Hepatocellular carcinoma is the most frequent form of primary liver cancer, and most patients are diagnosed when the disease is already advanced and therefore prognosis is poor despite available treatments. Understanding what contributes to the malignancy may help develop effective treatments.
Interferon (IFN)-α, on paper, should be quite effective against hepatocellular carcinoma, the most frequent form of primary liver cancer. IFN-α can suppress tumor growth directly by acting on tumor cells, as well as indirectly by activating cytotoxic CD8+ T cells. In addition, it can slow replication of hepatitis B virus, which is involved in 50% to 80% of cases of hepatocellular carcinoma. However, IFN-α on its own has performed disappointingly in clinical trials.
Hepatocellular carcinoma (HCC) is among the leading causes of cancer-related deaths worldwide due to lack of effective diagnosis at early stages and limited comprehension of its pathogenesis, thus limiting the development of effective treatments.
Hepatocellular carcinoma (HCC) is a fatal cancer and the third cause of cancer-related deaths worldwide. Current therapies have focused on CAR T cells for treating HCC. Glypican-3 (GPC3) is a membrane protein that is overexpressed in HCC but not in healthy adult liver tissue, thus becoming a promising therapeutic target for HCC management.
Rznomics Inc. scored a potential ₩1.9 trillion (US$1.35 billion) global license option agreement with Eli Lilly and Co. to codevelop a novel RNA editing gene therapy to treat hereditary hearing loss.
Hepatocellular carcinoma (HCC), which accounts for up to 80% of cases of primary liver cancer, is typically diagnosed in an advanced stage, meaning a poor prognosis. Understanding what drives progression may help identify proteins and pathways that can be targeted to slow down the disease.
Rznomics Inc. scored a potential ₩1.9 trillion (US$1.35 billion) global license option agreement with Eli Lilly and Co. to codevelop a novel RNA editing gene therapy to treat hereditary hearing loss.
Aberrant activation of β-catenin, often due to mutations in its encoding gene or loss-of-function mutations in APC, contributes to tumor progression and therapy resistance, as seen in advanced hepatocellular carcinoma (HCC), where approximately 30% of cases exhibit β-catenin activation.
Solute carrier family 25 member 19 (SLC25A19) is a transporter protein of thiamine pyrophosphate across cellular membranes, which is needed as a cofactor for multiple metabolic enzymes and is important for homeostasis regulation. It was hypothesized that SLC25A19 may be a pan-cancer marker and a therapeutic target, and more concretely in hepatocellular carcinoma (HCC).
