185P - Disease etiology impact on outcomes of hepatocellular carcinoma patients treated with atezolizumab plus bevacizumab: A real-world, multicenter study

Background

The impact of etiology on response to immunotherapy in advanced hepatocellular carcinoma (HCC) is being extensively debated. Early clinical trials suggested that PD-1/PD-L1 blockade prolonged survival of viral HCC patients, but not of those with non-viral HCC. However, a recent post-hoc analysis of the IMbrave-150 trial showed atezolizumab plus bevacizumab (AB) to exhibit similar efficacy in viral and non-viral groups. Here we investigated the role of etiology in AB-treated HCC patients in a real-world scenario to consolidate these findings and integrate them with previous comparative studies with lenvatinib.

Methods

We retrospectively analyzed 885 HCC patients treated with first-line AB from Eastern and Western countries, 53.9% having viral and 46.1% non-viral etiology. Baseline clinical and laboratory characteristics were analyzed with uni- and multi-variate models to assess the impact of etiology on overall survival (OS), time to progression (TTP), response rates and to identify prognostic factors in etiology subgroups.

Results

Overall, no statistically significant differences were found in OS (mOS: viral 15.9mo; non-viral 16.3mo), TTP (mTTP: viral 8.3mo; non-viral 7.2mo), and response rates based on etiology. However, certain prognostic factors differed between the two groups. Among patients with viral etiology, eosinophil count positively correlated with OS, while among non-viral patients AST and ALP levels were significantly related to OS. AFP, NLR, and ALBI score were prognostic for both groups. The toxicity profile of AB almost overlaps in the two etiology subgroups.

Conclusions

These findings indicate that underlying etiology does not significantly impact the outcome of HCC patients treated with AB. However, some prognostic factors differ between viral and non-viral patients, with immunological factors being mostly related to the former while metabolic to the latter, supporting potential biological differences. This may also account for different outcomes of AB observed in comparative studies with lenvatinib in etiology subgroups. Prospective and comparative trials stratifying by etiology are warranted to validate these findings and guide clinical practice.

Clinical trial identification

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

F. Finkelmeier: Financial Interests, Personal, Speaker, Consultant, Advisor: AbbVie, MSD, Ipsen, Esai and Fresenius. M. Scartozzi: Financial Interests, Personal, Speaker, Consultant, Advisor: Amgen, MSD, Merck, BMS, Servier, Eisai, GSK. A. Casadei Gardini: Financial Interests, Personal, Speaker, Consultant, Advisor: MSD, Eisai, Bayer, Bristol Myers Squibb, AstraZeneca and GSK. All other authors have declared no conflicts of interest.