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Overexpression of MUC13, a Poor Prognostic Predictor, Promotes Cell Growth by Activating Wnt Signaling in Hepatocellular Carcinoma

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AMERICAN JOURNAL OF PATHOLOGY 2018年第2期188卷 378-391页

作者： Dai, Yongdong Liu, Lulu Zeng, Tingting Liang, Jian-Zhong Song, Ye Chen, Kai Li, Yan Chen, Leilei Zhu, Ying-Hui Li, Jiangchao Li, Yan Xie, Dan Yuan, Yun-Fei Guan, Xin-Yuan Sun Yat Sen Univ Canc Ctr Collaborat Innovat Ctr Canc Med State Key Lab Oncol South China Guangzhou Guangdong Peoples R China Sir Run Run Shaw Hosp Coll Med Dept Obstet & Gynecol Assisted Reprod Unit Zhejiang Peoples R China Canc Biotherapy Ctr Zhejiang Peoples R China Zhejiang Univ Affiliated Hosp 1 Sch Med Hangzhou Zhejiang Peoples R China Southern Univ Sci & Technol Dept Biol Shenzhen Peoples R China Univ Hong Kong Dept Clin Oncol Hong Kong Hong Kong Peoples R China

Recently RNA sequencing revealed high mucin 13 (MUC13) expression in hepatocellular carcinoma (HCC) tissues. To understand the clinicopathologic significance of MUC13 in HCC, quantitative PCR and immunohistochemistry were used to detect its expression in paired tumor tissues and nontumor tissues. The oncoprotein role of MUC13 was determined by in vitro and in vivo assays. Overexpression of MUC13 was detected in 74 of 168 primary HCC cases (44%) and was significantly associated with tumor size (P = 0.027), stage (P = 0.006), encapsulation (P = 0.044), venous invasion (P = 0.024), and poor outcome (P = 0.004). Functional studies demonstrated MUC13 had strong oncogenic activity by promoting cell growth, colony formation, cell migration, and tumor formation in nude mice. The pro-oncogenic effect of MUC13 were effectively inhibited by RNA interference. MUC13 promoted cellular G(1)/S phase transition by activating Wnt signaling. Mechanistically, MUC13 bound to beta-catenin and increased its phosphorylation at Ser552 and Ser675 sites, which subsequently promoted nuclear translocation of beta-catenin and up-regulation of its downstream target genes Axing2, c-Myc, and CyclinDl. Knockdown of AKT with sh RNA in MUC13-overexpressing cells nullified the elevated phosphorylation of beta-catenin by MUC13. In clinical HCC samples, nuclear translocation of beta-catenin was significantly associated with MUC13 overexpression (P = 0.001). Overexpression of MUC13 plays a critical role in the development and progression of HCC by activating Wnt signaling.

关键词： Hepatocellular Cancer beta Catenin Wnt Signaling Pathway PID MUC13 gene Protein Overexpression Nuclear Translocation human-centered computing

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Longterm favorable results of limited hepatic resections for patients with hepatocellular carcinoma: 20 years of experience

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JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS 2007年第1期205卷 19-26页

作者： Yamashita, Yo-ichi Taketomi, Akinobu Itoh, Shinji Kitagawa, Dai Kayashima, Hiroto Harimoto, Norifumi Tsujita, Eiji Kuroda, Yosuke Maehara, Yoshihiko Kyushu Univ Dept Surg & Sci Grad Sch Med Sci Higashi Ku Fukuoka 8128582 Japan

