PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 22110230-3 2011 This study evaluates the usefulness of CEUS in the characterization of DN, early HCC and progressed HCC in cirrhotic livers. ceus 39-43 HCC Homo sapiens 100-103 22202426-2 2011 We analyzed patients who underwent multimodal treatment including surgical operation for advanced HCC after administration of sorafenib. Sorafenib 126-135 HCC Homo sapiens 98-101 21748762-4 2011 Interestingly, CypB protected tumor cells, even p53-defective HCC cells, against hypoxia- and cisplatin-induced apoptosis. Cisplatin 94-103 HCC Homo sapiens 62-65 21354447-1 2011 BACKGROUND & AIMS: The "Metroticket" prognostic model for survival post liver transplant for hepatocellular carcinoma (HCC) was developed from a European cohort of patients with predominantly alcoholic liver disease and hepatitis C-related HCC. Adenosine Monophosphate 12-15 HCC Homo sapiens 97-127 22171502-7 2011 It is well known that some patients with adenocarcinoma including HCC can develop respiratory failure owing to pulmonary tumor thrombotic microangiopathy (PTTM). pttm 155-159 HCC Homo sapiens 66-69 21801719-12 2011 Cyclin D1 and cyclin A are prognostic biomarkers associated with reduced OS in HCC. Osmium 73-75 HCC Homo sapiens 79-82 21880026-4 2011 Although, the epidemiologic evidence regarding the association of vitamin D and hepatocellular carcinoma (HCC) is still inconclusive, biochemical evidence clearly indicates that HCC cells are responsive to the inhibitory effect of vitamin D and its analogs. Vitamin D 66-75 HCC Homo sapiens 106-109 21880026-4 2011 Although, the epidemiologic evidence regarding the association of vitamin D and hepatocellular carcinoma (HCC) is still inconclusive, biochemical evidence clearly indicates that HCC cells are responsive to the inhibitory effect of vitamin D and its analogs. Vitamin D 231-240 HCC Homo sapiens 178-181 22322848-3 2011 Sorafenib, an oral multi-targeted tyrosine kinase inhibitor, was recently approved for the treatment of patients with HCC. Sorafenib 0-9 HCC Homo sapiens 118-121 22322848-5 2011 We present a case of transverse colon perforation during sorafenib therapy for advanced HCC. Sorafenib 57-66 HCC Homo sapiens 88-91 22322848-6 2011 A 68-year-old woman with advanced HCC was treated with sorafenib. Sorafenib 55-64 HCC Homo sapiens 34-37 21878637-7 2011 Intratumoral injection of cholesterol-conjugated miR-99a mimics significantly inhibited tumor growth and reduced the alpha-fetoprotein level in HCC-bearing nude mice. Cholesterol 26-37 HCC Homo sapiens 144-147 21769078-6 2011 The indications, technique and current results of radioembolization with yttrium-90 microspheres for the treatment of HCC are discussed in this review. Yttrium-90 73-83 HCC Homo sapiens 118-121 21627113-1 2011 Hydrogen-end-capped polyynes, H(C C)(n)H (n = 5-7), were photoirradiated in the presence of iodine molecules in nonpolar solvents to find a dramatic change in the UV/vis absorption spectrum. Hydrogen 0-8 HCC Homo sapiens 30-35 21627113-1 2011 Hydrogen-end-capped polyynes, H(C C)(n)H (n = 5-7), were photoirradiated in the presence of iodine molecules in nonpolar solvents to find a dramatic change in the UV/vis absorption spectrum. Polyynes 20-28 HCC Homo sapiens 30-35 21554201-2 2011 Epidemiological studies have identified major risk factors for HCC, including infection with hepatitis B and C virus (HBV and HCV), exposure to certain chemicals, high intake of alcohol, as well as metabolic diseases such as obesity and diabetes that are rapidly rising in the US. Alcohols 178-185 HCC Homo sapiens 63-66 21448954-5 2011 RESULTS: Mean RE(liver) (P = 0.013) and RE(HCC) (P < 0.001) were significantly higher on 1-h than on 3-h DPI, whereas CNR was significantly higher on 3-h than on 1-h DPI (P = 0.001). 3-aminodiphenyleneiodium 108-111 HCC Homo sapiens 40-47 21270118-3 2011 DESIGN: Retrospective analysis of HCC incidence in HBeAg-negative chronic hepatitis B patients from a retrospective-prospective cohort who were treated with nucleos(t)ide analogue(s) starting with lamivudine monotherapy for >=12 months. Lamivudine 197-207 HCC Homo sapiens 34-37 21350811-6 2011 A multi-kinase angiogenesis inhibitor, sorafenib, has been revealed as the first agent to show favorable overall survival in patients with advanced HCC. Sorafenib 39-48 HCC Homo sapiens 148-151 21351273-0 2010 Vitamin K enhancement of sorafenib-mediated HCC cell growth inhibition in vitro and in vivo. Vitamin K 0-9 HCC Homo sapiens 44-47 21633647-2 2011 Sorafenib has shown an overall survival benefit and has become the new standard of care for advanced HCC. Sorafenib 0-9 HCC Homo sapiens 101-104 21074623-6 2011 In the very recently published first monomeric structure of human cystatin C (hCC-stab1), dimerization was abrogated due to clasping of the beta-strands from the swapping domains by an engineered disulfide bridge. Disulfides 196-205 HCC Homo sapiens 78-81 20971570-4 2011 ANXA2 is a calcium-dependent phospholipid-binding protein that has been linked to malignant transformation and HCC development. Calcium 11-18 HCC Homo sapiens 111-114 21301005-9 2011 In conclusion, Sorafenib has demonstrated survival benefits in patients with advanced HCC, thus representing a new standard reference for systemic treatment in these cases. Sorafenib 15-24 HCC Homo sapiens 86-89 21829017-4 2011 Recently a multikinase inhibitor, sorafenib, has shown survival benefits in patients with advanced HCC. Sorafenib 34-43 HCC Homo sapiens 99-102 21829017-10 2011 Sorafenib, an oral multikinase inhibitor, has set a milestone in the management of HCC in that it is the first agent to significantly improve the overall survival in patients with advanced HCC in a double-blind, placebo-controlled, phase III study. Sorafenib 0-9 HCC Homo sapiens 83-86 21829017-10 2011 Sorafenib, an oral multikinase inhibitor, has set a milestone in the management of HCC in that it is the first agent to significantly improve the overall survival in patients with advanced HCC in a double-blind, placebo-controlled, phase III study. Sorafenib 0-9 HCC Homo sapiens 189-192 21829023-5 2011 Apparently the most studied systemic antiangiogenic agent for HCC is sorafenib. Sorafenib 69-78 HCC Homo sapiens 62-65 21829023-6 2011 An updated version of the aforementioned treatment algorithms recommends sorafenib therapy for advanced HCC patients with Child-Pugh A liver function and extrahepatic spread or major vascular invasion. Sorafenib 73-82 HCC Homo sapiens 104-107 21829023-7 2011 Moreover, sorafenib is recommended for use in HCC patients who are refractory or intolerant to transarterial chemoembolization (TACE) with well-preserved liver function (Child-Pugh A). Sorafenib 10-19 HCC Homo sapiens 46-49 21829023-11 2011 To further investigate the benefits of brivanib for advanced HCC, a broad-spectrum, global, phase III development plan, the Brivanib studies in HCC patients at RISK (BRISK) clinical program, has been initiated. brivanib 124-132 HCC Homo sapiens 144-147 21829023-12 2011 Clinical benefits seen with brivanib in the first-line setting, and following the failure of sorafenib therapy, highlight the potential to improve the clinical course of patients with advanced HCC, and this agent may provide a novel therapeutic option for the growing population of patients for whom no other treatment choice exists. brivanib 28-36 HCC Homo sapiens 193-196 22087137-3 2011 Emerging evidence indicates that there are other important lifestyle factors that contribute to the international burden of HCC, such as alcohol consumption, diabetes, obesity, and the intake of aflotoxin-contaminated food. aflotoxin 