Expression of interleukin-18, interferon-γ and interleukin-10 in hepatocellular carcinoma

Chia, Chok Seng; Ban, Kechen; Ithnin, Hairuszah; Singh, Harjit; Ravindran, Krishnan; Mokhtar, Suryati; Malihan, Nik; Seow, Heng Fong

doi:10.1016/s0165-2478(02)00176-1

Cited by 38 publications

(25 citation statements)

References 23 publications

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“…However, there was no further report about the significance of the IFN-g expression in those tissues or cells. IFN-g has also been reported weakly expressed in HCCs (Chia et al, 2002). But in the present study, neither protein nor mRNA of IFN-g was expressed in the 10 cases of HCCs, probably because that the methods we used are not sensitive enough.…”

Section: Western Blot Analysiscontrasting

confidence: 74%

“…IFN-g also regulates cell proliferation and apoptosis via activating the downstream JAK -STAT signalling pathway (Buard et al, 1998;Haque and Williams, 1998;WeberNordt et al, 1998;Lee et al, 2000). IFN-g-like immunoreactivity has been proved to appear in human adrenal cortical tumours, phaeochromocytomas and hepatocellular carcinomas (HCCs) by immunohistochemical method Song, 1995, 1996;Chia et al, 2002). However, immunohistochemistry analysis alone cannot confirm whether tumour cells produce IFN-g. To answer this question, we used immunohistochemistry combined with in situ hybridisation and Western blot method to screen a cluster of different types of tumours.…”

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confidence: 99%

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Expression of interferon-γ in human adrenal gland and kidney tumours

Zhang

Nie

et al. 2007

Br J Cancer

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It is known that interferon-g (IFN-g) is produced by activated T and NK lymphoid cells, mononuclear cells, and macrophage and dendritic cells. Our previous studies have shown that IFN-g-like immunoreactivity also appears in human adrenal cortical tumour and phaeochromocytoma. To investigate whether human tumour cells can produce IFN-g, we examined 429 biopsy specimens of 30 kinds of tumour and tumour-surrounding tissues in adrenal glands and in kidneys by using immunohistochemistry and in situ hybridisation. IFN-g immunoactivity was shown in 34.3% of the adrenal cortical adenomas, 50% of the adrenal cortical carcinomas, 26.7% of the phaeochromocytomas, 26.7% of the clear cell renal cell carcinomas (RCCs), 22% of the adrenal cortexes and 40% of medullas adjacent to tumours. The positive samples and expression areas were well overlapped between the IFN-g mRNA and the immunohistochemistry staining. Western blot analysis has further confirmed the immunohistochemistry results by showing a distinct IFN-g band corresponding to 17.4 kDa in tissue extracts from adrenal cortical adenoma, phaeochromocytoma and clear cell RCCs. These results indicate that IFN-g is produced by some types of tumour cells, suggesting it may play a dual role in the development of these tumours.

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Section: Western Blot Analysiscontrasting

confidence: 74%

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confidence: 99%

Expression of interferon-γ in human adrenal gland and kidney tumours

Zhang

Nie

et al. 2007

Br J Cancer

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“…Several groups have shown that IL-10 is highly expressed in HCC tumors and individuals with HCC versus non-tumorous-surrounding tissue controls or healthy cohorts (162,164,(173)(174)(175). These studies suggest that increases in IL-10 and perhaps other Th2 cytokines correlate with progression.…”

Section: Hepatic Stellate Cells (Hscs)mentioning

confidence: 96%

The tumor microenvironment in hepatocellular carcinoma (Review)

et al. 2012

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Abstract. The tumor microenvironment has been largely studied as a dynamic system orchestrated by inflammatory cells, including cancer cells, stroma as well as the extracellular matrix. It is useful to describe and predict the phenotypic characteristics of cancer. Furthermore, a better understanding of its interplay with the various aspects of the tumor cells may be utilized for the discovery of novel molecular targets. Liver cancer is considered a model of the relation occurring between the tumor microenvironment and tumor development. The chronic inflammatory status of the liver, sustained by the infection of hepatitis viruses, as well as the production of cytokines and growth factors within the parenchyma, lead to an intricate microenvironment. The identification of novel molecular therapeutic targets may improve the outcome of patients with liver cancer as it remains the third leading cause of cancer death worldwide. In the present study, the tumor microenvironment in hepatocellular carcinoma (HCC) was explored by a review of the literature. Studies on hepatitis virus infections and the consequent chronic inflammatory status were examined. In this context, immune-mediated and/or virusrelated molecular mechanisms have been hypothesized as being responsible for liver cancer development. The interlink among HCC microenvironment components, comprising cellular elements, cytokines, growth factors and several proteins is also described together with the role of matrix metalloproteinases in HCC development. Finally, the rationale for targeting tumorstromal interface is summarized in the context of new therapeutic opportunities.

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“…The constitutive expression of IFN-γ in the liver causes chronic active hepatitis through the recruitment of lymphomononuclear cells (Toyonaga et al, 1994). The expression of IFN-γ is slightly higher in HCC tissue than in adjacent normal tissue (Chia et al, 2002). Su et al (2012) found that IFN-γ-1615 GA/AA genotypes are significantly related to an elevated risk of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

“…Su et al (2012) found that IFN-γ-1615 GA/AA genotypes are significantly related to an elevated risk of breast cancer. IL-10 is a potent immunosuppressive anti-inflammatory cytokine that is highly expressed in HCC tissue and adjacent normal tissue (Chia et al, 2002). IL-10 is the most studied anti-inflammatory cytokine involved in cancer research.…”

Section: Introductionmentioning

confidence: 99%

Combined Effects of Six Cytokine Gene Polymorphisms and SNP-SNP Interactions on Hepatocellular Carcinoma Risk in Southern Guangxi, China

Bei

Bai²,

Yu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Cytokine gene single nucleotide polymorphisms (SNPs) are involved in the genesis and progression of hepatocellular carcinoma (HCC). We hypothesized that combined effects of cytokine gene SNPs and SNP-SNP interactions are associated with HCC risk. Six SNPs in cytokine genes (IL-2, IFN-γ, IL-1β, IL-6, and IL-10) were genotyped in a study of 720 Chinese HCC cases and 784 cancer-free controls. Although none of these SNPs individually had a significant effect on the risk of HCC, we found that the combined effects of these six SNPs may contribute to HCC risk (OR=1.821, 95% CI=1.078-3.075). This risk was pronounced among smokers, drinkers, and hepatitis B virus carriers. A SNP-SNP interaction between IL-2-330 and IFN-γ-1615 was associated with an increased HCC risk (OR=1.078, 95% CI=1.022-1.136). In conclusion, combined effects of SNPs and SNP-SNP interactions in cytokine genes may contribute to HCC risk.

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Expression of interleukin-18, interferon-γ and interleukin-10 in hepatocellular carcinoma

Cited by 38 publications

References 23 publications

Expression of interferon-γ in human adrenal gland and kidney tumours

Expression of interferon-γ in human adrenal gland and kidney tumours

The tumor microenvironment in hepatocellular carcinoma (Review)

Combined Effects of Six Cytokine Gene Polymorphisms and SNP-SNP Interactions on Hepatocellular Carcinoma Risk in Southern Guangxi, China

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