Emerging drugs for the treatment of hepatocellular carcinoma

ABSTRACT

Introduction

Hepatocellular carcinoma (HCC) remains a leading cause of liver-related mortality. Cirrhosis of any etiology is the major risk factor although HCC can develop in its absence in patients with hepatitis B and increasingly in those with nonalcoholic fatty liver disease. When detected at an early stage, curative options include surgical resection, liver transplantation, and/or ablative therapies. Unfortunately, most cases of HCC are recognized at an advanced stage when options are limited and noncurative. However, new systemic therapies with tyrosine kinase inhibitors and immunotherapy have expanded therapeutic options in advanced HCC. Advances in systemic therapy have given patients with advanced HCC hope and prolonged their survival.

Areas covered

We discuss recent data and ongoing research efforts to improve the treatment of hepatocellular carcinoma with discussion of current and upcoming systemic therapies combining agents of different classes.

Expert opinion

Systemic therapy for HCC is in evolution. The inclusion of immunotherapy to systemic therapy has revolutionized the field of HCC treatment. Identification of the appropriate combination and sequence of systemic therapy coupled with discovery of reliable HCC biomarkers will lead to improved survival and individualized HCC therapy.

KEYWORDS:

• Atezolizumab
• bevacizumab
• cabozantinib
• hepatocellular carcinoma
• immunotherapy
• ipilimumab
• lenvatinib
• nivolumab
• pembrolizumab
• ramucirumab
• regorafenib
• sorafenib
• tyrosine kinase inhibitors

Abbreviations

Hepatocellular carcinoma (HCC), tyrosine kinase inhibitors (TKIs), hepatitis B (HBV), Nonalcoholic steatohepatitis (NASH), Contrast-enhanced ultrasound (CEUS), Barcelona Clinic Liver Cancer (BCLC), American Joint Committee on Cancer (AJCC), the Eastern Cooperative Oncology Group Performance Status ([ECOG), hepatovenous pressure gradient (HVPG), programmed cell death protein-1 (PD-1), programmed death ligand 1 (PD-L1), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), vascular endothelial growth factor (VEGF) receptor, platelet-derived growth factor (PDGF), humanized monoclonal antibody (mAb), complete response (CR), overall response rate (ORR), progression-free survival (PFS), alpha fetoprotein (AFP).

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers of this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.