195-204 HCC Homo sapiens 124-127 22087137-10 2011 A diet rich that is in polyunsaturated fatty acids and, possibly, B-carotene could reduce the risk of HCC, and high dietary GL is associated with an increased risk independently of cirrhosis or diabetes. beta Carotene 66-76 HCC Homo sapiens 102-105 21548473-6 2011 The U.S. Food and Drug Administration (FDA) authorized use of sorafenib for "unresectable HCC", an indication which is very broad, vague, and confusing. Sorafenib 62-71 HCC Homo sapiens 90-94 21044630-14 2011 CONCLUSIONS: Patients with HCC treated by chemoembolization or radioembolization with Yttrium-90 microspheres had similar survival times. Yttrium-90 86-96 HCC Homo sapiens 27-30 21351273-1 2010 The multikinase inhibitor sorafenib is the first oral agent to show activity against human hepatocellular carcinoma (HCC). Sorafenib 26-35 HCC Homo sapiens 117-120 21351273-2 2010 Apoptosis has been shown to be induced in HCC by several agents, including sorafenib as well as by the naturally occurring K vitamins (VKs). Sorafenib 75-84 HCC Homo sapiens 42-45 21351273-3 2010 As few nontoxic agents have activity against HCC growth, we evaluated the activity of sorafenib and VKs, both independently and together on the growth of HCC cells in vitro and in vivo. Sorafenib 86-95 HCC Homo sapiens 154-157 21351273-5 2010 Conversely, VK enhanced sorafenib effects in several HCC cell lines on growth inhibition. Sorafenib 24-33 HCC Homo sapiens 53-56 21351273-9 2010 Sorafenib alone inhibited growth of transplantable HCC in vivo. Sorafenib 0-9 HCC Homo sapiens 51-54 21351273-11 2010 Thus, combination of VK1 plus sorafenib strongly induced growth inhibition and apoptosis in rodent and human HCC and inhibited the RAF/mitogen-activated protein kinase kinase/ERK pathway. Sorafenib 30-39 HCC Homo sapiens 109-112 21351273-14 2010 As both agents are available for human use, the combination has potential for improving sorafenib effects in HCC. Sorafenib 88-97 HCC Homo sapiens 109-112 21351273-0 2010 Vitamin K enhancement of sorafenib-mediated HCC cell growth inhibition in vitro and in vivo. Sorafenib 25-34 HCC Homo sapiens 44-47 20932754-1 2010 A series of novel furoxan-based nitric oxide (NO)-releasing derivatives of glycyrrhetinic acid (GA) were designed, synthesized, and evaluated for their in vitro cytotoxicity against human hepatocellular carcinoma (HCC) and non-tumor liver cells. Glycyrrhetinic Acid 75-94 HCC Homo sapiens 188-218 20625842-7 2010 RESULTS: GSEA revealed Ribosomal Proteins as a common regulatory pathway in B-type (P < .001) and C-type (P = .003) HCC recurrence. gsea 9-13 HCC Homo sapiens 119-122 20625842-8 2010 In addition, Proteasome (P < .001) and Pentose Phosphate Pathway (P = .01) were identified as specific pathways in each type of HCC recurrence, respectively. Pentosephosphates 42-59 HCC Homo sapiens 131-134 20238246-11 2010 AFP, bilirubin and age were found to be inter-related factors for HCC severity and survival. Bilirubin 5-14 HCC Homo sapiens 66-69 20443078-4 2010 We present a patient with HCC who underwent treatment with sorafenib, which resulted in a remarkable reduction in tumor burden to allow for liver transplant listing. Sorafenib 59-68 HCC Homo sapiens 26-29 20932754-2 2010 Five furoxan/GA hybrids, 7b-d, 7f, and 7g, displayed potent cytotoxicity against HCC cells (IC(50): 0.25-1.10 muM against BEL-7402 cells and 1.32-6.78 muM against HepG2 cells), but had a little effect on the growth of LO2 cells, indicating that these compounds had selective cytotoxicity against HCC cells. Glycyrrhetinic Acid 13-15 HCC Homo sapiens 296-299 20932754-4 2010 Apparently, the high concentrations of NO produced by NO donor moieties and the bioactivity of GA synergistically contribute to the cytotoxicity, but the NO is a major player against HCC cells in vitro. Glycyrrhetinic Acid 95-97 HCC Homo sapiens 183-186 21157578-5 2010 The current review article presents an evidence-based approach to the multidisciplinary management of HCC along with a new algorithm for the management of HCC that incorporates the BCLC staging system and the authors" local selection criteria for resection, ablative techniques, liver transplantation, transarterial chemoembolization, transarterial radioembolization and sorafenib in Alberta. Sorafenib 371-380 HCC Homo sapiens 155-158 20532728-5 2010 Our result demonstrated that common terms in both no-tumor hepatitis/cirrhotic liver tissues and HCC include secreted extracellular region, extracellular region part, extracellular space, signal peptide, signal, disulfide bond, glycosylation site N-linked (GlcNAc...), and glycoprotein, and these terms are less relative to invasion; therefore, we deduced the weaker AFP secreted network in HCC consistent with our number computation. n-linked 247-255 HCC Homo sapiens 97-100 20532728-5 2010 Our result demonstrated that common terms in both no-tumor hepatitis/cirrhotic liver tissues and HCC include secreted extracellular region, extracellular region part, extracellular space, signal peptide, signal, disulfide bond, glycosylation site N-linked (GlcNAc...), and glycoprotein, and these terms are less relative to invasion; therefore, we deduced the weaker AFP secreted network in HCC consistent with our number computation. 2-acetamido-2-deoxy-4-O-(beta-2-acetamid-2-deoxyglucopyranosyl)glucopyranose 257-263 HCC Homo sapiens 97-100 20739261-4 2010 Additional increase in HCC incidence is expected as a consequence of climate change, since risk of aflatoxin contamination in agricultural products increases with hot and dry growing conditions. Aflatoxins 99-108 HCC Homo sapiens 23-26 20956466-1 2010 UNLABELLED: This prospective study aimed to compare the diagnostic performance of (18)F-fluorocholine and (18)F-FDG for detecting and staging hepatocellular carcinoma (HCC) in patients with chronic liver disease and suspected liver nodules. fluorocholine 88-101 HCC Homo sapiens 168-171 20956466-12 2010 CONCLUSION: (18)F-fluorocholine was significantly more sensitive than (18)F-FDG at detecting HCC, in particular in well-differentiated forms. fluorocholine 18-31 HCC Homo sapiens 93-96 20956466-14 2010 Thus (18)F-fluorocholine appears to be a useful PET/CT tracer for the detection and surveillance of HCC; however, performing PET/CT with both radiopharmaceuticals seems to be the best option. fluorocholine 11-24 HCC Homo sapiens 100-103 20932754-1 2010 A series of novel furoxan-based nitric oxide (NO)-releasing derivatives of glycyrrhetinic acid (GA) were designed, synthesized, and evaluated for their in vitro cytotoxicity against human hepatocellular carcinoma (HCC) and non-tumor liver cells. Glycyrrhetinic Acid 96-98 HCC Homo sapiens 188-218 20932754-2 2010 Five furoxan/GA hybrids, 7b-d, 7f, and 7g, displayed potent cytotoxicity against HCC cells (IC(50): 0.25-1.10 muM against BEL-7402 cells and 1.32-6.78 muM against HepG2 cells), but had a little effect on the growth of LO2 cells, indicating that these compounds had selective cytotoxicity against HCC cells. 1,2,5-oxadiazole 2-oxide 5-12 HCC Homo sapiens 81-84 20932754-2 2010 Five furoxan/GA hybrids, 7b-d, 7f, and 7g, displayed potent cytotoxicity against HCC cells (IC(50): 0.25-1.10 muM against BEL-7402 cells and 1.32-6.78 muM against HepG2 cells), but had a little effect on the growth of LO2 cells, indicating that these compounds had selective cytotoxicity against HCC cells. 