PHAROH lncRNA is upregulated in hepatocellular carcinoma and functions by sequestering the translational suppressor TIAR via a 71 nucleotide hairpin to regulate c-MYC translation.

Human liver organoids provide a patient-derived platform to interrogate host and viral mechanisms of HBV replication, perform anti-HBV and toxicity drug screens, and investigate the molecular determinants of related tumorigenesis.

Inhibiting IRE1α decreases tumor cell proliferation and migration in hepatocellular carcinoma, therefore components of this ER-stress pathway may be therapeutically relevant for liver cancer.

ELYS, a multifunctional protein with critical roles in the cell cycle, is essential for the vigorous proliferation and survival of difficult-to-treat cancers carrying mutations in the KRAS oncogene, making it a compelling target for novel drug treatments.

Chromosomal instability through spindle assembly checkpoint alleviation facilitates malignant transformation of hepatocytes and T-cells in vivo, resulting in cancers with recurrent karyotypes.

Specific tissue environments provide selective pressures that give rise to distinct Ras oncogenic dosage in primary liver tumours and their metastatic-like outgrowths.

A cellular experiment and animal model reveals that nifuroxazide can inhibit the expression of PD-L1 through the proteasome pathway, rather than at the genetic level.

NOD-like receptor NLRP12 is a critical regulator of hepatocyte proliferation and its activation could be therapeutically used to suppress hepatocellular carcinoma.

Local infusion of bicarbonate into hepatocellular carcinoma markedly enhances local tumor control by transarterial chemoembolization.

Combination of glutaminase inhibitor CB-839 and ASCT2 inhibitor V-9302 showed efficient antitumor effect against glutamine addicted liver cancer cells via glutathione depletion and reactive oxygen species (ROS) induction.