Background: Recently, anatomic resection has been, in theory, considered preferable for eradicating portal venous tumor extension and intrahepatic metastasis in hepatocellular carcinoma (HCC). We have reported the effectiveness of limited hepatic resection for cirrhotic patients with HCC. Study Design: A retrospective study was carried out in 321 patients who underwent curative hepatic resection (anatomic resection, n=201;limited resection, n=120) as the initial treatment for solitary HCC<5 cm in our institution in the period 1985 to 2004 (median followup period 5.1 years). Results: Anatomic resection did not influence overall and recurrence-free survival rates after hepatic resection. In the liver damage A group (n=215), both 5-year overall and recurrence-free Survival rates in the anatomic resection group were considerably better than those in the limited resection group (87% versus 76%, p=0.02, and 63% versus 35%, p<0.01, respectively). In the liver damage B group (n=106), both 5-year overall and recurrence-free survival rates in the anatomic resection group were substantially worse than those in the limited resection group (48% versus 72%, p<0.01, and 28% versus 43%, p=0.01, respectively). The results of multivariate analysis revealed that anatomic resection was a notably poor factor in promoting recurrence-free survival in patients with liver damage B. Conclusions: Anatomic resection should be recommended for noncirrhotic patients (liver damage A) with HCC. Longterm results of limited hepatic resection proved its validity for cirrhotic patients (liver damage 13) with HCC.

关键词： Excision anatomic Hepatic Liver 肝 Hepatic Organ System ectomy hepatic damage Survival Rate Liver human-centered computing

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Projected future increase in aging hepatitis C virus-infected liver transplant candidates: A potential effect of hepatocellular carcinoma

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LIVER TRANSPLANTATION 2012年第12期18卷 1471-1478页

作者： Biggins, Scott W. Bambha, Kiran M. Terrault, Norah A. Inadomi, John Shiboski, Stephen Dodge, Jennifer L. Gralla, Jane Rosen, Hugo R. Roberts, John P. Univ Colorado Denver Div Gastroenterol & Hepatol Aurora CO 80045 USA Univ Colorado Denver Dept Pediat Aurora CO 80045 USA Univ Colorado Denver Dept Biostat & Informat Aurora CO 80045 USA Univ Calif San Francisco Div Gastroenterol & Hepatol San Francisco CA 94143 USA Univ Calif San Francisco Dept Epidemiol & Biostat San Francisco CA 94143 USA Univ Calif San Francisco Dept Surg San Francisco CA USA Univ Washington Div Gastroenterol & Hepatol Seattle WA 98195 USA

In the United States, the peak hepatitis C virus (HCV) antibody prevalence of 4% occurred in persons born in the calendar years 1940-1965. The goal of this study was to examine observed and projected age-specific trends in the demand for liver transplantation (LT) among patients with HCV-associated liver disease stratified by concurrent hepatocellular carcinoma (HCC). All new adult LT candidates registered with the Organ Procurement and Transplantation Network for LT between 1995 and 2010 were identified. Patients who had primary, secondary, or text field diagnoses of HCV with or without HCC were identified. There were 126,862 new primary registrants for LT, and 52,540 (41%) had HCV. The number of new registrants with HCV dramatically differed by the age at calendar year, and this suggested a birth cohort effect. When the candidates were stratified by birth year in 5-year intervals, the birth cohorts with the highest frequency of HCV were as follows (in decreasing order): 1951-1955, 1956-1960, 1946-1950, and 1941-1945. These 4 birth cohorts, spanning from 1941 to 1960, accounted for 81% of all new registrants with HCV. A 4-fold increase in new registrants with HCV and HCC occurred between the calendar years 2000 and 2010 in the 1941-1960 birth cohorts. By 2015, we anticipate that an increasing proportion of new registrants with HCV will have HCC and be =60 years old (born in or before 1955). In conclusion, the greatest demand for LT due to HCV-associated liver disease is occurring among individuals born between 1941 and 1960. This demand appears to be driven by the development of HCC in patients with HCV. During the coming decade, the projected increase in the demand for LT from an aging HCV-infected population will challenge the transplant community to reconsider current treatment paradigms. Liver Transpl, 2012. (c) 2012 AASLD.

关键词： Level Trigger Hepatocellular Cancer liver transplant Cohort Effect Parturition Liver Diseases human-centered computing birth Organ Procurement

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Recurrent chromosome alterations in hepatocellular carcinoma detected by comparative genomic hybridization

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GENES CHROMOSOMES & CANCER 2000年第2期29卷 110-116页

作者： Guan, XY Fang, Y Sham, JST Kwong, DLW Zhang, YQ Liang, QW Li, HM Zhou, H Trent, JM Univ Hong Kong Queen Mary Hosp Dept Clin Oncol Hong Kong Hong Kong Peoples R China Sun Yat Sen Univ Inst Canc Guangzhou Peoples R China Sun Yat Sen Univ Canc Hosp Guangzhou Peoples R China NHGRI Canc Genet Branch NIH Bethesda MD 20892 USA