1,2,5-oxadiazole 2-oxide 5-12 HCC Homo sapiens 296-299 20932754-2 2010 Five furoxan/GA hybrids, 7b-d, 7f, and 7g, displayed potent cytotoxicity against HCC cells (IC(50): 0.25-1.10 muM against BEL-7402 cells and 1.32-6.78 muM against HepG2 cells), but had a little effect on the growth of LO2 cells, indicating that these compounds had selective cytotoxicity against HCC cells. Glycyrrhetinic Acid 13-15 HCC Homo sapiens 81-84 21161015-0 2010 Surgical treatment of HCC in a patient with lamivudine-resistant hepatitis B cirrhosis with adefovir dipivoxil. Lamivudine 44-54 HCC Homo sapiens 22-25 21161015-0 2010 Surgical treatment of HCC in a patient with lamivudine-resistant hepatitis B cirrhosis with adefovir dipivoxil. adefovir dipivoxil 92-110 HCC Homo sapiens 22-25 21161015-4 2010 Three years after the start of additional adefovir treatment, hepatocellular carcinoma (HCC) was detected and the patient underwent a successful hepatectomy. adefovir 42-50 HCC Homo sapiens 62-92 21161015-5 2010 Our findings suggest that the addition of adefovir to ongoing lamivudine therapy cannot completely suppress hepatocarcinogenesis, but is useful for improving liver function in patients with lamivudine-resistant HBV-related cirrhosis, allowing HCC surgery. adefovir 42-50 HCC Homo sapiens 243-246 20483498-1 2010 BACKGROUND & AIMS: Chronic hepatitis B patients are at increased risk for hepatocellular carcinoma (HCC). Adenosine Monophosphate 12-15 HCC Homo sapiens 104-107 20483498-5 2010 HCC was diagnosed in 2.8% and 6.4% of treated and untreated patients, respectively, during a 46 (32-108) month period (p=0.003), in 10.8% and 0.5% of nucleos(t)ide naive patients with and without cirrhosis (p<0.001) and in 17.6% and 0% of lamivudine resistance patients with and without cirrhosis (p<0.001). Lamivudine 242-252 HCC Homo sapiens 0-3 20591786-6 2010 It can be stated, that the antiviral therapy (interferon and nucleoside analogues) is able to decrease the risk of HCC or the recurrence of the tumor after curative treatment of HCC, in case of non responder state, as well. Nucleosides 61-71 HCC Homo sapiens 115-118 20591786-6 2010 It can be stated, that the antiviral therapy (interferon and nucleoside analogues) is able to decrease the risk of HCC or the recurrence of the tumor after curative treatment of HCC, in case of non responder state, as well. Nucleosides 61-71 HCC Homo sapiens 178-181 20570793-4 2010 However, the most important environmental risk factor for HCC is still the heavy long-term alcohol use. Alcohols 91-98 HCC Homo sapiens 58-61 20570793-7 2010 Since geographical distribution of aflatoxin as well as HBV overlaps with each other, they have a synergistic effect on inducing HCC. Aflatoxins 35-44 HCC Homo sapiens 129-132 20570793-13 2010 Dietary antioxidants, selenium, statins and coffee drinking have protective effect against HCC. Selenium 22-30 HCC Homo sapiens 91-94 20471129-1 2010 BACKGROUND & AIMS: To assess the risk for the development of hepatocellular carcinoma (HCC) according to the underlying liver status and on-treatment viral response during long-term lamivudine therapy in patients with hepatitis B virus-related liver disease. Adenosine Monophosphate 12-15 HCC Homo sapiens 91-94 20524812-1 2010 Hepatocellular carcinoma (HCC), following liver cirrhosis as a complication of chronic hepatitis B or C viruses (HBV or HCV)and iron overload, has been reported in thalassemia patients. Iron 128-132 HCC Homo sapiens 26-29 20524812-4 2010 Three (33.3%) TI patients with liver siderosis and fibrosis and late introduction of iron chelation developed HCC without a history of hepatitis. Iron 85-89 HCC Homo sapiens 110-113 20524812-6 2010 The main risk factor for HCC was HCV infection in TM patients but it was iron activity in TI patients. Iron 73-77 HCC Homo sapiens 25-28 20661702-1 2010 The purpose of this report was to describe pseudolesions of the liver that mimicked residual hypervascular hepatocellular carcinoma (HCC), as observed on gadoxetate disodium-enhanced magnetic resonance imaging (EOB-MRI) obtained shortly after transarterial chemoembolization (TACE). gadolinium ethoxybenzyl DTPA 154-173 HCC Homo sapiens 133-136 20661702-3 2010 In all three patients, nontumorous liver tissue adjacent to the treated HCC exhibited focal arterial enhancement on dynamic phase and subsequent diminished uptake of gadoxetate disodium on hepatocellular phase images, which mimicked residual HCC. gadolinium ethoxybenzyl DTPA 166-185 HCC Homo sapiens 72-75 20616600-2 2010 Sorafenib, an oral multikinase inhibitor, has set a milestone in the management of HCC in that it is the first agent to significantly improve the overall survival in patients with advanced HCC in a double-blind, placebo-controlled, phase III study. Sorafenib 0-9 HCC Homo sapiens 83-86 20616600-2 2010 Sorafenib, an oral multikinase inhibitor, has set a milestone in the management of HCC in that it is the first agent to significantly improve the overall survival in patients with advanced HCC in a double-blind, placebo-controlled, phase III study. Sorafenib 0-9 HCC Homo sapiens 189-192 20616600-4 2010 There is no doubt that sorafenib has a firm position at the core of HCC therapy, and its indications are anticipated to widen in the near future to intermediate HCC or as an adjuvant agent with or without combination modality. Sorafenib 23-32 HCC Homo sapiens 68-71 20227796-3 2010 The most important advance is possibly the demonstration that sorafenib, a multikinase inhibitor with antiproliferative and antiangiogenic properties, is an effective treatment, able to increase survival in patients with advanced-stage HCC. Sorafenib 62-71 HCC Homo sapiens 236-239 20471129-1 2010 BACKGROUND & AIMS: To assess the risk for the development of hepatocellular carcinoma (HCC) according to the underlying liver status and on-treatment viral response during long-term lamivudine therapy in patients with hepatitis B virus-related liver disease. Lamivudine 186-196 HCC Homo sapiens 91-94 20471129-8 2010 In patients without cirrhosis and with decompensated cirrhosis, the preventive effects of lamivudine on the development of HCC were not observed (p=0.446 and p=0.123, respectively). Lamivudine 90-100 HCC Homo sapiens 123-126 20471129-9 2010 CONCLUSION: Lamivudine therapy reduced the incidence of HCC in patients with compensated cirrhosis when the viral suppression was sustained. Lamivudine 12-22 HCC Homo sapiens 56-59 20037280-4 2009 Hepatitis B virus (HBV) is the most important risk factor, which represents approximately 70% of all HCC, and hepatitis C virus (HCV) and alcohol are the next in order of major risk factors for the development of HCC in Korea. Alcohols 138-145 HCC Homo sapiens 213-216 20388796-5 2010 In nude mice xenograft studies, a lentivirus expressing AEG-1 short hairpin RNA, in combination with doxorubicin, profoundly inhibited growth of aggressive human HCC cells compared with either agent alone. Doxorubicin 101-112 HCC Homo sapiens 162-165 20404792-7 2010 PEI offers favorable outcomes in small HCC but has increased recurrence and decreased long-term survival compared with RFA. pei 0-3 HCC Homo sapiens 39-42 20404795-5 2010 The multikinase inhibitor sorafenib has provided survival benefit in patients with advanced HCC and well-preserved liver function. Sorafenib 26-35 HCC Homo sapiens 92-95 19788684-0 2010 Development of HCC in patients receiving adefovir dipivoxil for lamivudine-resistant hepatitis B virus mutants. adefovir dipivoxil 41-59 HCC Homo sapiens 15-18 19788684-0 2010 Development of HCC in patients receiving adefovir dipivoxil for lamivudine-resistant hepatitis B virus mutants. Lamivudine 64-74 HCC Homo sapiens 15-18 19788684-1 2010 AIM: To identify factors for the development of hepatocellular carcinoma (HCC) in the patients who receive adefovir add-on lamivudine for treatment of lamivudine-resistant hepatitis B virus (HBV) mutants. adefovir 