Systematic review of hepatocellular carcinoma mortality rates among hepatitis B virus-infected renal transplant recipients, with supplemental analyses of liver failure and all-cause mortality

Blackadar, Clarke Brian

doi:10.1016/j.ijid.2012.08.002

Cited by 6 publications

(2 citation statements)

References 102 publications

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“…The author compared the HCC mortality in HBV positive kidney transplant recipients with that of HBV positive general populations, and found that the HCC mortality rate was increased in low and intermediate seroprevalence areas, but inconclusive in high seroprevalence areas. 18 Different surveillance programs may contribute to differences in HCC mortality in various studies. The HCC mortality rate in our HBV positive kidney transplant recipients was 263/100,000 person-years, which was comparable with that of the HBV positive general population in high seroprevalence areas such as Taiwan (283.5/100,000 personyears).…”

Section: Discussionmentioning

confidence: 99%

Hepatocellular carcinoma after kidney transplantation: analysis of Hong Kong Renal Registry

et al. 2014

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Kidney transplant recipients have increased risk of cancers when compared with the general population. Hepatocellular carcinoma (HCC) is extremely important in Asia where hepatitis B virus (HBV) infection is endemic. The aim is to study the epidemiological and clinical aspects of all de novo HCC in our kidney transplant recipients. Moreover, various preventive strategies which may help to optimize the outcome will also be discussed. A retrospective review of all patients who developed HCC after kidney transplantation between May 1972 and December 2011 in Hong Kong, based on the data from Hong Kong Renal Registry. After a follow-up period of 40,246 person-years, 20 patients (males 15: females 5) developed HCC. The annual incidence was 49.7/100,000 persons per year. Among them, 16 were HBV carriers, 2 were hepatitis C (HCV) carriers and 2 had HBV and HCV co-infection. Presence of HBV infection was associated with 78-fold higher risk for HCC development. Majority (85%) were asymptomatic when HCC was diagnosed by ultrasound or alpha-fetoprotein surveillance. All patients diagnosed by surveillance received active treatment while 2/3 of symptomatic patients could only receive symptomatic care and died rapidly. In conclusion, HBV infection is the major etiological factor for HCC development in kidney transplant recipients in HBV endemic areas. Regular HCC surveillance appeared to be able to detect early stage cancers which are amenable to treatment and offer the best hope of cure.

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Section: Discussionmentioning

confidence: 99%

Hepatocellular carcinoma after kidney transplantation: analysis of Hong Kong Renal Registry

et al. 2014

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“…Therefore, investigation into novel methods to improve the treatment and survival of liver cancer patients is essential. The pathogenesis of liver cancer is complex, and studies have demonstrated that uncontrolled proliferation, various ion disorders and resistance to apoptosis are key features of this process ( 4 ). However, the exact mechanisms of pathogenesis are unclear, particularly that of apoptosis resistance.…”

Section: Introductionmentioning

confidence: 99%

Antitumor action of the peroxisome proliferator-activated receptor-γ agonist rosiglitazone in hepatocellular carcinoma

et al. 2015

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The inhibition of apoptosis in cancer cells is the major pathological feature of hepatic carcinoma. Rosiglitazone (RGZ), a ligand for peroxisome proliferator-activated receptor γ (PPAR-γ), has been shown to induce apoptosis in hepatic carcinoma cells. However, the mechanism underlying this effect remains to be elucidated. The present study aimed to investigate the effect of RGZ on cell viability and apoptosis, and its mechanisms in cultured HepG2 cells using MTT assay, flow cytometry and western blotting. The results revealed that treatment with RGZ may attenuate HepG2 cell viability and induce the apoptosis of the cells. The mechanism of RGZ-induced apoptosis involves an increase in the level of activated PPAR-γ (p-PPAR-γ) and a decrease in p85 and Akt expression. In addition, the PPAR-γ antagonist GW9662 suppressed the effect of RGZ in the HepG2 cells. Taken together, the results suggest that RGZ induces the apoptosis of HepG2 cells through the activation of PPAR-γ, suppressing the activation of the PI3K/Akt signaling pathway. Such mechanisms may contribute to the favorable effects of treatment using RGZ in HepG2 cells.

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Human Microbiome and Malignancy: Principles, Mechanisms, and Challenges

Ruwali

Shukla

2019

Pathogenicity and Drug Resistance of Human Pathogens

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Systematic review of hepatocellular carcinoma mortality rates among hepatitis B virus-infected renal transplant recipients, with supplemental analyses of liver failure and all-cause mortality

Abstract: Mortality due to HCC was increased in low and intermediate seroprevalence areas, but the evidence was inconclusive for high seroprevalence areas.

Cited by 6 publications

References 102 publications

Hepatocellular carcinoma after kidney transplantation: analysis of Hong Kong Renal Registry

Hepatocellular carcinoma after kidney transplantation: analysis of Hong Kong Renal Registry

Antitumor action of the peroxisome proliferator-activated receptor-γ agonist rosiglitazone in hepatocellular carcinoma

Human Microbiome and Malignancy: Principles, Mechanisms, and Challenges

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