• Media type: E-Article
  • Title: CXCL9 inhibits tumour growth and drives anti-PD-L1 therapy in ovarian cancer
  • Contributor: Seitz, Stefanie; Dreyer, Tobias F.; Stange, Christoph; Steiger, Katja; Bräuer, Rosalinde; Scheutz, Leandra; Multhoff, Gabriele; Weichert, Wilko; Kiechle, Marion; Magdolen, Viktor; Bronger, Holger
  • Published: Springer Science and Business Media LLC, 2022
  • Published in: British Journal of Cancer, 126 (2022) 10, Seite 1470-1480
  • Language: English
  • DOI: 10.1038/s41416-022-01763-0
  • ISSN: 0007-0920; 1532-1827
  • Origination:
  • Footnote:
  • Description: Abstract Background Response to immune checkpoint blockade (ICB) in ovarian cancer remains disappointing. Several studies have identified the chemokine CXCL9 as a robust prognosticator of improved survival in ovarian cancer and a characteristic of the immunoreactive subtype, which predicts ICB response. However, the function of CXCL9 in ovarian cancer has been poorly studied. Methods Impact of Cxcl9 overexpression in the murine ID8-Trp53−/− and ID8-Trp53−/–Brca2−/− ovarian cancer models on survival, cellular immune composition, PD-L1 expression and anti-PD-L1 therapy. CXCL9 expression analysis in ovarian cancer subtypes and correlation to reported ICB response. Results CXCL9 overexpression resulted in T-cell accumulation, delayed ascites formation and improved survival, which was dependent on adaptive immune function. In the ICB-resistant mouse model, the chemokine was sufficient to enable a successful anti-PD-L1 therapy. In contrast, these effects were abrogated in Brca2-deficient tumours, most likely due to an already high intrinsic chemokine expression. Finally, in ovarian cancer patients, the clear-cell subtype, known to respond best to ICB, displayed a significantly higher proportion of CXCL9high tumours than the other subtypes. Conclusions CXCL9 is a driver of successful ICB in preclinical ovarian cancer. Besides being a feasible predictive biomarker, CXCL9-inducing agents thus represent attractive combination partners to improve ICB in this cancer entity.
  • Access State: Open Access