107-115 HCC Homo sapiens 74-77 19788684-1 2010 AIM: To identify factors for the development of hepatocellular carcinoma (HCC) in the patients who receive adefovir add-on lamivudine for treatment of lamivudine-resistant hepatitis B virus (HBV) mutants. Lamivudine 123-133 HCC Homo sapiens 74-77 19788684-1 2010 AIM: To identify factors for the development of hepatocellular carcinoma (HCC) in the patients who receive adefovir add-on lamivudine for treatment of lamivudine-resistant hepatitis B virus (HBV) mutants. Lamivudine 151-161 HCC Homo sapiens 74-77 21071991-3 2010 Currently, sorafenib is available for advanced HCC. Sorafenib 11-20 HCC Homo sapiens 47-50 21071991-5 2010 METHODS: We retrospectively looked at 54 patients who received sorafenib for advanced HCC. Sorafenib 63-72 HCC Homo sapiens 86-89 21071991-6 2010 Out of 54 patients, we analyzed 9 who received sorafenib after OLT for HCC reoccurrence at Cleveland Clinic. Sorafenib 47-56 HCC Homo sapiens 71-74 21071991-14 2010 CONCLUSION: Sorafenib can be used in patients with recurrent HCC after liver transplantation with tolerable toxicity; however, dose adjustment may be required. Sorafenib 12-21 HCC Homo sapiens 61-64 20679973-3 2010 One such therapy, a tyrosine kinase inhibitor (sorafenib) is now used to treat patients with advanced hepatocellular carcinoma (HCC) and metastatic renal cell carcinoma. Sorafenib 47-56 HCC Homo sapiens 128-131 20679973-4 2010 This article will explore the role of the oncology nurse in managing patients receiving sorafenib for advanced HCC. Sorafenib 88-97 HCC Homo sapiens 111-114 20679973-5 2010 A brief overview of sorafenib as a current treatment approved for advanced HCC in the palliative setting is presented. Sorafenib 20-29 HCC Homo sapiens 75-78 19788684-9 2010 HCC developed more frequently in the patients with than without cirrhosis at the start of adefovir (10/59 [16.9%] vs. 8/188 [4.3%], P = 0.002). adefovir 90-98 HCC Homo sapiens 0-3 19788684-10 2010 CONCLUSION: HCC can develop in cirrhotic patients receiving adefovir add-on lamivudine. adefovir 60-68 HCC Homo sapiens 12-15 19788684-10 2010 CONCLUSION: HCC can develop in cirrhotic patients receiving adefovir add-on lamivudine. Lamivudine 76-86 HCC Homo sapiens 12-15 20595072-11 2010 Sorafenib is the first medical treatment shown to be effective in the treatment of HCC. Sorafenib 0-9 HCC Homo sapiens 83-86 19577120-6 2009 A multikinase inhibitor, sorafenib, is the first molecular targeted oral therapy that has recently been shown to provide a survival benefit in HCC in select patients. Sorafenib 25-34 HCC Homo sapiens 143-146 19693687-3 2009 Consumption of aflatoxin contaminated foods is a recognised risk factor for human hepatocellular carcinoma (HCC) and may contribute to the high incidence of HCC in Southeast Asia. Aflatoxins 15-24 HCC Homo sapiens 82-112 19693687-3 2009 Consumption of aflatoxin contaminated foods is a recognised risk factor for human hepatocellular carcinoma (HCC) and may contribute to the high incidence of HCC in Southeast Asia. Aflatoxins 15-24 HCC Homo sapiens 108-111 19524575-1 2009 BACKGROUND & AIMS: Dietary exposure to aflatoxin B(1) (AFB(1)), in addition to other known factors, increases risk for human hepatocellular carcinoma (HCC). Aflatoxin B1 43-54 HCC Homo sapiens 129-159 19524575-1 2009 BACKGROUND & AIMS: Dietary exposure to aflatoxin B(1) (AFB(1)), in addition to other known factors, increases risk for human hepatocellular carcinoma (HCC). afb 59-62 HCC Homo sapiens 129-159 19524575-9 2009 CONCLUSIONS: In this model system, AFB(1)-induced DNA adduction and mutagenesis recapitulate the unique mutational features of TP53 in AFB(1)-associated human HCC. Aflatoxin B1 35-41 HCC Homo sapiens 159-162 19488072-8 2009 In 2007, the multitargeted kinase inhibitor, sorafenib, was found to prolong survival significantly for patients with advanced HCC. Sorafenib 45-54 HCC Homo sapiens 127-130 19026166-1 2008 AIM: To investigate the in vitro and in vivo activities and related mechanism of apogossypolone (ApoG2) alone or in combination with adriamycin (ADM) against human hepatocellular carcinoma (HCC). apogossypolone 81-95 HCC Homo sapiens 164-194 19507591-1 2009 OBJECTIVE: To investigate the value of in vivo proton magnetic resonance spectroscopy (1H MRS) in the assessment of hepatocellular carcinoma (HCC) and cholangiocarcinoma. Hydrogen 87-89 HCC Homo sapiens 142-145 19507591-2 2009 METHODS: 1H MRS was performed in normal volunteers and in patients with pathologically confirmed HCC and cholangiocarcinomas using a whole-body 1.5-T scanner. Hydrogen 9-11 HCC Homo sapiens 97-100 19507591-5 2009 The ratio of choline-to-lipid was significantly higher in HCC compared than those in cholangiocarcinomas or normal livers (P < 0.05). Choline 13-20 HCC Homo sapiens 58-61 19507591-7 2009 CONCLUSION: In vivo 1H MRS can reflect the pathological changes of HCC and cholangiocarcinomas at metabolic level and thus is useful in the diagnosis of these two cancers. Hydrogen 20-22 HCC Homo sapiens 67-70 19223512-3 2009 The objective of our study was to quantitatively assess N-glycans originating from serum glycoproteins as alternative markers for the detection of HCC. n-glycans 56-65 HCC Homo sapiens 147-150 19223512-6 2009 RESULTS: The abundance of 57 N-glycans was significantly altered in HCC patients compared with controls. n-glycans 29-38 HCC Homo sapiens 68-71 19223512-7 2009 The sensitivity of six individual glycans evaluated for separation of HCC cases from population controls ranged from 73% to 90%, and the specificity ranged from 36% to 91%. Polysaccharides 34-41 HCC Homo sapiens 70-73 19223512-8 2009 A combination of three selected N-glycans was sufficient to classify HCC with 90% sensitivity and 89% specificity in an independent validation set of patients with chronic liver disease. n-glycans 32-41 HCC Homo sapiens 69-72 19223512-9 2009 The three N-glycans remained associated with HCC after adjustment for chronic viral infection and other known covariates, whereas the other glycans increased significantly at earlier stages of the progression of chronic viral infection to HCC. n-glycans 10-19 HCC Homo sapiens 45-48 19223512-9 2009 The three N-glycans remained associated with HCC after adjustment for chronic viral infection and other known covariates, whereas the other glycans increased significantly at earlier stages of the progression of chronic viral infection to HCC. Polysaccharides 12-19 HCC Homo sapiens 45-48 19223512-10 2009 CONCLUSION: A set of three identified N-glycans is sufficient for the detection of HCC with 90% prediction accuracy in a population with high rates of hepatitis C viral infection. n-glycans 38-47 HCC Homo sapiens 83-86 19195059-10 2009 Compared to other causes of liver cirrhosis such as chronic viral hepatitis, alcohol, or hemochromatosis, the incidence of HCC is significantly lower. Alcohols 77-84 HCC Homo sapiens 123-126 19140229-1 2009 AIM: To search for transcription dysregulation that could (1) differentiate hepatocellular carcinoma (HCC)-free from HCC-related cirrhosis (2) differentiate HCC-free cirrhosis related to HCV from that related to alcohol intake. Alcohols 212-219 HCC Homo sapiens 102-105 19094780-14 2008 CONCLUSION: LH is a safe and feasible method for the treatment of HCC. Luteinizing Hormone 12-14 HCC Homo sapiens 66-69 18986218-1 2008 INTRODUCTION: We conducted a molecular imaging and gene therapy method in alpha-fetoprotein (AFP)-producing hepatocellular carcinoma (HCC) by tumor-specific expression of the human sodium/iodide symporter (hNIS) using an AFP promoter. Sodium 181-187 HCC Homo sapiens 134-137 19030192-6 2008 Recently, encouraging results have been shown in using sorafenib in the treatment of advanced HCC patients. Sorafenib 55-64 HCC Homo sapiens 94-97 18986218-1 2008 INTRODUCTION: We conducted a molecular imaging and gene therapy method in alpha-fetoprotein (AFP)-producing hepatocellular carcinoma (HCC) by tumor-specific expression of the human sodium/iodide symporter (hNIS) using an AFP promoter. Iodides 188-194 HCC Homo sapiens 134-137 17938995-1 2008 PURPOSE: To examine the results of segmental transcatheter arterial chemoembolization with doxorubicin-loaded DC Bead in the treatment of hepatocellular carcinoma (HCC) in non-surgical candidates. Doxorubicin 91-102 HCC Homo sapiens 164-167 18391920-3 2008 However a survival advantage was recently established for sorafenib, instituting a new standard of care for unresectable HCC. Sorafenib 58-67 HCC Homo sapiens 121-124 18854000-8 2008 Furthermore, the cumulative incidence rate of HCC in 39 patients with high 8-OHdG expression levels was significantly greater than that in 65 patients with low 8-OHdG expression levels (P = 0.043). 