Scientists are a step closer to developing new treatments for dozens of types of cancer after they used big data to better understand the disease’s survival tactics.

       Some cancers are caused by mutations such as faults in the BRCA1/2 genes, which make it harder for the body to repair damaged DNA.

       Drugs can target those tumours by disrupting the back-up repair processes cancer cells rely on for survival, causing them to die.

       However, this approach has so far mainly been successful in patients with BRCA-mutated breast, ovarian, prostate and pancreatic cancers.

       Now, research suggests many more types of cancer may contain similar pairs of “synthetic-lethal partner genes”, where cancer cells can survive if one process is disrupted but not two.

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       Experts at The Institute of Cancer Research in London (ICR) analysed data from more than 9,300 patients and identified 32 tumour types that rely on such back-up processes, and could be targeted in a similar way.

       Dr Syed Haider, leader of the ICR’s Breast Cancer Research Bioinformatics Group, said: “This research tells us how some cancer cells survive despite having faulty mutations in key genes.

       “We’ve learned that when cancers lose a particular tumour-suppressor gene, which usually work to protect our cells from becoming cancerous, they ramp up the activity of back-up processes controlled by other genes in order to stay alive.

       “This is an effect known as buffering. Buffering in cells has been known about for a long time, but our large-scale analysis of over 9300 patients with different cancers shows that buffering occurs in most cancers and the genes that are increased for the cancer to survive are different, depending upon which tumour suppressor gene is lost.

       “This could mean more potential new treatments for even more types of cancer.”

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       Funded by Cancer Research UK (CRUK), Breast Cancer Now and Walk the Walk, the study has given researchers a better understanding of how some cancers survive despite having mutations in key genes.

       And it has revealed hundreds of potential targets for drugs that could lead to a new generation of therapies.

       Study co-author Professor Chris Lord, also from the ICR and group leader of the Cancer Research UK Gene Function Laboratory, said: “In the short- to medium-term, our findings suggest there might be more precise ways to design cancer drugs for specific cancers. Our immediate plans are to now use these approaches to do just that.

       “In the longer term, we hope that using the tools we have developed, we will eventually be able to design drugs that are effective for very specific types of cancer that are difficult to treat.“

       Dr Simon Vincent, director of research, support and influencing at Breast Cancer Now, said the work highlighted “the power of big data in cancer research to potentially help identify better ways to treat cancer, including breast cancer.

       “By identifying the genetic alterations that cancer cells rely on to survive, the researchers have discovered hundreds of potential targets for developing new drugs.

       “This approach will help researchers develop more ‘synthetic lethal’ treatments, like PARP inhibitors. Drugs like these will treat breast cancer and other cancers in a way that largely leaves a patient’s healthy cells unharmed.

       “We look forward to seeing results from future research and further insights into how this breakthrough may lead to new targeted treatments for this devastating disease.”

       CRUK’s research information manager, Dr Hattie Brooks, said: “We are living in a golden age of research where we can use patient data in new ways to help us better understand cancer and how to beat it.

       “We were pleased to fund this research and look forward to seeing how this work might contribute to the development of new cancer drugs, which may help more people live longer, better lives, free from the fear of cancer.”

       The findings were published in the journal Nature Genetics. The study was supported by The Cancer Genome Atlas (TCGA) Research Network and the NIHR Biomedical Research Centre at The Royal Marsden NHS Foundation Trust.