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Percutaneous Ablation of Hepatocellular Carcinoma: Current Status

JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY 2010年第8期21卷 S204-S213页

作者： McWilliams, Justin P. Yamamoto, Shota Raman, Steven S. Loh, Christopher T. Lee, Edward W. Liu, David M. Kee, Stephen T. Univ Calif Los Angeles Med Ctr Dept Intervent Radiol Los Angeles CA 90095 USA Univ Calif Los Angeles Med Ctr Dept Radiol Sci Los Angeles CA 90095 USA Univ British Columbia Fac Med Dept Radiol Vancouver BC Canada Vancouver Gen Hosp Dept Radiol Intervent Radiol Sect Vancouver BC V5Z 1M9 Canada

Hepatocellular carcinoma (HCC) is an increasingly common disease with dismal long-term survival. Percutaneous ablation has gained popularity as a minimally invasive, potentially curative therapy for HCC in nonoperative candidates. The seminal technique of percutaneous ethanol injection has been largely supplanted by newer modalities, including radiofrequency ablation, microwave ablation, cryoablation, and high-intensity focused ultrasound ablation. A review of these modalities, including technical success, survival rates, and complications, will be presented, as well as considerations for treatment planning and follow-up.

关键词： High-Intensity Focused Ultrasound Ablation Complication Modality treatment planning Cryosurgery radiofrequency ablation human-centered computing Popularity

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Glucose-Regulated Protein 78 Is a Novel Contributor to Acquisition of Resistance to Sorafenib in Hepatocellular Carcinoma

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ANNALS OF SURGICAL ONCOLOGY 2010年第2期17卷 603-612页

作者： Chiou, Jeng-Fong Tai, Cheng-Jeng Huang, Ming-Te Wei, Po-Li Wang, Yu-Huei An, Jane Wu, Chih-Hsiung Liu, Tsan-Zon Chang, Yu-Jia Taipei Med Univ & Hosp Dept Radiat Oncol Taipei Taiwan Taipei Med Univ & Hosp Ctr Canc Taipei Taiwan New York Med Coll Valhalla NY 10595 USA Taipei Med Univ Shuang Ho Hosp Dept Surg Taipei Taiwan Taipei Med Univ & Hosp Dept Surg Taipei Taiwan

Background. Sorafenib is a newly established cancer drug found to be an effective systemic treatment for advanced hepatocellular carcinoma (HCC). However, little is known about any potential effectors that modify tumor cell sensitivity towards sorafenib. Here, we present the first evidence that glucose-regulated protein 78 (GRP78) is intimately associated with acquisition of resistance towards sorafenib. Methods. The role of GRP78 in acquisition of resistance towards sorafenib was determined using HepJ5 (a GRP78-overexpressing subline) and HepG2 as its pair-matched control. RNA interference in cancer cells was applied to determine the influence of GRP78 expression on sensitivity to sorafenib treatment. Results. We found that HepG2 cells exhibited higher sensitivity toward sorafenib, with 50% inhibition concentration (IC50) >20 mu M for HepJ5 and 4.8 mu M for HepG2. Specifically, when HepG2 cells received 20 mu M sorafenib treatment for 24 h, over 80% of cells underwent apoptosis compared with only 32% of HepJ5 cells under similar experimental conditions. Similarly, GRP78 knockdown in HepJ5 cells by small interfering RNA (siRNA) technique enhanced the efficacy of sorafenib-mediated cell death. This was reflected by a shift of IC50 values from >20 mu M to 4.8 mu M. Conclusions. GRP78 is a positive modifier for sorafenib resistance acquisition in HCC and represents a prime target for overcoming sorafenib resistance.