8-ohdg 75-81 HCC Homo sapiens 46-49 18854000-8 2008 Furthermore, the cumulative incidence rate of HCC in 39 patients with high 8-OHdG expression levels was significantly greater than that in 65 patients with low 8-OHdG expression levels (P = 0.043). 8-ohdg 160-166 HCC Homo sapiens 46-49 18854000-10 2008 CONCLUSIONS: 8-OHdG is a risk factor for the development of HCC in patients with chronic HCV infection. 8-ohdg 13-19 HCC Homo sapiens 60-63 18854000-11 2008 Patients with chronic HCV who express 8-OHdG should be monitored carefully for the development of HCC. 8-ohdg 38-44 HCC Homo sapiens 98-101 19080480-15 2008 CONCLUSION: Endostatin gene therapy synergizes with doxorubicin to suppress HCC. Doxorubicin 52-63 HCC Homo sapiens 76-79 18471552-3 2008 However, the rising incidence of HCC in several regions around the world coupled with emerging evidence for efficacy of screening in high-risk patients, liver transplantation as a curative option in select patients, ability to make definitive diagnosis using high-resolution imaging of the liver, less dependency on obtaining tissue diagnosis, and proven efficacy of transarterial chemoembolization and sorafenib as palliative therapy have improved the outlook for HCC patients. Sorafenib 403-412 HCC Homo sapiens 33-36 18854000-3 2008 The aim of this study was to determine whether expression of 8-OHdG is a risk factor for the development of hepatocellular carcinoma (HCC) in patients with hepatitis C virus (HCV) infection. 8-ohdg 61-67 HCC Homo sapiens 134-137 18854000-7 2008 RESULTS: On multivariate analysis, 8-OHdG and fibrosis were independent and significant risk factors for HCC development (relative risk, 2.48; P = 0.023; relative risk, 5.35; P = 0.001, respectively). 8-ohdg 35-41 HCC Homo sapiens 105-108 18695135-7 2008 A Cox proportional hazards model was used to estimate the risk of HCC associated with HBV genotype and precore and BCP mutants after adjustment for other risk factors. bcp 115-118 HCC Homo sapiens 66-69 18695135-12 2008 The multivariable-adjusted hazard ratio of developing HCC was 1.76 (95% CI = 1.19 to 2.61) for genotype C vs genotype B, 0.34 (95% CI = 0.21 to 0.57) for precore G1896A vs wild type, and 1.73 (95% CI = 1.13 to 2.67) for BCP A1762T/G1764A vs wild type. bcp 220-223 HCC Homo sapiens 54-57 18486261-2 2008 We aimed to assess safety and efficacy of doxorubicin-eluting bead (DEB)-enhanced RF ablation in the treatment of human hepatocellular carcinoma (HCC). Doxorubicin 42-53 HCC Homo sapiens 120-150 18632827-1 2008 UNLABELLED: The purpose of this study was to retrospectively investigate the feasibility of 11C-choline PET, compared with 18F-FDG PET, for the detection of hepatocellular carcinoma (HCC). methyl carbon-11 choline 92-103 HCC Homo sapiens 183-186 18632827-2 2008 METHODS: A total of 16 HCC lesions in 12 patients were examined with both 11C-choline PET and 18F-FDG PET. methyl carbon-11 choline 74-85 HCC Homo sapiens 23-26 18632827-5 2008 RESULTS: 11C-choline PET showed a slightly higher detection rate than did 18F-FDG PET for detection of HCC (63% vs. 50%, respectively), although this difference was not statistically significant. methyl carbon-11 choline 9-20 HCC Homo sapiens 103-106 18632827-6 2008 11C-choline PET had a better detection rate for moderately differentiated HCC lesions but not for those poorly differentiated (75% vs. 25%, respectively). methyl carbon-11 choline 0-11 HCC Homo sapiens 74-77 18632827-8 2008 The mean 11C-choline SUV and T/L ratio in moderately differentiated HCC lesions were higher than those in poorly differentiated HCC lesions. methyl carbon-11 choline 9-20 HCC Homo sapiens 68-71 18632827-11 2008 CONCLUSION: 11C-choline PET had a better detection rate for moderately differentiated HCC lesions but not for poorly differentiated HCC lesions, whereas 18F-FDG PET produced the opposite result. methyl carbon-11 choline 12-23 HCC Homo sapiens 86-89 18632827-12 2008 11C-choline is a potential tracer to complement 18F-FDG in detection of HCC lesions. methyl carbon-11 choline 0-11 HCC Homo sapiens 72-75 18313840-4 2008 The DNA concentrations were significantly higher in HCC patients compared to HBV and HCV carriers without cancer, and to sero-negative individuals. sero 121-125 HCC Homo sapiens 52-55 18313840-8 2008 In parallel, studies on DNA extracted from 20 HCC biopsies showed the presence of ser-249 mutation in two cases (10%). Serine 82-85 HCC Homo sapiens 46-49 18319685-2 2008 The major risk factor associated with the development of hepatocellular carcinoma (HCC) is cirrhosis caused by hepatitis B, hepatitis C virus or chronic alcohol consumption. Alcohols 153-160 HCC Homo sapiens 83-86 18319685-4 2008 When HCC is diagnosed at early stages, prognosis is better with five-year disease free survival of around 50% with resection, or local ablative treatments such as radio-frequency ablation or percutaneous ethanol injection, and 70-80% with liver transplantation. Ethanol 204-211 HCC Homo sapiens 5-8 17249202-8 2006 In spectra, the choline compound peak of HCC elevated compared with uninvolved liver parenchyma. Choline 16-23 HCC Homo sapiens 41-44 19092267-7 2008 Recent clinical data have shown that interferon and lamivudine treatment is effective in preventing the occurrence of HCC attributed to HCV and HBV infection, respectively, and that an aggressive vaccination program against the latter reduces the incidence of HCC. Lamivudine 52-62 HCC Homo sapiens 118-121 17914972-1 2007 AIM: The aim of this study was to determine whether antiviral therapy with lamivudine is beneficial in patients after initial treatment for hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Lamivudine 75-85 HCC Homo sapiens 198-201 17914972-3 2007 Comparison was made between 16 patients who received lamivudine therapy at a dose of 100 mg/day after treatment for HCC (lamivudine group) and 33 patients who did not (control group) in terms of changes in remnant liver function, HCC recurrence and survival. Lamivudine 53-63 HCC Homo sapiens 116-119 17914972-6 2007 All patients in the lamivudine group were able to receive curative treatment for recurrent HCC. Lamivudine 20-30 HCC Homo sapiens 91-94 17914972-9 2007 CONCLUSION: It is suggested that lamivudine therapy is beneficial for patients after initial treatment for HBV-related HCC because it contributes to improving remnant liver function, thus decreasing the risk of liver failure and increasing the chances of receiving available treatment modalities for recurrent HCC. Lamivudine 33-43 HCC Homo sapiens 119-122 17914972-9 2007 CONCLUSION: It is