Management of hepatocellular carcinoma

Fitzmorris, Paul; Shoreibah, Mohamed; Anand, B S; Singal, Ashwani K.

doi:10.1007/s00432-014-1806-0

Cited by 92 publications

(63 citation statements)

References 125 publications

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“…These discrepancies need to be explored. In Western countries and Japan, infection with hepatitis C virus (HCV) is the more common cause of HCC, while in China, HBV infection is the dominant risk factor [24], with Fan et al reporting that about 90 % of HCC patients undergoing transplantation in Chinese transplant centers have HCC that is HBV-related [15]. Consequently, we study focused on HCC recurrence due to HBV infection.…”

Section: Discussionmentioning

confidence: 96%

Donor interleukin 6 gene polymorphisms predict the recurrence of hepatocellular carcinoma after liver transplantation

et al. 2016

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Section: Discussionmentioning

confidence: 96%

Donor interleukin 6 gene polymorphisms predict the recurrence of hepatocellular carcinoma after liver transplantation

et al. 2016

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“…Hepatocellular carcinoma (HCC) is the most common primary liver cancer (1,2). Many HCC patients lose the opportunity for surgical resection due to late diagnosis (3).…”

Section: Introductionmentioning

confidence: 99%

COX-2/PGE2 Axis Regulates HIF2α Activity to Promote Hepatocellular Carcinoma Hypoxic Response and Reduce the Sensitivity of Sorafenib Treatment

Dong

Liu

Zhi

et al. 2018

Clinical Cancer Research

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Tumor hypoxia and hypoxia-related sorafenib resistance adversely affected the prognosis of HCC patients. Hypoxia-inducible factor (HIF) s are defined as the central transcriptional mediator of hypoxic response. Recent efforts have identified HIF-2α that has been involved in sorafenib resistance. However, the regulatory mechanisms of HIF-2α activity in HCC remain obscure. Here, using both in vitro and in vivo HCC models, we show that the cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) axis is a driver of HIF-2α expression and activity, which then promotes HCC growth, metastasis and angiogenesis. We further show that COX-2 specific inhibitors synergistically enhanced the antitumour activity of sorafenib treatment by regulating the HIF-2α level and activity. These observations support further clinical developments of COX-2-specific inhibitors for HCC treatment and particularly for enhancing the response to sorafenib treatment.Research.

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“…Surgery remains the most efficacious and mainstream solution for the eradication of cancer nodules; however, relapse and distant organ invasion are common following tumor dissection (3). Anti-tumor agents have demonstrated strong cytotoxicity against cancer cells and oral administration of chemotherapeutics is recommended for the clearance of tumor cells that survive tumor dissection (4). Therefore, choosing appropriate anti-tumor agents and planning their administration is an indispensable part of systemic treatment HCC.…”

Section: Introductionmentioning

confidence: 99%

Chrysin induces cell apoptosis via activation of the p53/Bcl-2/caspase-9 pathway in hepatocellular carcinoma cells

Zhang

Liu

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Chrysin is a major active ingredient of flavonoids, known to exhibit protective effects against various types of cancer. However, the anticancer role of chrysin against hepatocellular carcinoma (HCC) and the underlying molecular mechanisms remain unclear. In order to evaluate the effects of chrysin on cell viability and apoptosis in human HCC, HepG2 and QGY7701 cells were used in the present study. Cell viability was monitored using an MTT assay. In addition, an Annexin V-fluorescein isothiocyanate/propidium iodide kit was used for the labeling of the apoptotic cells, which were then measured using flow cytometry. Western blotting was used to examine the protein expression of p53, B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X (Bax), Bcl-2-associated death promoter (Bad), Bcl-2 homologous antagonist/killer (Bak), caspases-3 and -9, and cleaved-caspases-3 and -9. The results of the present study revealed that chrysin suppressed the cell viability of HepG2 and QGY7701 cells in a concentration-dependent manner. In addition, chrysin induced significant apoptosis in HepG2 and QGY7701 cells. Furthermore, it was demonstrated that chrysin treatment increased the expression of proapoptotic proteins, including p53, Bax, Bad and Bak, while it decreased the protein level of antiapoptotic protein Bcl-2. It was also demonstrated that chrysin induced apoptosis in the HCC cells by regulating the p53/Bcl-2/caspase-9 signaling pathway. In conclusion, the results of the present study suggested that chrysin may be a potential candidate agent for the induction of cell apoptosis in human HCC.

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Management of hepatocellular carcinoma

Abstract: In spite of significant advancement in HCC management, its incidence continues to rise. There remains an urgent need to continue refining understanding of HCC and develop strategies to increase utilization of the available preventive measures and curative treatment modalities for HCC.

Cited by 92 publications

References 125 publications

Donor interleukin 6 gene polymorphisms predict the recurrence of hepatocellular carcinoma after liver transplantation

Donor interleukin 6 gene polymorphisms predict the recurrence of hepatocellular carcinoma after liver transplantation

COX-2/PGE2 Axis Regulates HIF2α Activity to Promote Hepatocellular Carcinoma Hypoxic Response and Reduce the Sensitivity of Sorafenib Treatment

Chrysin induces cell apoptosis via activation of the p53/Bcl-2/caspase-9 pathway in hepatocellular carcinoma cells

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