- The Expression of Apolipoprotein D in Hepatocellular Carcinoma.
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Hongxiu Han, Chan Kum Park
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Korean J Pathol. 2010;44(2):187-190.
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DOI: https://doi.org/10.4132/KoreanJPathol.2010.44.2.187
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 Abstract
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- BACKGROUND
Apolipoprotein D (Apo D) has recently been identified as a novel tumor suppressor gene. Apo D may have a profound effect on the carcinogenesis and progression of hepatocellular carcinoma. This study was designed to evaluate the expression of Apo D in hepatocellular carcinoma and to investigate the relationship between the expression of Apo D and the clinicopathological characteristics and the patients' survival.
METHODS
An immunohistochemical study was performed on the tumors and tissues from 43 hepatocellular carcinoma (HCC) patients with controls to determine the expression of Apo D protein.
RESULTS
Our data showed that a higher expression of Apo D was seen in 10 of 43 cases (23.3%), while a lower and no expression of Apo D was observed in 28 of 43 cases (65.1%) and 5 of 43 cases (11.6%), respectively. A reduced expression of Apo D was correlated with the tumor stage (p = 0.037) and tumor size (p = 0.017). However, the patients' 5-year survival was not associated with the expression of Apo D (p = 0.903).
CONCLUSIONS
The results suggest that a reduced Apo D protein expression may play an important role in HCC progression as associated with the tumor stage and size, but it does not affect the survival of HCC patients.
- Enhanced Protein Expression of Signal Transducer and Activator of Transcription 3 and Protein Kinase Substrate p36 in Hepatocellular Carcinoma.
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Hongxiu Han, Si Hyong Jang, Chan Kum Park
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Korean J Pathol. 2009;43(5):393-399.
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DOI: https://doi.org/10.4132/KoreanJPathol.2009.43.5.393
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Abstract
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- BACKGROUND
Signal transducers and activators of transcription 3 (STAT3) and protein kinase substrate p36 may be involved in cell proliferation, differentiation and growth.
METHODS
Immunohistochemistry for STAT3 and p36 was performed in 46 patients with hepatocellular carcinoma (HCC).
RESULTS
STAT3 staining was present in the cytoplasm and/or nucleus, while p36 staining was present in the nucleus.
STAT3 and p36 expression occurred in 78.3% (36/46) and 47.8% (22/46) of HCC patients, respectively. However, no correlation was found between STAT3 and p36 protein expression (p>0.05). Enhanced expression of STAT3 was negatively correlated with portal vein invasion (p=0.033).
Expression of STAT3 in the nucleus was correlated with tumor grade (p=0.004). Enhanced expression of p36 was correlated with tumor grade (p=0.031). HCC was correlated with HBV infection (p=0.032). The patients'5-year survival was related to expression of p36 (p=0.044), but not to total STAT3 or nuclear STAT3 (p>0.05).
CONCLUSIONS
The enhanced expression of STAT3 in the nucleus and the enhanced expression of p36 are associated with the aggressive phenotype of HCC. Enhanced p36 expression may contribute to poor survival of patients with HCC.
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