关键词： molecular chaperone GRP78 systemic treatment sorafenib Antineoplastic Agents Neoplastic Cell human-centered computing

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Identification of genes preferentially methylated in hepatitis C virus-related hepatocellular carcinoma

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CANCER SCIENCE 2010年第6期101卷 1501-1510页

作者： Deng, Ying-Bing Nagae, Genta Midorikawa, Yutaka Yagi, Koichi Tsutsumi, Shuichi Yamamoto, Shogo Hasegawa, Kiyoshi Kokudo, Norihiro Aburatani, Hiroyuki Kaneda, Atsushi Univ Tokyo RCAST Genome Sci Div Tokyo Japan Univ Tokyo Grad Sch Med Dept Hepatobiliary Pancreat Surg Tokyo Japan Univ Tokyo TSBMI Tokyo Japan Japan Sci & Technol Agcy PRESTO Tokyo Japan

Chronic infections by hepatitis B virus (HBV) and hepatitis C virus (HCV) appear to be the most significant causes of hepatocellular carcinoma (HCC). Aberrant promoter methylation is known to be deeply involved in cancer, including in HCC. In this study, we analyzed aberrant promoter methylation by methylated DNA immunoprecipitation-on-chip analysis on a genome-wide scale in six HCCs including three HBV-related and three HCV-related HCCs, six matched noncancerous liver tissues, and three normal liver tissues. Candidate genes with promoter methylation were detected more frequently in HCV-related HCC. Candidate genes methylated preferentially to HBV-related or HCV-related HCCs were detected and selected, and methylation levels of the selected genes were validated by quantitative methylation analysis using MALDI-TOF mass spectrometry using 125 liver tissue samples, including 61 HCCs (28 HBV-related HCCs and 33 HCV-related HCCs) and 59 matched noncancerous livers, and five normal livers. Among analyzed genes, preferential methylation in HBV-related HCC was validated in one gene only. However, 15 genes were found to be methylated preferentially in HCV-related HCC, which was independent from age. Hierarchical clustering of HCC using these genes stratified HCV-related HCC as a cluster of frequently methylated samples. The 15 genes included genes inhibitory to cancer-related signaling such as RAS/RAF/ERK and Wnt/beta-catenin pathways. Methylation of dual specificity phosphatase 4 (DUSP4), cytochrome P450, family 24, subfamily A, polypeptide 1 (CYP24A1), and natriuretic peptide receptor A (NPR1) significantly correlated with recurrence-free survival. It was indicated that genes methylated preferentially in HCV-related HCC exist, and that DNA methylation might play an important role in HCV-related HCC by silencing cancer-related pathway inhibitors, and might perhaps be useful as a prognostic marker. (Cancer Sci 2010).

关键词： atrial natriuretic factor receptor A Methylated Methylation liver tissue human-centered computing Hepatitis C Virus-Related Hepatocellular Carcinoma

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Hepatocellular Carcinoma: Current Management

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CURRENT PROBLEMS IN SURGERY 2010年第1期47卷 10-67页

作者： Cha, Charles H. Saif, M. Wasif Yamane, Brett H. Weber, Sharon M. Yale Univ Sch Med Dept Surg New Haven CT USA Yale Univ Sch Med Dept Med Yale Canc CtrGI Canc Program New Haven CT USA Univ Wisconsin Madison WI USA

The age-adjusted incidence of hepatocellular carcinoma (HCC) has tripled in the United States over the past 2 decades, fueled by the dramatic increase of hepatitis C during that same time period. Currently, there are an estimated 3 million people with chronic hepatitis C and 1.2 million with chronic hepatitis B in the United States. These patients are estimated to develop HCC at a rate of 0.5% to 5% per year.1 The incidence of HCC in the United States still lags behind many parts of the world where hepatitis B is endemic, such as China, Southeast Asia, and southern Africa. Worldwide, HCC is the third most common cause of cancer death and there are an estimated 1 million cases worldwide. The median survival in unresectable cases is less than 4 months and under a year for untreated patients with less advanced ***, the long-term survival rates from HCC in the United States have doubled over the past 2 decades, and a part of this increase is likely due to advances in surgical therapy for HCC, particularly as cancers are being detected earlier and therefore are still localized.8 Both surgical resection and transplantation are highly effective in the treatment of patients with localized HCC. Typically these surgical modalities complement each other, as patients with preserved liver function are candidates for resection and those with poor underlying liver function would be directed toward transplantation. However, their relative roles in the treatment of HCC have generated quite a bit of debate. Ultimately, as the multitude of treatment modalities proliferate, HCC must be treated in a multidisci-plinary fashion, involving hepatologists, oncologists, surgeons, radiologists, and pathologists, to come up with the best treatment plan for any individual patient.

