Unique tumour microenvironment: when ferroptosis activation boosts ICI of liver cancer

Immune checkpoint inhibition (ICI) has revolutionised cancer therapy in the past decade including liver cancer. Combined ICI (eg, atezolizumab) and anti-angiogenic (eg, bevacizumab) agents have become the new first-line treatment for advanced liver cancer over the multikinase inhibitor sorafenib.1 Nonetheless, this novel combined treatment does not cure disease but prolongs overall survival by approximately 6–9 months. There is recent evidence to suggest that the type of aetiology driving liver cancer affects the efficacy of response to combinatorial ICI: non-alcoholic steatohepatitis (NASH)-induced liver cancer was shown to be less efficient to such interventions.2 Therefore, there is still a huge interest to increase the sensitivity of ICI in liver cancer by either overcoming therapy resistance or increasing therapy efficacy. To this end, the recent article by Conche et al3 in Gut proposes the induction of hepatocyte ferroptosis combined with blockade of myeloid-derived tumour cells (MDSCs)...
Source: Gut - Category: Gastroenterology Authors: Tags: Gut Commentary Source Type: research