{
  "abstract": "Targeting signalling by the rat sarcoma virus (Ras) family of oncoproteins remains one of the biggest challenges in oncology, with RAS mutations being prevalent drivers of tumours of poor prognosis such as pancreatic ductal adenocarcinoma (PDAC, 90–95%), non-small cell lung cancer (30%) or colorectal cancer (40%).1 The prognosis is particularly bad in the case of pancreatic ductal adenocarcinoma (PDAC), with 5-year survival for metastatic disease remaining under 3% with standard therapies.2 Despite the very much awaited development of selective inhibitors targeting mutant RAS, these have unfortunately been confronted with rapid resistance due to feedback reactivation or allele switching, and their clinical efficacy in PDAC has been modest.3 Furthermore, other aspects of PDAC such as its abundant and complex stroma significantly limit the impact of monotherapies. This highlights the need to identify combinatorial therapeutic strategies which integrate RAS pathway inhibition with compounds targeting an RAS-independent vulnerability that cannot be bypassed by the reactivation of RAS signalling. And this is where Wu and colleagues focused their efforts.4",
  "authors": [
    {
      "affiliations": [
        "Genomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Madrid, Spain"
      ],
      "name": "Jorge Mota-Pino"
    },
    {
      "affiliations": [
        "Genomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Madrid, Spain",
        "Science for Life Laboratory, Division of Genome Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden",
        "Networking Research Center on Neurodegenerative Diseases (CIBER-NED), Instituto de Salud Carlos III, Madrid, Spain"
      ],
      "name": "Oscar Fernandez-Capetillo"
    }
  ],
  "title": "Exploiting a purine imbalance to target KRAS mutant pancreatic adenocarcinomas",
  "uid": "70167d10-1d6b-56e6-960a-f08cec9aa6b5"
}