关键词： United States treatment planning Transplantation ectomy Hepatitis B human-centered computing Hepatitis C liver function

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Gas chromatography/time-of-flight mass spectrometry-based metabonomics of hepatocarcinoma in rats with lung metastasis: elucidation of the metabolic characteristics of hepatocarcinoma at formation and metastasis

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RAPID COMMUNICATIONS IN MASS SPECTROMETRY 2010年第18期24卷 2765-2775页

作者： Li, Zong-Fang Wang, Juan Huang, Chen Zhang, Shu Yang, Jun Jiang, An Zhou, Rui Pan, Dun Xi An Jiao Tong Univ Sch Med Dept Gen Surg Affiliated Hosp 2 Xian 710004 Shaanxi Prov Peoples R China Xi An Jiao Tong Univ Sch Med Lab Environm & Genes Related Dis Educ Minist Xian 710061 Peoples R China Xi An Jiao Tong Univ Sch Med Affiliated Hosp 2 Dept Pathol Xian 710004 Peoples R China

Hepatocarcinoma (HCC) has a very high mortality rate and the high recurrence and metastasis rates contribute to the poor prognosis of HCC patients. To understand HCC formation and metastasis, we assessed the metabonomics of rat HCC and HCC with lung metastasis (HLM). The HLM rat model was established by exposure to diethylnitrosamine (DEN). Levels of serum and urine metabolites were quantified with gas chromatography/time-of-flight mass spectrometry (GC/TOFMS), and data were analyzed with partial least-squares discrimination analysis (PLS-DA). Serum and urine levels of some metabolites differed significantly between the control, HCC, and HLM groups. The products and intermediates from glycolysis and glutamate metabolism were elevated, while the tricarboxylic acid (TCA) cycle was inhibited, in both HCC and HLM. HLM samples revealed enhanced metabolism of nucleic acids, amino acids and glucuronic acid. PLS-DA indicated that principal component weighting was greatest for serum serine, phenylalanine, lactic acid, tyrosine and glucuronic acid, and urine glycine, serine, 5-oxyproline, malate, hippuric acid and uric acid. These data provide novel information that will improve understanding of the pathophysiological processes involved in HCC and HLM, and revealed potential metabolic markers for HCC invasion and metastasis. Copyright (c) 2010 John Wiley & Sons, Ltd.

关键词： Metabolomics lung metastasis Hepatocellular Cancer Glucuronic Acids Mortality Mass spectroscopy human-centered computing metastasis Rats

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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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Enhanced Detection of Early Hepatocellular Carcinoma by Serum SELDI-TOF Proteomic Signature Combined with Alpha-Fetoprotein Marker

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ANNALS OF SURGICAL ONCOLOGY 2010年第9期17卷 2518-2525页

作者： Chen, Lei Ho, David W. Y. Lee, Nikki P. Y. Sun, Stella Lam, Brian Wong, Kwong-Fai Yi, Xin Lau, George K. Ng, Eddy W. Y. Poon, Terence C. W. Lai, Paul B. S. Cai, Zongwei Peng, Jirun Leng, Xisheng Poon, Ronnie T. P. Luk, John M. Univ Hong Kong Queen Mary Hosp Dept Surg Hong Kong Hong Kong Peoples R China Univ Hong Kong Queen Mary Hosp Dept Med Hong Kong Hong Kong Peoples R China Peking Univ Peoples Hosp Dept Hepatobiliary Surg Beijing 100871 Peoples R China Univ Cambridge Metab Res Labs Inst Metab Sci Addenbrookes Hosp NHS Turst Cambridge England Chinese Univ Hong Kong Dept Med & Therapeut Hong Kong Hong Kong Peoples R China Hong Kong Baptist Univ Dept Chem Hong Kong Hong Kong Peoples R China Natl Univ Singapore Dept Pharmacol Singapore 117548 Singapore Natl Univ Singapore Dept Surg Singapore 117548 Singapore