suggested that lamivudine therapy is beneficial for patients after initial treatment for HBV-related HCC because it contributes to improving remnant liver function, thus decreasing the risk of liver failure and increasing the chances of receiving available treatment modalities for recurrent HCC. Lamivudine 33-43 HCC Homo sapiens 310-313 18417044-9 2008 A new oral agent, sorafenib, was recently shown to prolong survival in patients with advanced HCC. Sorafenib 18-27 HCC Homo sapiens 94-97 17510798-1 2008 The aim of this work was to study the benefit of supplementation with a branched chain amino acids enriched nutrient mixture on the physical and mental condition following hepatic surgery in patients with hepatocellular carcinoma (HCC). Amino Acids, Branched-Chain 72-98 HCC Homo sapiens 231-234 17510798-7 2008 This preliminary case control study suggested that the perioperative supplementation of a branched chain amino acids enriched nutrient mixture is of clinical benefit for nutritional support of patients surgically managed for HCC in chronic liver disease. Amino Acids, Branched-Chain 90-116 HCC Homo sapiens 225-228 18188819-11 2008 Due to its antiproliferative effects, the immunosuppressive drug sirolimus may play a role for secondary prevention of HCC following transplantation. Sirolimus 65-74 HCC Homo sapiens 119-122 20485632-1 2007 BACKGROUND/AIMS: This study evaluated the prevention by lamivudine of hepatocellular carcinoma (HCC) in chronic hepatitis B patients. Lamivudine 56-66 HCC Homo sapiens 96-99 20485632-3 2007 A Cox regression model revealed that four factors increased the prevalence of HCC: gender (females; OR=0.53, p=0.006), age (>/=40 years; OR=4.64, p<0.001), platelet count (>/=100x10(3)/mm(3); OR=0.35, p<0.001), and alcohol consumption (>/=80 g/day; OR=1.79, p=0.004). Alcohols 227-234 HCC Homo sapiens 78-81 20485632-6 2007 RESULTS: HCC occurred in 10 patients (1.7%) of the lamivudine group, with an incidence rate of 0.61% patients/year, and in 65 patients (11.0%) of the control group, with an incidence rate of 2.16% patients/year. Lamivudine 51-61 HCC Homo sapiens 9-12 20485632-7 2007 The cumulative incidence of HCC was lower in the lamivudine group than in the control group (p=0.0117, log-rank test). Lamivudine 49-59 HCC Homo sapiens 28-31 20485632-8 2007 CONCLUSIONS: Lamivudine can reduce the incidence of HCC in patients suffering from chronic hepatitis B. Lamivudine 13-23 HCC Homo sapiens 52-55 16712928-5 2007 The functionality of transporters expressed in hCC was confirmed by their ability to take up and export estradiol 17beta-d-glucuronide in a self-inhibitable and temperature-sensitive manner. estradiol-17 beta-glucuronide 104-134 HCC Homo sapiens 47-50 17249202-11 2006 1H MRS can monitor the early stage metabolic changes of HCC after TACE but limitation like quantification still exists. Hydrogen 0-2 HCC Homo sapiens 56-59 17197759-2 2006 We report a case of HCC with liver cirrhosis and lung metastases who had been treated successfully by combination chemotherapy of 5-fluorouracil (5-FU) and interferon-alpha (IFN-alpha). Fluorouracil 130-144 HCC Homo sapiens 20-23 17197759-7 2006 Although systemic combination chemotherapy of 5-FU and IFN-alpha induced the bone marrow suppression, it was effective for lung metastases and palliates symptoms and signs in our case of HCC. Fluorouracil 46-50 HCC Homo sapiens 187-190 17125609-2 2006 METHODS: The total RNAs of matched HCC, PCT and NLT of HCC patients were isolated using one step Trizol method. trizol 97-103 HCC Homo sapiens 55-58 16967451-5 2006 METHODS: The effect of the administration of colchicine on the development of HCC was evaluated in 186 patients with hepatitis virus-related liver cirrhosis in a retrospective cohort study. Colchicine 45-55 HCC Homo sapiens 78-81 16967451-9 2006 RESULTS: The percentage of patients who developed HCC was significantly smaller in the colchicine group when compared with the noncolchicine group (9% vs. 29%; P = .001). Colchicine 87-97 HCC Homo sapiens 50-53 16967451-11 2006 The average time for the development of HCC was 222 months +/- 15 months and 150 months +/- 12 months in the patients who received and who did not receive colchicine, respectively. Colchicine 155-165 HCC Homo sapiens 40-43 16967451-12 2006 CONCLUSIONS: The results suggest that treatment with colchicine prevents and delays the development of HCC in patients with hepatitis virus-related cirrhosis. Colchicine 53-63 HCC Homo sapiens 103-106 16967451-13 2006 The protective mechanisms of colchicine over the development of HCC could be related to antiinflammatory properties and inhibition of mitosis. Colchicine 29-39 HCC Homo sapiens 64-67 17006925-2 2006 This randomized controlled trial evaluated whether postoperative adjuvant therapy with oral uracil-tegafur (UFT) prevents recurrence of HCC. Tegafur-Uracil 92-106 HCC Homo sapiens 136-139 17006925-2 2006 This randomized controlled trial evaluated whether postoperative adjuvant therapy with oral uracil-tegafur (UFT) prevents recurrence of HCC. Tegafur 108-111 HCC Homo sapiens 136-139 16901768-1 2006 BACKGROUND & AIMS: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. Adenosine Monophosphate 12-15 HCC Homo sapiens 49-52 17197759-2 2006 We report a case of HCC with liver cirrhosis and lung metastases who had been treated successfully by combination chemotherapy of 5-fluorouracil (5-FU) and interferon-alpha (IFN-alpha). Fluorouracil 146-150 HCC Homo sapiens 20-23 21614248-13 2006 Rhenium-188 lipiodol is a new radioconjugate, and using it we treated 70 patients with inoperable HCC. rhenium-188 lipiodol 0-20 HCC Homo sapiens 98-101 16898008-1 2006 We have reported a remarkably high anti-tumor efficacy using intra arterial 5-FU infusion chemotherapy combined with subcutaneous interferon-alpha injection to treat advanced hepatocellular carcinoma (HCC) with portal vein thrombus. Fluorouracil 76-80 HCC Homo sapiens 201-204 15886943-9 2005 TAE with the use of microspheres and Lipiodol and cyanoacrylate for unresectable HCC is a feasible treatment modality. tae 0-3 HCC Homo sapiens 81-84 16457596-5 2006 We show here that increased levels of core fucosylation can be observed via glycan analysis of total serum and are associated with the development of HCC. Polysaccharides 76-82 HCC Homo sapiens 150-153 16396674-8 2006 CONCLUSION: Combination chemotherapy with doxorubicin, cisplatin and capecitabine produced modest antitumor activity with tolerable adverse effects in patients with metastatic HCC. Doxorubicin 42-53 HCC Homo sapiens 176-179 16396674-8 2006 CONCLUSION: Combination chemotherapy with doxorubicin, cisplatin and capecitabine produced modest antitumor activity with tolerable adverse effects in patients with metastatic HCC. Cisplatin 55-64 HCC Homo sapiens 176-179 16396674-8 2006 CONCLUSION: Combination chemotherapy with doxorubicin, cisplatin and capecitabine produced modest antitumor activity with tolerable adverse effects in patients with metastatic HCC. Capecitabine 69-81 HCC Homo sapiens 176-179 16032439-1 2005 Several techniques have been developed for radionuclide therapy of hepatocellular carcinoma (HCC). Radioisotopes 43-55 HCC Homo sapiens 93-96 16032439-5 2005 The additive value of a single 131I-Lipiodol administration following partial liver resection for HCC was evaluated and evidence is available that adjuvant radionuclide treatment reduces the recurrence rate. 131i-lipiodol 31-44 HCC Homo sapiens 98-101 16032439-10 2005 The use of radiolabelled Lipiodol and microspheres allows for selective targeting of HCC with limited toxicity. Ethiodized Oil 25-33 HCC Homo sapiens 85-88 16329776-2 2005 Aim