Researchers studying cancer’s DNA have made recent leaps forward in understanding two aspects of the disease. The first has been in unravelling how the genetic chaos inside a tumour accrues over time.
In 2012, for example, Professor Swanton’s team showed that – just as Darwin might have predicted – kidney tumours evolve from a single group of damaged cells, but rapidly diversify as they grow and spread – ending up as a variegated, motley crew of disordered clumps, each harbouring its own unique spectrum of DNA errors.
Others have revealed a similar situation – known as ‘intratumour heterogeneity’ – in other types of cancer, including breast, prostate and ovarian cancers; leukaemia; and glioma brain tumours. The stark message is that, to cure patients with advanced cancer, the rules governing how tumours evolve need to be worked out urgently.
The second has been to uncover the fundamental processes causing this genetic chaos.
Two classics of this genre emerged in 2009 from the Wellcome Trust Sanger Institute in Cambridge. Focusing on lung cancer and melanoma skin cancer, researchers pinpointed the fingerprints of tobacco smoke and sunlight in the faulty ‘letters’ of a tumour’s DNA.
They followed this up with a tour de force in 2013, discovering at least 20 different chemical processes leaving telltale fingerprints in cancer’s DNA.
So researchers now have two powerful weapons to crack open cancer’s secrets: a way to reconstruct a tumour’s genetic history; and the ability to identify the forces that shape it.
But can these two approaches be combined? Can the different processes acting during a tumour’s evolutionary history be unravelled?
Read full, original article: Lung cancer evolution – a journey through space and time
