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Clinical Translational Research

Role of Albumin in Growth Inhibition in Hepatocellular Carcinoma

Bağırsakçı E.a, b · Şahin E.a, b · Atabey N.a, b · Erdal E.a, b · Guerra V.c · Carr B.I.a

Author affiliations

aIzmir International Biomedicine and Genome Institute, and bDepartment of Medical Biology, Faculty of Medicine, Dokuz Eylul University, Izmir, Turkey; cDepartment of Epidemiology, IRCCS de Bellis Medical Center, Castellana Grotte, Italy

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Oncology 2017;93:136-142

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Article / Publication Details

First-Page Preview
Abstract of Clinical Translational Research

Received: February 21, 2017
Accepted: March 16, 2017
Published online: May 10, 2017
Issue release date: August 2017

Number of Print Pages: 7
Number of Figures: 5
Number of Tables: 1

ISSN: 0030-2414 (Print)
eISSN: 1423-0232 (Online)

For additional information: https://www.karger.com/OCL

Abstract

Objective: Levels of serum albumin have recently emerged, together with C-reactive protein, as an important prognostic indicator for hepatocellular carcinoma (HCC). It has recently been reported that larger HCCs are associated with lower albumin levels. However, the albumin-mediated growth decrease has yet to be determined. Methods: We examined a large HCC cohort and then by direct exposure of HCC cells in vitro, the relationship of albumin levels to HCC growth. Results: We found that patients with lower albumin levels had significantly larger maximum tumor diameters, more portal vein thrombosis, more tumor multifocality, higher α-fetoprotein levels, and a lower survival than patients with higher albumin levels. Direct addition of exogenous albumin at physiological concentrations resulted in decreased growth in several HCC cell lines in vitro. We found a decrease in MAP kinase levels and in levels of Cdk2 and Cdk4, cyclinE, as well as in α-fetoprotein. Conclusion: These results indicate that in addition to its role as a monitor of systemic inflammation, albumin may have a direct role in HCC growth inhibition, either through modulation of α-fetoprotein or through its actions on growth-controlling kinases.

© 2017 S. Karger AG, Basel


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Article / Publication Details

First-Page Preview
Abstract of Clinical Translational Research

Received: February 21, 2017
Accepted: March 16, 2017
Published online: May 10, 2017
Issue release date: August 2017

Number of Print Pages: 7
Number of Figures: 5
Number of Tables: 1

ISSN: 0030-2414 (Print)
eISSN: 1423-0232 (Online)

For additional information: https://www.karger.com/OCL


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