of this study is to report an initial series of patients affected by HCC treated by hepatic resection utilizing a new water-cooled, high-density, monopolar device, the Tissuelink Monopolar Floating Ball (Tissuelink Medical Inc., Dover, NH, U.S.A.), in order to avoid bleeding during hepatic surgery. Water 122-127 HCC Homo sapiens 73-76 16286955-2 2005 However, the outcomes in patients with hepatocellular carcinoma (HCC) treated with lamivudine have not been established. Lamivudine 83-93 HCC Homo sapiens 65-68 16286955-3 2005 This study was conducted to evaluate the outcomes of lamivudine treatment for patients with HCC using an untreated, matched control group. Lamivudine 53-63 HCC Homo sapiens 92-95 16286955-10 2005 A significant improvement in liver function was achieved by lamivudine treatment, even in patients with HCC. Lamivudine 60-70 HCC Homo sapiens 104-107 16286955-11 2005 These results suggest that lamivudine treatment for patients with HCC may prevent death due to liver failure. Lamivudine 27-37 HCC Homo sapiens 66-69 16108176-16 2005 Interferon and lamivudine therapy have demonstrated reduction of HCC among responders. Lamivudine 15-25 HCC Homo sapiens 65-68 15983686-9 2005 Of the 2 patients with a history of heavy alcohol intake, one had concomitant chronic viral hepatitis infection, and alcohol alone was the etiology of HCC in only one case (1.40%). Alcohols 117-124 HCC Homo sapiens 151-154 15886943-9 2005 TAE with the use of microspheres and Lipiodol and cyanoacrylate for unresectable HCC is a feasible treatment modality. Ethiodized Oil 37-45 HCC Homo sapiens 81-84 15886943-9 2005 TAE with the use of microspheres and Lipiodol and cyanoacrylate for unresectable HCC is a feasible treatment modality. Cyanoacrylates 50-63 HCC Homo sapiens 81-84 15455319-18 2004 Thus, IOUS remains a mandatory tool in patients treated by locoregional surgical modalities such as resection, cryotherapy, and intraoperative ethanol instillation for HCC even after refinement of radiological technologies. Ethanol 143-150 HCC Homo sapiens 168-171 15871304-7 2005 All liver lesions (altered foci, adenomata, HCC) occurred significantly less frequently in the tamoxifen-treated group than the group given only ethylnitrosourea (HCC developed in 2 of 47 (4%) vs 11 of 44 (25%); P < .001). Tamoxifen 95-104 HCC Homo sapiens 44-47 15871304-7 2005 All liver lesions (altered foci, adenomata, HCC) occurred significantly less frequently in the tamoxifen-treated group than the group given only ethylnitrosourea (HCC developed in 2 of 47 (4%) vs 11 of 44 (25%); P < .001). Tamoxifen 95-104 HCC Homo sapiens 163-166 15871304-7 2005 All liver lesions (altered foci, adenomata, HCC) occurred significantly less frequently in the tamoxifen-treated group than the group given only ethylnitrosourea (HCC developed in 2 of 47 (4%) vs 11 of 44 (25%); P < .001). Ethylnitrosourea 145-161 HCC Homo sapiens 163-166 15871304-9 2005 Tamoxifen significantly decreased the incidence of chemical hepatocarcinogenesis in this model, suggesting an important role for estrogens in the pathogenesis of HCC and suggesting that it should be tested in human beings as a chemopreventive agent against HCC. Tamoxifen 0-9 HCC Homo sapiens 162-165 15871304-9 2005 Tamoxifen significantly decreased the incidence of chemical hepatocarcinogenesis in this model, suggesting an important role for estrogens in the pathogenesis of HCC and suggesting that it should be tested in human beings as a chemopreventive agent against HCC. Tamoxifen 0-9 HCC Homo sapiens 257-260 15827527-1 2005 PURPOSE: To evaluate the feasibility of enhanced sonography using arterial injection of pure carbon dioxide gas (CO(2)) for detecting small hepatocellular carcinoma (HCC) nodules. Carbon Dioxide 93-107 HCC Homo sapiens 166-169 15827527-1 2005 PURPOSE: To evaluate the feasibility of enhanced sonography using arterial injection of pure carbon dioxide gas (CO(2)) for detecting small hepatocellular carcinoma (HCC) nodules. Carbon Dioxide 113-118 HCC Homo sapiens 166-169 15827527-9 2005 CONCLUSION: Enhanced sonography of arterial injection of pure CO(2) is a feasible technique for detecting small HCC nodules. Carbon Dioxide 62-67 HCC Homo sapiens 112-115 15339156-2 2004 Measurements of ET rates from photoexcited CcP substituted with Zn porphyrin to either yeast Fe(III)Cc or horse Fe(III)Cc in crystals reveal that the molecular associations found in the respective crystal structures determine solution reactivity. zn porphyrin 64-76 HCC Homo sapiens 43-45 15339156-2 2004 Measurements of ET rates from photoexcited CcP substituted with Zn porphyrin to either yeast Fe(III)Cc or horse Fe(III)Cc in crystals reveal that the molecular associations found in the respective crystal structures determine solution reactivity. zn porphyrin 64-76 HCC Homo sapiens 100-102 15339156-2 2004 Measurements of ET rates from photoexcited CcP substituted with Zn porphyrin to either yeast Fe(III)Cc or horse Fe(III)Cc in crystals reveal that the molecular associations found in the respective crystal structures determine solution reactivity. ferric sulfate 93-100 HCC Homo sapiens 43-45 15339156-2 2004 Measurements of ET rates from photoexcited CcP substituted with Zn porphyrin to either yeast Fe(III)Cc or horse Fe(III)Cc in crystals reveal that the molecular associations found in the respective crystal structures determine solution reactivity. ferric sulfate 112-119 HCC Homo sapiens 43-45 15261064-7 2004 It suggested that HCC would be synchronized preferably in G1 and S phase with thymine-2-deoxyriboside and colchicines, the adhesive molecule integrin beta1 expressed in a high lever in HCC and presented differences in vary cell cycle, and integrin beta1 played an important roles in adhesion of HCC to HUVEC. Thymidine 78-101 HCC Homo sapiens 18-21 15261064-7 2004 It suggested that HCC would be synchronized preferably in G1 and S phase with thymine-2-deoxyriboside and colchicines, the adhesive molecule integrin beta1 expressed in a high lever in HCC and presented differences in vary cell cycle, and integrin beta1 played an important roles in adhesion of HCC to HUVEC. Colchicine 106-117 HCC Homo sapiens 18-21 15261064-7 2004 It suggested that HCC would be synchronized preferably in G1 and S phase with thymine-2-deoxyriboside and colchicines, the adhesive molecule integrin beta1 expressed in a high lever in HCC and presented differences in vary cell cycle, and integrin beta1 played an important roles in adhesion of HCC to HUVEC. Colchicine 106-117 HCC Homo sapiens 185-188 15261064-7 2004 It suggested that HCC would be synchronized preferably in G1 and S phase with thymine-2-deoxyriboside and colchicines, the adhesive molecule integrin beta1 expressed in a high lever in HCC and presented differences in vary cell cycle, and integrin beta1 played an important roles in adhesion of HCC to HUVEC. Colchicine 106-117 HCC Homo sapiens 185-188 15756142-3 2005 Most HCC develops in cirrhosis caused by known and preventable risk factors (hepatitis B virus, HBV, hepatitis C virus, HCV, alcohol and possibly non-alcoholic steatohepatitis, NASH). Alcohols 125-132 HCC Homo sapiens 5-8 15508108-1 2004 More than 18 million adults in the United States abuse alcohol, a prevalence 5 times higher than that of hepatitis C. Chronic alcohol use of greater than 80 g/day for more than 10 years increases the risk for hepatocellular carcinoma (HCC) approximately 5-fold; alcohol use of less than 80 g/day is associated with a nonsignificant increased risk for HCC. Alcohols 55-62 HCC Homo sapiens 235-238 15508108-1 2004 More than 18 million adults in the United States abuse alcohol, a prevalence 5 times