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and has a very poor prognosis. Fifty primary HCC cases have been analyzed in the present study to explore the association between genomic alteration in primary HCC and clinical features. Several recurrent chromosomal abnormalities were identified in this study. The most frequently detected chromosomal gains involved chromosome arms Iq (33/50 cases, 66%), 8q (24/50 cases, 48%), and 20q (10/50 cases, 20%). High-copy-number amplifications involving Iq (4 cases), 8q (3 cases), and 20q (3 cases) were detected, and a minimum overlapping amplified region at 1q12-q22 was identified. The most frequently detected loss of chromosomal material involved 16q (35/50 cases, 70%), 17p (26/50 cases, 52%), 19p (21/50 cases, 42%), 4q (20/50 cases, 40%), 1p(18/50 cases, 36%), 8p(16/50 cases, 32%), and 22q (14/50 cases, 28%). The associations between genomic alterations detected in the present study and clinical features including clinical stage, tumor size, HBV infection, chronic liver disease, and liver cirrhosis were explored. Our CGH results suggest that the gain of 20q and deletion of 8p are late genetic alterations in HCC, because the incidence of these alterations was obviously increased in the advanced clinical stages. Another finding showed that loss of 8p and gain of 8q and 20q are associated with tumor size. The recurrent gain and loss of chromosomal regions identified in this study provide candidate regions that may contain oncogenes or tumor suppressor genes respectively involved in HCC development and progression. (C) 2000 Wiley-Liss, Inc.

关键词： Carcinoma Hepatocellular Chromosome Abnormalities Liver Neoplasms 癌肝细胞染色体异常肝肿瘤 Chromosome Aberrations Carcinoma Tumor Suppressor Genes Oncogenes Liver Neoplasms tumor size human-centered computing cases (containers) Gain clinical stages

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Multimodality management of hepatocellular carcinoma larger than 10 cm

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JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS 2003年第5期197卷 730-738页

作者： Mok, KT Wang, BW Lo, GH Liang, HL Liu, SI Chou, NH Tsai, CC Chen, IS Yeh, MH Chen, YC Vet Gen Hosp Dept Surg Div Gen Surg Kaohsiung 813 Taiwan Vet Gen Hosp Div Gastroenterol Dept Internal Med Kaohsiung 813 Taiwan Vet Gen Hosp Dept Radiol Kaohsiung 813 Taiwan Natl Yang Ming Univ Sch Med Taipei 112 Taiwan

BACKGROUND: Hepatic resection for huge hepatocellular carcinoma (HCC) is challenging. The role of multimodality nonsurgical therapy for HCC larger than 10 cm is unclear. STUDY DESIGN: We retrospectively investigated 131 HCC patients with main tumors larger than 10 cm in diameter seen between October 1990 and October 2001. Fifty-six patients (group A) underwent hepatectomy and 75 patients (group B) underwent nonsurgical multidisciplinary therapy including hepatic arterial infusion, transcatheter arterial embolization, and percutaneous acetic acid injection. RESULTS: Patients in group B were older, had lower serum albumin levels, and there were more patients with liver cirrhosis and great vessel invasion. Median survivals of group A and B patients were 17 months and 7 months, respectively (p < 0.001). But the 1-, 3-, 5-year survival rates in group B using 38 patients undergoing 3 or more sessions of nonsurgical treatment were not significantly worse than those for group A using 53 patients with followup (57.1%, 19.0%, 16.3% versus 60.7%, 24.5%, 24.5%, respectively). Group A patients had 37.7% and 71.7% recurrence rates at 6 and 12 months, respectively, after operation, and they had a significantly higher frequency of overall extrahepatic recurrence compared with group B patients (43.4% versus 18.7%, p = 0.005). In group B, only 3 of 35 patients younger than 60 years had tumor. shrinkage after nonsurgical treatment modalities in comparison to 17 of 40 patients in the elderly group (p = 0.003). Younger patients had a significantly higher prevalence of hepatitis B surface antigen positivity (85.7% versus 47.5%) and infiltrating tumor growth pattern (74.3% versus 45.0%) compared with older patients. CONCLUSIONS: Our study suggests that the advantage of hepatic resection in patients with huge HCC is marginal. An effective adjuvant therapy is needed to improve outcomes after hepatic resection. The experience in using nonsurgical treatment shows that the result is poor in yo

