![]() ![]() Making restriction maps was my first use of “Molecular Biology” software It will take time but I am confident we will get there.Assembling fragments, detecting SNPs, and managing raw sequence data And in the coming years, we will test a lot more until we find the best one to tackle ecDNA and halt its pro-cancerous activities. We have also discovered a drug that has a promising effect on this protein. This point was backed by Chang: “We are now looking to pinpoint the achilles heel of ecDNA and have identified a protein that helps hold it together. “The crucial point is that once we have found the cause of the problem then it becomes possible to develop and try out all sorts of drugs and therapies to tackle that.” “It should be noted that ecDNA is a feature of cancer and not healthy tissue, so that raises hopes that when we find ways to remove it – through drugs or some form of therapy – then it will not have unpleasant side-effects,” said Dr Mariam Jamal-Hanjani of University College London Cancer Institute. Nevertheless scientists are confident that they will be able to find ways of removing ecDNA from patients. “That provides almost infinite adaptability.” ![]() “It can almost completely disappear from a tumour and then come back after you stop drug treatments,” said Professor Charlie Swanton of the Francis Crick Institute in London. Then it reappeared once it was safe for it to start causing damage again.”įrom this perspective, ecDNA is not just a villain. ![]() They are actually on extrachromosomal DNA,” said Mischel.“The vulnerable gene had quickly disappeared when threatened by cancer drugs and was hidden in ecDNA. We have now discovered that, in some of the most aggressive forms of cancer, the oncogenes aren’t where we thought they were. “However, resistance to those drugs or therapies often appears after a while, and this allows the cancer to return. These genes are known as oncogenes and they can be targeted by a range of drugs and therapies. In recent years, scientists have shown that tumours occur because normal genes in a cell go wrong and cause that cell to divide uncontrollably. In this case, it has provided £20m to fund the work on ecDNA’s involvement in cancers and has involved teams of chemists, biologists, geneticists, mathematicians, and immunologists – based in California, London and other centres – collaborating to show how these little loops of DNA cause such biological harm. ![]() It has been set up to fund multidisciplinary research programmes that could develop novel routes for tackling cancer. The breakthrough is part of a major initiative, known as the Cancer Grand Challenges, that is backed by Cancer Research UK and the US National Cancer Institute. “Now, at last, we have revealed the agents of these events. Scientists could see all sorts of strange, unaccountable things happening – tumours spreading with unanticipated speed or cancers becoming resistant to drugs that had initially been effective in attacking them. Then, at some point, you finally meet the villain who is revealed to be the agent of all this mayhem.” At first, in a film, you see different explosions, killings and disasters occurring and you don’t know why they are happening or who is responsible. “They behave like villains in a Bond film. “We have found that ecDNA act as cancer-causing genes that have somehow separated themselves from a person’s chromosomes and have started to behave in ways that circumvent the normal rules of genetics,” said Stanford university geneticist Howard Chang. Photograph: Patrick McMullan/Getty Images Howard Chang, geneticist at Stanford University. ![]()
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