{
  "abstract": "Intrahepatic cholangiocarcinoma (iCCA) is an aggressive malignant tumour of the biliary epithelium whose incidence is increasing worldwide.1 Despite advances in molecular classification and targeted therapies, most patients present with advanced disease and have poor survival outcomes.2 The biological complexity of iCCA is due not only to its genomic heterogeneity, but also to a profoundly remodelled tumour microenvironment (TME) characterised by chronic inflammation, immune dysfunction and extensive stromal desmoplasia.3 In this inflammatory landscape, interleukin-6 (IL-6) has long been recognised as a central cytokine associated with disease progression and adverse prognosis in biliary tract cancers.4 However, the functional consequences of tumour-derived IL-6 signalling in CCA biology remain incompletely understood.",
  "authors": [
    {
      "affiliations": [
        "Immunology, Ophthalmology and ENT, Complutense University of Madrid Faculty of Medicine, Madrid, Spain",
        "Instituto de Investigación Sanitaria Gregorio Marañón, Madrid, Spain",
        "CIBEREHD, Madrid, Community of Madrid, Spain"
      ],
      "name": "Francisco Javier Cubero"
    },
    {
      "affiliations": [
        "CIBEREHD, Madrid, Community of Madrid, Spain",
        "HEVEPHARM, Physiology and Pharmacology, University of Salamanca, Salamanca, Spain"
      ],
      "name": "Rocio I R Macias"
    }
  ],
  "title": "Tumour-autonomous IL-6 signalling creates a metabolic vulnerability in intrahepatic cholangiocarcinoma",
  "uid": "0b28645d-48d8-5d22-9660-5e4f72e278fb"
}