AIM: To determine fibrosis progression and hepatocellular carcinoma (HCC), using simultaneous gene expression analysis. METHODS: Total RNA samples were extracted from liver biopsies from 19 patients with hepatitis C virus (HCV) infection and 3 patients without HCV infection. Among the 19 HCV-infected patients, 7 and 12 patients had grade F1-2 and F3-4 fibrosis, respectively. Of the 12 patients with F3-4 fibrosis, 8 had HCC. Gene expression in the liver samples was determined using an oligonucleotide microarray. The following comparisons were performed: normal livers vs HCV-infected livers; F1-2 vs F3-4; and F3-4 with HCC vs F3-4 without HCC. Genes that were differentially expressed between these groups were identified based on signal-to-noise ratios. RESULTS: In the HCV-infected livers, genes involved in immune responses were highly expressed. Expression levels of genes for plasma proteins and drug-metabolizing enzymes were decreased and those of genes involved in the cell cycle and oncogenesis were increased in the F3-4 cases as compared to the F1-2 cases. Among the F3-4 cases, genes involved in carbohydrate metabolism tended to be more highly expressed in patients with HCC than in patients without HCC. CONCLUSION: We identified genes that are associated with fibrosis progression and hepatocarcinogenesis. This information may be used to detect increased carcinogenic potential in the livers of patients with HCV infection.
AIM: To determine fibrosis progression and hepatocellular carcinoma (HCC), using simultaneous gene expression analysis. METHODS: Total RNA samples were extracted from liver biopsies from 19 patients with hepatitis C virus (HCV) infection and 3 patients without HCV infection. Among the 19 HCV-infected patients, 7 and 12 patients had grade F1-2 and F3-4fibrosis, respectively. Of the 12 patients with F3-4 fibrosis, 8 had HCC. Gene expression in the liver samples was determined using an oligonucleotide microarray. The following comparisons were performed: normal livers vs HCV-infected livers; F1-2 vs F3-4; and F3-4 with HCC vs F3-4 without HCC. Genes that were differentially expressed between these groups were identified based on signal-to-noise ratios. RESULTS: In the HCV-infected livers, genes involved in immune responses were highly expressed. Expression levels of genes for plasma proteins and drug-metabolizing enzymes were decreased and those of genes involved in the cell cycle and oncogenesis were increased in the F3-4 cases as compared to the F1-2 cases. Among the F3-4 cases, genes involved in carbohydrate metabolism tended to be more highly expressed in patients with HCC than in patients without HCC. CONCLUSION: We identified genes that are associated with fibrosis progression and hepatocarcinogenesis. This information may be used to detect increased carcinogenic potential in the livers of patients with HCV infection.
Authors: Maria W Smith; Zhaoxia N Yue; Gary K Geiss; Natalya Y Sadovnikova; Victoria S Carter; Loreto Boix; Catherine A Lazaro; Gary B Rosenberg; Roger E Bumgarner; Nelson Fausto; Jordi Bruix; Michael G Katze Journal: Cancer Res Date: 2003-02-15 Impact factor: 12.701
Authors: Robert A Anders; Lisa M Yerian; Maria Tretiakova; Jon M Davison; Richard J Quigg; Peter H Domer; Jamie Hoberg; John Hart Journal: Am J Pathol Date: 2003-03 Impact factor: 4.307
Authors: H Okabe; S Satoh; T Kato; O Kitahara; R Yanagawa; Y Yamaoka; T Tsunoda; Y Furukawa; Y Nakamura Journal: Cancer Res Date: 2001-03-01 Impact factor: 12.701
Authors: Young Kwan Sung; Sun Young Hwang; Mi Kyung Park; Mohammad Farooq; In Sook Han; Han Ik Bae; Jung-Chul Kim; Moonkyu Kim Journal: Cancer Sci Date: 2003-03 Impact factor: 6.716
Authors: Maria W Smith; Zhaoxia N Yue; Marcus J Korth; Hao A Do; Loreto Boix; Nelson Fausto; Jordi Bruix; Robert L Carithers; Michael G Katze Journal: Hepatology Date: 2003-12 Impact factor: 17.425