Oncotarget

Research Papers:

Platelet-derived growth factor receptor α in hepatocellular carcinoma is a prognostic marker independent of underlying liver cirrhosis

Jung-Hwan Yu, Joon Mee Kim, Ja Kyung Kim, Suk Jin Choi, Kwan Sik Lee, Jin-Woo Lee, Hye Young Chang and Jung Il Lee _

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Oncotarget. 2017; 8:39534-39546. https://doi.org/10.18632/oncotarget.17134

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Abstract

Jung-Hwan Yu1,*, Joon Mee Kim2,*, Ja Kyung Kim1, Suk Jin Choi2, Kwan Sik Lee1, Jin-Woo Lee3, Hye Young Chang4 and Jung Il Lee1

1Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea

2Department of Pathology, Inha University School of Medicine, Incheon, Republic of Korea

3Department of Internal Medicine, Inha University School of Medicine, Incheon, Republic of Korea

4Medical Research Center, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea

*These authors have contributed equally and share the first authorship

Correspondence to:

Jung Il Lee, email: [email protected]

Keywords: platelet-derived growth factor receptor α, liver fibrosis, liver cirrhosis, hepatic stellate cell, hepatocellular carcinoma

Received: October 07, 2016    Accepted: February 22, 2017    Published: April 17, 2017

ABSTRACT

Background and Aims: Platelet-derived growth factor receptor alpha (PDGFRα) is suggested as a prognosis marker for hepatocellular carcinoma (HCC). Since PDGFRα is also known as a marker for activated hepatic stellate cells (HSCs), this study aimed to investigate whether PDGFRα expression in HCC was dependent on the background liver fibrous condition.

Results: Strong PDGFRα expression in the tumor lesions was associated with decreased survival after curative HCC resection. Expression of PDGFRα in the tumor correlated with increased collagen α1(I), lecithin retinol acyltransferase, and smooth muscle α-actin suggesting increased HSCs in tumor sites. The expression of PDGFRα in the tumor sites was associated neither with underlying liver fibrosis/cirrhosis nor with the expression of PDGFRα in adjacent non-tumor sites of the liver.

Materials and Methods: Patients with HCC who underwent liver resection as curative treatment were included in this study. Using liver samples of 95 patients, tissue microarray was constructed and immunohistochemical study of PDGFRα was conducted in both tumor and non-tumor sites. PDGFRα expression in tumor and matching non-tumor sites was compared. Freshly frozen liver tissue specimens of 16 HCC patients were used for gene expression analysis of PDGFRα and fibrosis related genes.

Conclusions: Our results suggest that PDGFRα overexpression in HCC is a prognostic marker independent of adjacent non-tumor site liver fibrosis status.


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