Background. Biomarkers for accurate diagnosis of early hepatocellular carcinoma (HCC) are limited in number and clinical validation. We applied SELDI-TOF-MS Protein-Chip technology to identify serum profile for distinguishing HCC and liver cirrhosis (LC) and to compare the accuracy of SELDI-TOF-MS profile and alpha-fetoprotein (AFP) level in HCC diagnosis. Patients and Methods. Serum samples were obtained from 120 HCC and 120 LC patients for biomarker discovery and validation studies. Protein Chip technology was employed for generating SELDI-TOF proteomic features and analyzing serum proteins/peptides. Results. A diagnostic model was established by CART algorithm, which is based on 5 proteomic peaks with m/z values at 3324, 3994, 4665, 4795, and 5152. In the training set, the CART algorithm could differentiate HCC from LC subjects with a sensitivity and specificity of 98% and 95%, respectively. The results were assessed in blind validation using separate cohorts of 60 HCC and 60 LC patients, with an accuracy of 83% for HCC and 92% for LC patients. The diagnostic odd ratio (DOR) indicated that SELDI-TOF proteomic signature could achieve better diagnostic performance than serum AFP level at a cutoff of 20 ng/mL (AFP(20)) (92.72 vs 9.11), particularly superior for early-stage HCC (87% vs 54%). Importantly, a combined use of both tests could enhance the detection of HCC (sensitivity, 95%;specificity, 98%;DOR, 931). Conclusion. Serum SELDI-TOF proteomic signature, alone or in combination with AFP marker, promises to be a good tool for early diagnosis and/screening of HCC in at-risk population with liver cirrhosis.

关键词： Protein Array Analysis Liver Cirrhosis line controller proteomics surface enhanced laser desorption ionization time of flight mass spectrometry Serum AFP Population at Risk human-centered computing alpha-Fetoproteins

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Evolution of prognostic factors in hepatocellular carcinoma in Japan

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ALIMENTARY PHARMACOLOGY & THERAPEUTICS 2010年第3期31卷 407-414页

作者： Nouso, K. Kobayashi, Y. Nakamura, S. Kobayashi, S. Toshimori, J. Kuwaki, K. Hagihara, H. Onishi, H. Miyake, Y. Ikeda, F. Shiraha, H. Takaki, A. Iwasaki, Y. Kobashi, H. Yamamoto, K. Okayama Univ Dept Mol Hepatol Grad Sch Med Dent & Pharmaceut Sci Okayama 7008558 Japan Okayama Univ Dept Gastroenterol & Hepatol Grad Sch Med Dent & Pharmaceut Sci Okayama 7008558 Japan

P>Background The surveillance of hepatocellular carcinoma (HCC) has become prevalent, and the modalities for its treatment have improved. Aim To understand the changes that occur in the characteristics and prognostic factors of HCC with time. Methods Newly diagnosed HCC patients were divided into two groups;patients treated before 31 December 2000 (n = 504), and after 1 January 2001 (n = 746), and their clinical backgrounds and prognostic factors were analysed. Results The number of patients negative for both Hepatitis B surface antigen (HBsAg) and Hepatitis C virus antibody (HCVAb) increased with time (NBNC-HCC). The size of HCC decreased in patients who were positive for HBsAg (B-HCC) or HCVAb (C-HCC), whereas no difference was observed in NBNC-HCC. The patient survival of C-HCC improved;however, no difference was detected for NBNC-HCC. In multivariate analysis, low albumin, high aspartate aminotransferase (AST), ascites, large tumour size, multiple tumour number and high alpha-fetoprotein were risk factors for survival before 2000, whereas the presence of HBsAg was additionally selected as a good prognostic factor and AST was excluded after 2001. Conclusions The prognostic factors as well as clinical background of HCC changed with time, and the presence of HBsAg was found to be an additional good prognostic factor after 2001.