关键词： Antineoplastic Combined Chemotherapy Protocols Carcinoma Hepatocellular 癌肝细胞化学栓塞治疗性肝切除术肝肿瘤 Antineoplastic Combined Chemotherapy Protocols Patients Carcinoma multimodality Hepatocellular Cancer human-centered computing Hepatic Organ System

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Diagnostic accuracy of osteopontin plus alpha-fetoprotein in the hepatocellular carcinoma: A meta-analysis

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CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY 2017年第5期41卷 543-553页

作者： Li, Jinwan Chen, Xiaoli Dai, Meiyu Huang, Shifeng Chen, Jingfan Dai, Shengming Guangxi Med Univ Affiliated Hosp 4 Med Sci Lab 1 Liushi Rd Liuzhou City 545005 Guangxi Provinc Peoples R China Guangxi Med Univ Affiliated Hosp 4 Dept Gen Surg Liuzhou 545005 Guangxi Peoples R China

Objective: Osteopontin (OPN) has been reported as a potential biomarker for diagnosis of hepatocellular carcinoma (HCC) in many inconsistent results. This study demonstrates a systematic meta-analysis for the evaluation on diagnostic accuracy of serum or plasma OPN and alpha-fetoprotein (AFP) alone and combined assays for HCC.& para;& para;Methods: Relevant literatures were searched in PubMed up to August 2016. The quality of each study was evaluated by QUADAS-2 (quality assessment for studies of diagnostic accuracy). Statistical analysis was performed by Meta-Disc 1.4 and Stata 12.0. The random-effect models were used to estimate pooled sensitivity, specificity and other diagnostic indicators of OPN and/or AFP in HCC.& para;& para;Results: A total of 14 case-control literatures (15 studies) met the inclusion criteria in this meta-analysis. The respective pooled diagnostic sensitivity and specificity were 0.71 (95% Cl: 0.69-0.74) and 0.80 (95% Cl: 0.78-0.82) for OPN;0.61 (95% Cl: 0.58-0.63) and 0.92 (95% Cl: 0.91-0.94) for AFP;0.82 (95% Cl: 0.79-0.84) and 0.77 (95% Cl: 0.74-0.80) for OPN plus AFP. Their area under the curve (AUC) values were 0.8786, 0.8718 and 0.9005, respectively.& para;& para;Conclusion: Combination of OPN and AFP was better than OPN or AFP alone in diagnosis of HCC. (C) 2017 Elsevier Masson SAS. All rights reserved.

关键词： Osteopontin diagnosis quality/standard SPP1 gene Meta-Analysis human-centered computing Sensitivity and Specificity

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Differences Between Hepatocellular Carcinoma and Hepatitis B Virus Infection in Patients With and Without Cirrhosis

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ANNALS OF SURGICAL ONCOLOGY 2014年第2期21卷 458-465页

作者： Kim, Jong Man Kwon, Choon Hyuck David Joh, Jae-Won Park, Jae Berm Lee, Joon Hyeok Kim, Sung Joo Paik, Seung Woon Park, Cheol Keun Yoo, Byung Chul Sungkyunkwan Univ Sch Med Samsung Med Ctr Dept Surg Seoul South Korea Sungkyunkwan Univ Sch Med Samsung Med Ctr Dept MedDiv Gastroenterol Seoul South Korea Sungkyunkwan Univ Sch Med Samsung Med Ctr Dept Pathol Seoul South Korea

