Journal of Liver Cancer

Original Article

Effect of PTEN Polymorphism on the Development of Hepatitis B Virus-associated Hepatocellular Carcinoma: Soon Sun Kim, Jung Woo Eun, Hyo Jung Cho, Hyun-Young Lee, Chul Won Seo, Gil Ho Lee, So Young Yoon, Choong Kyun Noh, Sung Won Cho, Jae Youn Cheong; J Liver Cancer. 2019;19(1):46-54. Published online March 31, 2019; DOI: https://doi.org/10.17998/jlc.19.1.46

4,452 Views
129 Downloads
1 Citation

Background/Aim
s: Phosphatase and tensin homolog (PTEN) is a known tumor suppressor gene that is downregulated in hepatocellular carcinoma (HCC). Here, we investigated the association between single nucleotide polymorphisms (SNPs) of PTEN and HCC development in patients with hepatitis B virus (HBV) infection.
Methods
Six SNPs of PTEN at positions rs1234221, rs1903860, rs1234220, rs1903858, rs2299941, and rs17431184 were analyzed in a development population (417 chronic HBV carriers without HCC and 281 chronic HBV carriers with HCC). PTEN rs1903858, rs1903860, and rs2299941 SNPs were further assessed for the development of HCC in a validation population of 200 patients with HBV-related liver cirrhosis.
Results
In the development population, PTEN rs1903860 C allele, rs1903858 G allele, and rs2299941 G allele were associated with a low risk of HCC. The haplotype A-T-A-A-A was associated with an increased risk of HCC (recessive model; odds ratio=2.277, 95% confidence interval [CI] =1.144-4.532, P=0.019). In the validation population, PTEN rs2299941 G allele was the only significant protective genetic polymorphism related to HCC development after adjustment for age and sex (hazard ratio=0.582, 95% CI =0.353-0.962, P=0.035).
Conclusions
These findings suggest that genetic polymorphisms in PTEN may affect HCC development in patients with chronic HBV infection.

Citations

Citations to this article as recorded by

Association of genetic variations in phosphatase and tensin homolog (PTEN) gene with polycystic ovary syndrome in South Indian women: a case control study
Swapna Siddamalla, Suresh Govatati, Veena Kunjumol Venu, Nagendram Erram, Mamata Deenadayal, Sisinthy Shivaji, Manjula Bhanoori
Archives of Gynecology and Obstetrics.2020; 302(4): 1033. CrossRef

Review Article

Hepatocellular Carcinoma Prediction Models for Patients with Chronic Hepatitis B Virus Infection in the Era of Potent Antiviral Therapy: Lee, Hye Won , Kim, Beom Kyung; J Liver Cancer. 2018;18(2):87-93. Published online September 30, 2018; DOI: https://doi.org/10.17998/jlc.18.2.87

2,987 Views
121 Downloads
5 Citations

Abstract PDF

Appropriate prediction of hepatocellular carcinoma (HCC) development is of paramount importance in terms of decision on antiviral therapy and HCC surveillance. To date, many HCC risk prediction models had been derived based on well-known risk factors such as age, male gender, the degree of fibrosis, and serum hepatitis B virus (HBV)-DNA load. Overall, such models showed high negative predictive values of approximately >90%, excluding the possibility of HCC development in 3 to 10 years with considerable accuracy. On the other hands, on the basis that potent antiviral therapy can substantially reduce the risk of HCC, its indications are steadily getting expanded for prevention of disease progression. Since antiviral therapy is a very strong disease modifier, the uniform application of HCC risk scores developed before the era of potent antiviral therapy would overestimate the risk of HCC. Furthermore, the tools to assess the fibrotic burden have remarkably evolved, from subjective determination based upon clinical symptom sign and ultrasonographic finding to more objective and delicate non-invasive tests based upon imaging and/or serological methods. Therefore, in the current era of potent antiviral therapy, the clinical significance of recently developed HCC risk models for patients with chronic HBV infection should be reappraised further.

Citations

Citations to this article as recorded by

Metabolic dysfunction associated fatty liver disease and the risk of hepatocellular carcinoma
Byeong Geun Song, Sung Chul Choi, Myung Ji Goh, Wonseok Kang, Dong Hyun Sinn, Geum-Youn Gwak, Yong-Han Paik, Moon Seok Choi, Joon Hyeok Lee, Seung Woon Paik
JHEP Reports.2023; : 100810. CrossRef
External validation of CAGE‐B and SAGE‐B scores for Asian chronic hepatitis B patients with well‐controlled viremia by antivirals
Jung Hyun Ji, Soo Young Park, Won Jeong Son, Hye Jung Shin, Hyein Lee, Hye Won Lee, Jae Seung Lee, Seung Up Kim, Jun Yong Park, Do Young Kim, Sang Hoon Ahn, Beom Kyung Kim
Journal of Viral Hepatitis.2021; 28(6): 951. CrossRef
An optimized hepatocellular carcinoma prediction model for chronic hepatitis B with well‐controlled viremia
Hye W. Lee, Soo Y. Park, Myeongjee Lee, Eun J. Lee, Jinae Lee, Seung U. Kim, Jun Y. Park, Do Y. Kim, Sang H. Ahn, Beom K. Kim
Liver International.2020; 40(7): 1736. CrossRef
External validation of the modified PAGE‐B score in Asian chronic hepatitis B patients receiving antiviral therapy
Hye Won Lee, Seung Up Kim, Jun Yong Park, Do Young Kim, Sang Hoon Ahn, Kwang‐Hyub Han, Beom Kyung Kim
Liver International.2019; 39(9): 1624. CrossRef
Changes in real-life practice for hepatocellular carcinoma patients in the Republic of Korea over a 12-year period: A nationwide random sample study
Beom Kyung Kim, Do Young Kim, Kwang-Hyub Han, Jinsil Seong, Jung Weon Lee
PLOS ONE.2019; 14(10): e0223678. CrossRef

