that increase cancer risk is shaping the screening programmes of the future.
As Professor Eeles explained, the NHS currently decides who to screen for cancer based mainly on their age. For example, younger women are screened for cervical cancer, while older women are screened for breast cancer – following our understanding of who is most at risk.
But scientists are learning more and more about inherited genetic changes that can increase a person’s risk of cancer. Professor Eeles and her colleagues are looking at how they can use this knowledge to improve screening and detect more cancers early.
Professor Doug Easton, a Cambridge-based senior Cancer Research UK scientist, spoke about breast and prostate cancer screening. He explained how our growing knowledge of genetic changes that boost risk (the subject of his research) could help to give personal risk estimates to people who have a family history of these cancers.
He and his colleagues in Cambridge have already developed computer program called BOADICEA that can give breast cancer risk estimates, and ongoing research into cancer genetics should make techniques like this possible for other types of cancer in the future. (We wrote in detail about BOADICEA last year)
Next up was Dr Harry de Koning, of Erasmus Medical Centre in the Netherlands and Johns Hopkins Bloomberg School of Public Health in the US. He focused on how screening for breast cancer can be tailored for women with inherited faults in their BRCA genes, who are at very high risk of developing the disease at a young age.
His data suggested that MRI scans are much better than mammograms at detecting cancer in younger women with these gene faults, and should be offered every year between the ages of 25 and 60. At the moment in the UK some women with a family history of the disease are offered MRI scans, but more research like this could give us a better idea of exactly who should be offered special screening and at what age.
The final speaker was Dr Mark Robson, from the Memorial Sloan Kettering Cancer Center in New York. His talk took a slightly different slant, asking how genetic information can help to treat women with breast cancer once they’ve been diagnosed.
Breast cancers can be split into many different types that may need different approaches to treatment, and Dr Robson outlined some of the recent research in this area. For example, it looks as if the types of tumours caused by BRCA faults could actually be more sensitive to some types of chemotherapy. And another interesting area of research is finding out if women with certain genetic changes could be more susceptible to the side effects of hormone-blocking drugs like aromatase inhibitors – understanding these patterns could help to personalise treatment for women with breast cancer.
The cancer genome
Given the heavy focus on cancer genetics at this year’s conference – and how it holds the key to future treatment – it was fitting that the closing session should be given by one of the world’s leading experts in the field – Professor Mike Stratton, of the Wellcome Sanger Institute in Cambridge.
Professor Stratton is perhaps best known in the cancer community for being part of the Cancer Research UK-funded teams that discovered the BRCA2 gene and its link with breast cancer, as well as helping pin down the involvement of mutations in another gene – BRAF – in melanoma skin cancer.
Stratton’s team has now analysed the entire genome of thousands of different cancers, and looked at the patterns that emerge. What he’s been uncovering has been challenging the fundamentals of how we think about cancer as a disease.
We often, for example, talk about cancer being caused by ‘the slow accumulation of DNA damage over a person’s lifetime’. But this seems to be wide of the mark. In studying the nature, type and origin of the ‘driver’ DNA mutations in cancer – those that cause the disease rather than being caused by it – it appears that the overwhelming majority occur after cancer has developed.
Looking at data from analyses of breast cancer samples, Stratton spoke of the 400+ genes they’d found associated with the disease. Astoundingly, over half of the cancers Stratton’s team analysed are driven by rare mutations in genes not previously linked to cancer – as Stratton remarked, “breast cancer is a hugely diverse disease”. This has obvious implications for the new era of treatments which aim to target cancers with specific defects.
Building on this theme, Professor Stratton talked of two extremes – in the first, every cancer with a different genetic signature is a unique form of the disease, which will require separate studies, trials and treatments.
In the second possible scenario, these hundreds of different genetic variations can be grouped into a smaller number of clinically similar types – a much more manageable and less daunting scenario. But which of these reflects reality?
Stratton feels it’s is likely to lie somewhere in between these extremes, but quite where we don’t know. He evidently intends to find out.
So that brings us to the end of our daily conference summaries. Every year’s conference brings new revelations, and a feeling of incremental but substantial progress – and this year was no different. Although there was a shortage of truly ‘blockbuster’ announcements, there was a real sense that slowly but surely, a new age of more personalised, tailored cancer treatment is arriving.
But as Professor Stratton’s closing talk reminded us, for all the promise of this new era, there’s still so much more to know and understand about what makes cancer tick.
Needless to say, the UK’s thriving research community will take up this challenge and help find out. We look forward to what next year’s conference will bring, and wish the doctors, nurses, researchers and others all the best in the meantime.
Henry, Kat, Nell and Julie