Background. In patients with hepatitis B virus (HBV) infections, differences in hepatocellular carcinoma (HCC) between those with liver cirrhosis and those without cirrhosis have not been elucidated. The aim of this study was to compare clinicopathological characteristics and survival between noncirrhotic and cirrhotic patients and to determine prognostic factors for tumor recurrence after hepatectomy in patients with HBV and HCC. Methods. Between 2005 and 2010, 441 curative hepatectomies for HCC in patients with cirrhosis and 454 for HCC in patients without cirrhosis were performed. Results. Cirrhotic patients had lower platelet counts, protein induced by vitamin K antagonist-II (PIVKA-II) levels, and tumor size than noncirrhotic patients. HCC differentiation in noncirrhotic patients was poorer than in cirrhotic patients. The 1-, 2-, and 3-year disease-free survival rates were 72.0, 65.6, and 61.0 % in noncirrhotic patients, and 68.6, 56.5, and 51.5 % in cirrhotic patients, respectively (P = 0.013). However, the 1-, 2-, and 3-year overall survival rates were 92.4, 85.5, and 81.7 % in noncirrhotic patients, and 91.9, 86.1, and 82.4 % in cirrhotic patients, respectively (P = 0.683). Risk factors for tumor recurrence in each group varied in multivariate analyses. Increased age, high platelet counts, microvascular invasion, serosal invasion, and intrahepatic metastasis predisposed to tumor recurrence in noncirrhotic patients, but elevated PIVKA-II and alkaline phosphatase levels, low serum albumin levels, portal vein invasion, intrahepatic metastasis, and tumor size were predisposing factors for recurrence in cirrhotic patients. Conclusions. The clinicopathologic characteristics and risk factors for tumor recurrence in cirrhotic and noncirrhotic HCC patients with HBV infection differ.

关键词： Liver Cirrhosis Patients Recurrent Neoplasm Hepatocellular Cancer Hepatitis B virus Cirrhosis acarboxy prothrombin tumor size Hepatectomy Predisposing Factors human-centered computing

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Inhibition of human methionine adenosyltransferase 1A transcription by coding region methylation

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JOURNAL OF CELLULAR PHYSIOLOGY 2012年第4期227卷 1583-1591页

作者： Tomasi, Maria Lauda Li, Tony W. H. Li, Mei Mato, Jose M. Lu, Shelly C. Keck Sch Med USC So Calif Res Ctr ALPD & Cirrhosis USC Res Ctr Liver Dis Div Gastroenterol & Liver Dis Los Angeles CA 90033 USA Ciberehd CIC BioGUNE Derio Bizkaia Spain

Two genes (MAT1A and MAT2A) encode for the essential enzyme methionine adenosyltransferase (MAT). MAT1A is silenced in hepatocellular carcinoma (HCC), and absence of MAT1A leads to spontaneous development of HCC in mice. Previous report correlated promoter methylation to silencing of MAT1A but definitive proof was lacking. Here we investigated the role of methylation in regulating MAT1A expression. There are three MspI/HpaII sites from -1,913 to +160 of the human MAT1A gene (numbered relative to the translational start site) at position -977, +10, and +88. Bisulfite treatment and DNA sequencing, and Southern blot analysis showed that methylation at +10 and +88, but not -977, correlated with lack of MAT1A expression. MAT1A promoter construct methylated at -977, +10 or +88 position has 0.7-fold, 3-fold, and 1.6-fold lower promoter activity, respectively. Methylation at -977 and +10 did not inhibit the promoter more than methylation at +10 alone;while methylation at +10 and +88 reduced promoter activity by 60%. Mutation of +10 and +88 sites also resulted in 40% reduction of promoter activity. Reactivation of MAT1A correlated with demethylation of +10 and +88. In vitro transcription assay showed that methylation or mutation of +10 and +88 sites reduced transcription. In conclusion, our data support the novel finding that methylation of the MAT1A coding region can inhibit gene transcription. This represents a key mechanism for decreased MAT1A expression in HCC and a target for therapy. To our knowledge, this is the first example of coding region methylation inhibiting transcription of a mammalian gene. J. Cell. Physiol. 227: 1583-1591, 2012. (C) 2011 Wiley Periodicals, Inc.