Original Article

17-DMAG has the Potentiated Anticancer Effects Against Hepatocellular Carcinoma Cells by Transfection of the Gene Encoding Hepatitis B Viral X Protein: Chul-Seung Lee, Ok-Hee Kim, Ha-Eun Hong, Sang-Jin Jeon, Seong-Soo Wong, Say-June Kim; J Liver Cancer. 2017;17(2):126-135. Published online September 30, 2017; DOI: https://doi.org/10.17998/jlc.17.2.126

2,371 Views
17 Downloads

Abstract PDF: Background/Aim
s: Hepatitis B viral protein X (HBx) is implicated in the pathogenesis of hepatocellular carcinoma (HCC) as well as the elevation of heat shock proteins (HSPs) after hepatitis B virus (HBV) infection. We thus investigated the anticancer effects of an HSP90 inhibitor 17-Dimethylaminoethylamino-17-demethoxygeldanamycin (17-DMAG) in HBxtransfected hepatocellular carcinoma cells.
Methods
pcDNA-HBx was made by inserting the HBx gene derived from the HBV-infected patient into pcDNA3.1 using the restriction enzymes (XbaI/HindIII). HBx-expressing HepG2 cells were then generated by transfecting HepG2 cells with pcDNA containing HBx gene. To compare the anticancer effects of 17-DMAG between pcDNA-HBx transfected HepG2 cells and the control cells (pcDNA-transfected HepG2 cells), we performed various molecular studies, including Ez-cytox proliferation assay, Western blot analysis, and flow cytometry.
Results
17-DMAG inhibited the proliferation of pcDNA-HBx transfected HepG2 cells better than control cells (P<0.05). After treating with a various concentration of 17-DMAG (50–1,000 nM), pcDNA-HBx transfected HepG2 cells exhibited higher expression of pro-apoptotic proteins (c-caspase-3, c-caspase-8, and c-caspase-9) than did control cells (P<0.05). pcDNAHBx transfected HepG2 cells showed higher activities of caspase-3, caspase-8, and caspase-9 than did control cells (P<0.05). Finally, we found that the expression of pro-apoptotic proteins (PARP and c-caspase-3) was considerably decreased by the use of a caspase inhibitor suggesting that 17-DMAG induces the cell death of HepG2 cells caspase-dependently.
Conclusions
Our study strongly suggests that 17-DMAG has antiviral effects against HBV as well as anticancer effects against HepG2 cells. Thus, the application of 17-DMAG appears to be particularly advantageous to the HCC patients related with HBV infection.

Review Article

Application of CRISPR/Cas9 in Treating Hepatitis B Virus: Ju-Yeon Cho; J Liver Cancer. 2017;17(2):111-116. Published online September 30, 2017; DOI: https://doi.org/10.17998/jlc.17.2.111

3,095 Views
102 Downloads

Abstract PDF: The advent of oral antiviral agents has revolutionized hepatitis B treatment. It has led to decreased incidence and mortality related to hepatocellular carcinoma. However, although nucleos(t)ide analogs (NA) are fast and potent in inhibiting hepatitis B virus (HBV) polymerase and reverse transcriptase activity, complete cure of the virus is not possible. The complete eradication of HBV requires the covalently-closed-circular DNA (cccDNA) to be eliminated. Novel gene editing methods, such as zing finger nucleases, transcription activator-like effector nucleases, and the clustered regularly interspaced short palindromic repeats/Cas9 (CRISPR/ Cas9) system, designed to target specific DNA sequences has great potential for therapeutic application. Among these, the CRISPR/Cas9 system may be the most feasible approach to eradicate HBV cccDNA. Further studies are needed to develop a more efficient and safer
method
of delivery using the CRISPR/Cas9 system to achieve complete cure of chronic hepatitis B.

Case Report

Two Cases of Acute Hepatic Decompensation after Concurrent Chemoradiotherapy in Patients with Advanced Hepatocellular Carcinoma: Myoung Hwan Kim, Sang Hoon Ahn, Yong Han Paik, Kwan Sik Lee, Chae Yoon Chon, Young Myoung Moon, Jinsil Seong, Kwang Hyub Han; Journal of the Korean Liver Cancer Study Group. 2005;5(1):52-56. Published online June 30, 2005

490 Views
0 Download

Abstract PDF: Advanced hepatocellular carcinoma with portal vein thrombosis has a poor prognosis. Concurrent chemoradiation (CCRT) therapy achieved favorable results in advanced hepatocellular carcinoma with portal vein thrombosis and can be considered as a treatment option for the management of advanced hepatocellular carcinoma.2 But, exacerbation of liver function during concurrent chemoradiotherapy is a critical complication in patients with hepatitis B virus (HBV) related HCC. Reactivation of HBV replication is a well-known complication in cancer patients receiving chemotherapy. We report two cases with acute exacerbation of liver function. The one
result
ed in hepatic decompensation after CCRT probably due to HCC progression and/or chemoradiotherapy and the other is due to reactivation of HBV replication after CCRT, who recovered after lamivudine and corticosteroid therapy.

First
Prev
Page of 1
Next
Last

Search