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Recent findings indicate that Poly(ADP-ribose)polymerase1 (PARP-1) is implicated in\n                      <jats:italic>KRAS<\/jats:italic>\n                      -driven cancers, but its exact role in cholangiocarcinogenesis remains undefined.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Design<\/jats:title>\n                    <jats:p>\n                      <jats:italic>PARP-1<\/jats:italic>\n                      inhibition was performed in patient-derived and established iCCA cells using RNAi, CRISPR\/Cas9 and pharmacological inhibition in\n                      <jats:italic>KRAS<\/jats:italic>\n                      -mutant, non-mutant cells. In addition,\n                      <jats:italic>Parp-1<\/jats:italic>\n                      knockout mice were combined with iCCA induction by hydrodynamic tail vein injection to evaluate an impact on phenotypic and molecular features of\n                      <jats:italic>Kras<\/jats:italic>\n                      -driven and\n                      <jats:italic>Kras<\/jats:italic>\n                      -wildtype iCCA. Clinical implications were confirmed in authentic human iCCA.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      PARP-1 was significantly enhanced in\n                      <jats:italic>KRAS<\/jats:italic>\n                      -mutant human iCCA. PARP-1-based interventions preferentially impaired cell viability and tumourigenicity in human\n                      <jats:italic>KRAS<\/jats:italic>\n                      -mutant cell lines. Consistently, loss of\n                      <jats:italic>Parp-1<\/jats:italic>\n                      provoked distinct phenotype in\n                      <jats:italic>Kras\/Tp53-<\/jats:italic>\n                      induced versus\n                      <jats:italic>Akt\/Nicd-<\/jats:italic>\n                      induced iCCA and abolished\n                      <jats:italic>Kras<\/jats:italic>\n                      -dependent cholangiocarcinogenesis. Transcriptome analyses confirmed preferential impairment of DNA damage response pathways and replicative stress response mediated by CHK1. Consistently, inhibition of CHK1 effectively reversed PARP-1 mediated effects. Finally,\n                      <jats:italic>Parp-1<\/jats:italic>\n                      depletion induced molecular switch of\n                      <jats:italic>KRAS<\/jats:italic>\n                      -mutant iCCA recapitulating good prognostic human iCCA patients.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Our findings identify the novel prognostic and therapeutic role of\n                      <jats:italic>PARP-1<\/jats:italic>\n                      in iCCA patients with activation of oncogenic\n                      <jats:italic>KRAS<\/jats:italic>\n                      signalling.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/gutjnl-2023-331237","type":"journal-article","created":{"date-parts":[[2024,6,10]],"date-time":"2024-06-10T13:22:50Z","timestamp":1718025770000},"page":"1712-1724","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":12,"title":["PARP-1 selectively impairs\n                    <i>KRAS<\/i>\n                    -driven phenotypic and molecular features in intrahepatic cholangiocarcinoma"],"prefix":"10.1136","volume":"73","author":[{"given":"Friederike L","family":"Keggenhoff","sequence":"first","affiliation":[{"name":"First Department of Internal Medicine, University Medical Center of the Johannes Gutenberg University, Mainz, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Darko","family":"Castven","sequence":"additional","affiliation":[{"name":"Department of Medicine I, University Medical Center Schleswig Holstein Campus L\u00fcbeck, L\u00fcbeck, 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