关键词： Hepatitis C Antibodies Prognostic Factors Risk Factors Number of tumors AST human-centered computing Hepatitis B Surface Antigens Patients

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Genistein synergizes with arsenic trioxide to suppress human hepatocellular carcinoma

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CANCER SCIENCE 2010年第4期101卷 975-983页

作者： Jiang, Hongchi Ma, Yong Chen, Xiaoning Pan, Shangha Sun, Bei Krissansen, Geoffrey W. Sun, Xueying Harbin Med Univ Affiliated Hosp 1 Hepatosplen Surg Ctr Dept Gen Surg Harbin Peoples R China Univ Auckland Dept Mol Med & Pathol Fac Med & Hlth Sci Auckland 1 New Zealand

Arsenic trioxide (ATO) is of limited therapeutic benefit for the treatment of solid tumors. Genistein exhibits anticancer and prooxidant activities, making it a potential candidate to enhance the efficacy of ATO whose cytotoxicity is oxidation-sensitive. This study sought to determine whether genistein synergizes with ATO to combat hepatocellular carcinoma (HCC). Three human HCC cell lines, namely HepG2, Hep3B, and SK-Hep-1, were incubated with ATO, genistein, or ATO + genistein. The cells were also pretreated with antioxidant agents N-acetyl-L-cysteine (NAC) or butylated hydroxyanisole (BHA). Cell viability, apoptosis, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (Delta Psi m), expression of Bcl-2, Bax, caspase-9, and -3, and release of cytochrome c into the cytosol were examined. The synergistic effect of ATO and genistein was also assessed using HepG2 xenografts subcutaneously established in BALB/c nude mice. The results show that genistein synergized with ATO to reduce viability, induce apoptosis, and diminish the Delta Psi m of cells. The combination therapy down-regulated Bcl-2 expression, up-regulated Bax expression, enhanced the activation of caspase-9 and-3, and increased the release of cytochrome c. The synergistic effect of ATO and genistein was diminished by pretreatment with NAC or BHA. Genistein increased the production of intracellular ROS, while ATO had little effect. Genistein synergized with a low dose of ATO (2.5 mg/kg) to significantly inhibit the growth of HepG2 tumors, and suppress cell proliferation and induce apoptosis in situ. There were no obvious side effects, as seen with a high dose of ATO (5 mg/kg). Combining genistein with ATO warrants investigation as a therapeutic strategy to combat HCC. (Cancer Sci 2010;101: 975-983)

关键词： Reactive Oxygen Species NLRP1 gene Side Effect Synergism ARSENIC OXIDES Genistein Caspase 9 human-centered computing Cytochromes c arsenic trioxide

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Expression and prognostic significance of osteopontin and caspase-3 in hepatocellular carcinoma patients after curative resection

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CANCER SCIENCE 2010年第5期101卷 1314-1319页

作者： Huang, Hua Zhang, Xiao-Fei Zhou, Hai-Jun Xue, Yu-Hua Dong, Qiong-Zhu Ye, Qing-Hai Qin, Lun-Xiu Fudan Univ Liver Canc Inst Shanghai 200433 Peoples R China Fudan Univ Zhongshan Hosp Shanghai 200433 Peoples R China Fudan Univ Inst Biomed Sci Shanghai 200433 Peoples R China

(Cancer Sci 2010;101: 1314-1319).

关键词： Caspase 3 rise level SPP1 gene human-centered computing CASP3 gene Recurrent Neoplasm

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