关键词： Open Reading Frames human-centered computing MAT2A gene Methylation MAT1A gene Genetic Transcription

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Small Interfering RNAs Induce Target-Independent Inhibition of Tumor Growth and Vasculature Remodeling in a Mouse Model of Hepatocellular Carcinoma

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AMERICAN JOURNAL OF PATHOLOGY 2010年第6期177卷 3192-3201页

作者： Berge, Mathieu Bonnin, Philippe Sulpice, Eric Vilar, Jose Allanic, David Silvestre, Jean Sebastien Levy, Bernard I. Tucker, Gordon C. Tobelem, Gerard Rainon, Tatyana Merkulova Univ Paris 07 INSERM Inst Vaisseaux & Sang U965 Paris France Univ Paris 07 Equipe Labellisee LIGUE 2009 Paris France Univ Paris 07 Hop Lariboisiere AP HP Paris France INSERM U970 Paris France Univ Paris 05 Paris France Inst Rech SERVIER Canc Res & Drug Discovery Croissy Sur Seine France

RNA interference mediated by small interfering RNAs (siRNAs) has emerged as a potential therapeutic approach to treat various diseases including cancer Recent studies with several animal models of post traumatic revascularization demonstrated that synthetic siRNAs may produce therapeutic effects m a target independent manner through the stimulation of the toll hike receptor 3 (TLR3)/interferon pathway and suppression of angiogenesis To analyze the impact of siRNAs on tumor angiogenesis we injected transgenic mice developing hepatocellular carcinoma (HCC) with either control siRNAs or siRNA targeting neuropilin 1 We found that treatment with these siRNAs led to a comparable reduction in tumor liver volume and to inhibition of tumor vasculature remodeling We further determined that TLR3 which recognizes double stranded siRNA was up regulated m mouse HCC Treatment of HCC mice with polyinosinic polycytidylic acid [poly(I C)], a TLR3 agonist led to both a reduction of tumor liver enlargement and a decrease in hepatic arterial blood flow indicating that TLR3 is functional and may mediate both anti angiogenic and anti tumor responses We also demonstrated that siRNAs increased interferon gamma levels in the liver In vitro interferon gamma inhibited proliferation of endothelial cells In addition we found that siRNAs inhibited endothelial cell proliferation and morphogenesis in an interferon gamma-independent manner Our results suggest that synthetic siRNAs inhibit target independently HCC growth and angiogenesis through the activation of the innate interferon response and by directly inhibiting endothelial cell function (Am J Pathol 2010 177 3192-3201 DOI 10 2353/ajpath 2010 100157)

关键词： Toll-Like Receptor 3 Cell Proliferation Angiogenesis Endothelial Cells Hepatocellular Cancer Interferon-gamma Remodeling Small Interfering RNA mouse model tumor growth Liver Neoplasms small disturbance human-centered computing cancer angiogenesis

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Does antiviral therapy prevent hepatocellular carcinoma?

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ANTIVIRAL THERAPY 2011年第6期16卷 787-795页

作者： Kwon, Hellan Lok, Anna S. Univ Michigan Div Gastroenterol & Hepatol Ann Arbor MI 48109 USA

Chronic infection with HBV or HCV can lead to the development of hepatocellular carcinoma (HCC). The major risk factors for HBV-related HCC are persistent presence of hepatitis B e antigen (HBeAg) and/or high serum HBV DNA levels, and cirrhosis. The major risk factor for HCV-related HCC is cirrhosis. One randomized double blind controlled trial of lamivudine in patients with HBeAg and/or high serum HBV DNA levels showed that antiviral therapy prevented disease progression and reduced the incidence of HCC. A beneficial effect of antiviral therapy on the risk of HCC has also been shown in cohort studies and meta-analyses, particularly among responders. Several randomized controlled trials of interferon in patients with HCV-related cirrhosis showed that treated patients had a lower incidence of HCC. A greater effect was observed in patients who achieved sustained virological response, while the benefit in non-responders is unclear. Antiviral therapies for hepatitis B and hepatitis C can prevent but not completely eliminate HCC. Improvement in identification of infected persons, accessibility of care and affordability of treatment is needed for antiviral therapy to have a major impact on the global incidence of HCC.

关键词： antiviral therapy Hepatitis B e Antigens Hepatocellular Cancer Hepatitis B virus human-centered computing Risk Factors Hepatitis B and hepatitis C chronic infection

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