Local injection therapy for hepatocellular carcinoma

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the world and ranks the third most common cause of cancer-related death. Surgical resection, liver transplantation and percutaneous ablation are generally considered the only curative treatment for early stage HCC. Besides the limitations of insufficient organ donors and a long waiting time for liver transplantation, however, resection is applied only to patients with good hepatic reserve and localized tumors, with a resectability of 30%. DATA SOURCES: Local ablation therapy, which is minimally invasive but contributes to the significant improvement of survival in patients with unresectable tumor, hasbeen widely used in treating small HCC. Among the techniques of local therapy, percutaneous ethanol injection (PEI) with a complete response in 80% of HCCs less than 3 cm has been accepted as an alternative to surgery in patients with small HCC. Moreover, percutaneous hepatic quantified ethanol injection (PHQEI) or PEI according to the standard criteria has been confirmed to benefit patients with HCC, especially when quantified ethanol is given at a short interval (QESI, the interval was 2-3 days). RESULT: Several limitations related to local percutaneous methods may result in incomplete therapeutic effect in case of larger HCC nodules (>3 cm). CONCLUSION: The combined use of different methods according to the clinical status of patients or tumors may be essential to the effective treatment of HCC.

HepG2 cells recovered from apoptosis show altered drug responses and invasiveness

BACKGROUND: Cancer relapse, associated with increased drug resistance and rate of metastasis, often follows completion of chemotherapy but the cancer escape mechanisms are still incompletely understood. Percutaneous ethanol injection(PEI)has been used for treating hepatocellular carcinoma(HCC)for decades, while the recurrence after PEI treatment remains a major limitation. Recent evidence mounted that cancer cells could survive from chemical induced apoptosis, suggesting a potential route through which cancer relapse may occur. This study focuses on the consequence of HepG2 recovery from ethanol-induced apoptotic event.METHODS: The model of HepG2 recovery from ethanolinduced apoptotic event was established by live cell imaging,BrdU assay and Western blotting. MTT assay, wound healing assay and invasion assay were used to investigate the behavior of HepG2 after recovery.RESULTS: HepG2 cells could recover from ethanol-induced apoptosis. These cells changed their behaviors such as drug resistance, mobility and invasiveness. On average, the recovered HepG2 cell clones were found to be 46% more resistant to ethanol and 84% higher in mobility. The recovered clones became 58.2% more sensitive to 5-fluorouracil.CONCLUSIONS: HepG2 cells can recover from ethanolinduced apoptotic event. These cells became more resistant to ethanol and more invasive. Although the recovered cell clones were more resistant to ethanol, they became more sensitive to5-fluorouracil treatment.

Advances in the interventional therapy of hepatocellular carcinoma originating from the caudate lobe

Hepatocellular carcinoma originating from the caudate lobe, also known as segment I hepatocellular carcinoma, is difficult to treat because of its special location, complex vascular supply, and the proximity of important vessels,bile ducts, and organs. This research is conducted to examine the efficacy and safety of interventional therapy for hepatocellular carcinoma in the caudate lobe.Conclusion: Superselective chemoembolization and ablation techniques for the treatment of caudate lobe hepatocellular carcinoma still need to be improved. The combination of multiple interventional methods and the application of multiple imaging techniques can improve the effectiveness and safety of interventional therapy for hepatocellular carcinoma in the caudate lobe. Multidisciplinary treatment is also essential to improve the prognosis of patients with caudate lobe hepatocellular carcinoma.