higher than that of hepatitis C. Chronic alcohol use of greater than 80 g/day for more than 10 years increases the risk for hepatocellular carcinoma (HCC) approximately 5-fold; alcohol use of less than 80 g/day is associated with a nonsignificant increased risk for HCC. Alcohols 55-62 HCC Homo sapiens 351-354 15508108-1 2004 More than 18 million adults in the United States abuse alcohol, a prevalence 5 times higher than that of hepatitis C. Chronic alcohol use of greater than 80 g/day for more than 10 years increases the risk for hepatocellular carcinoma (HCC) approximately 5-fold; alcohol use of less than 80 g/day is associated with a nonsignificant increased risk for HCC. Alcohols 126-133 HCC Homo sapiens 235-238 15508108-1 2004 More than 18 million adults in the United States abuse alcohol, a prevalence 5 times higher than that of hepatitis C. Chronic alcohol use of greater than 80 g/day for more than 10 years increases the risk for hepatocellular carcinoma (HCC) approximately 5-fold; alcohol use of less than 80 g/day is associated with a nonsignificant increased risk for HCC. Alcohols 126-133 HCC Homo sapiens 351-354 15508108-2 2004 The risk for HCC in decompensated alcohol induced cirrhosis approaches 1% per year. Alcohols 34-41 HCC Homo sapiens 13-16 15508108-4 2004 Alcohol use in chronic hepatitis C doubles the risk for HCC as compared with the risk in hepatitis C alone. Alcohols 0-7 HCC Homo sapiens 56-59 15508108-5 2004 Furthermore, there may be synergism between alcohol and hepatitis C in the development of HCC, and in these patients HCC may occur at an earlier age and the HCC may be histologically more advanced. Alcohols 44-51 HCC Homo sapiens 90-93 15508108-5 2004 Furthermore, there may be synergism between alcohol and hepatitis C in the development of HCC, and in these patients HCC may occur at an earlier age and the HCC may be histologically more advanced. Alcohols 44-51 HCC Homo sapiens 117-120 15508108-5 2004 Furthermore, there may be synergism between alcohol and hepatitis C in the development of HCC, and in these patients HCC may occur at an earlier age and the HCC may be histologically more advanced. Alcohols 44-51 HCC Homo sapiens 117-120 15508108-6 2004 Studies in the United States and Italy suggest that alcohol is the most common cause of HCC (accounting for 32%-45% of HCC). Alcohols 52-59 HCC Homo sapiens 88-91 15508108-6 2004 Studies in the United States and Italy suggest that alcohol is the most common cause of HCC (accounting for 32%-45% of HCC). Alcohols 52-59 HCC Homo sapiens 119-122 15508108-7 2004 The mechanisms by which alcohol causes HCC are incompletely understood, but may include chromosomal loss, oxidative stress, a decreased retinoic acid level in the liver, altered DNA methylation, and genetic susceptibility. Alcohols 24-31 HCC Homo sapiens 39-42 15508108-7 2004 The mechanisms by which alcohol causes HCC are incompletely understood, but may include chromosomal loss, oxidative stress, a decreased retinoic acid level in the liver, altered DNA methylation, and genetic susceptibility. Tretinoin 136-149 HCC Homo sapiens 39-42 15508108-8 2004 Alcohol use is increasing in many countries, suggesting that alcohol will continue to be a common cause of HCC throughout the world. Alcohols 0-7 HCC Homo sapiens 107-110 15508108-8 2004 Alcohol use is increasing in many countries, suggesting that alcohol will continue to be a common cause of HCC throughout the world. Alcohols 61-68 HCC Homo sapiens 107-110 15498315-2 2004 METHODS: 21 HCC cases received orthotopic liver transplantation and treated with adjuvant individualized chemotherapy based on ATP tumor chemosensitivity assay (ex vivo) between April 2001 and January 2003 were retrospective reviewed, compared with 52 cases received orthotopic liver transplantation only. Adenosine Triphosphate 127-130 HCC Homo sapiens 12-15 15498315-7 2004 The individualized protocol based on ATP-TCA may be effective for patients with HCC after liver transplantation. atp-tca 37-44 HCC Homo sapiens 80-83 16210821-5 2003 The iron-overloaded liver provided a natural source of paramagnetic contrast for detection of HCC. Iron 4-8 HCC Homo sapiens 94-97 14598418-2 2003 METHODS: The efficacy of, and tolerance to, preoperative intra-arterial injection of (131)I-labelled lipiodol was examined in 34 patients with HCC, including 29 with cirrhosis. Ethiodized Oil 101-109 HCC Homo sapiens 143-146 14571807-0 2003 A case of hepatocellular carcinoma (HCC): treatment with local application of alcohol and interleukin 2 (IL-2). Alcohols 78-85 HCC Homo sapiens 10-40 12506476-0 2002 [Modified pharmacokinetic modulation chemotherapy (PMC) with medication of UFT and intraarterial infusion of 5-FU for advanced unresectable HCC]. Fluorouracil 109-113 HCC Homo sapiens 140-143 12557138-1 2003 BACKGROUND & AIMS: Hepatitis B viral (HBV) genotype C is associated with the development of hepatocellular carcinoma (HCC) compared with genotype B; however, the virologic factors contributing to the pathogenic differences remain unknown. Adenosine Monophosphate 12-15 HCC Homo sapiens 122-125 12138235-8 2002 CONCLUSIONS: Intra-arterial chemotherapy using cisplatin and etoposide seems to have some anti-tumor effect against advanced HCC, although a high rate of life- threatening complications precludes the indication of this regimen at least for patients with non-compensated cirrhosis. Cisplatin 47-56 HCC Homo sapiens 125-128 12161001-3 2002 In addition, elevated levels of serum testosterone (T) and increased T to Estradiol (E(2)) ratio have been reported to predict an increased risk of HCC for male cirrhotic patients. Testosterone 38-50 HCC Homo sapiens 148-151 12161001-3 2002 In addition, elevated levels of serum testosterone (T) and increased T to Estradiol (E(2)) ratio have been reported to predict an increased risk of HCC for male cirrhotic patients. Estradiol 74-83 HCC Homo sapiens 148-151 12537564-6 2002 CGMA was applied to HCC gene-expression profiles to identify regions of frequent cytogenetic change and to identify genes whose expression is misregulated within these regions. cgma 0-4 HCC Homo sapiens 20-23 12537564-8 2002 CGMA identified 13 regions of frequent cytogenetic change in the HCC samples. cgma 0-4 HCC Homo sapiens 65-68 12534775-6 2002 However, measures to reduce the high levels of aflatoxin exposure, where chronic HBV infection is currently epidemic, would also significantly contribute to reducing HCC incidence. Aflatoxins 47-56 HCC Homo sapiens 166-169 12138235-8 2002 CONCLUSIONS: Intra-arterial chemotherapy using cisplatin and etoposide seems to have some anti-tumor effect against advanced HCC, although a high rate of life- threatening complications precludes the indication of this regimen at least for patients with non-compensated cirrhosis. Etoposide 61-70 HCC Homo sapiens 125-128 11791378-5 2001 A retinoid analog, acyclic retinoid, induces differentiation and apoptosis of HCC cell lines in vitro. Retinoids 2-10 HCC Homo sapiens 78-81 11867196-7 2002 The serum retinol levels in both cirrhotic patients and HCC patients were significantly lower than those in healthy subjects. Vitamin A 10-17 HCC Homo sapiens 56-59 11867196-9 2002 The prediagnostic retinol levels were significantly lower in cirrhotic patients who developed HCC compared with patients who did not. Vitamin A 18-25 HCC Homo sapiens 94-97 11867196-10 2002 The odds ratio of cirrhotic patients who developed HCC in the lowest tertile to highest tertile of retinol status was 6.75 (95% CI=1.26--36.0; P=0.015). Vitamin A 99-106 HCC Homo sapiens 51-54 11169832-2 2001 Twenty patients with hepatocellular carcinoma (HCC) underwent 3DFISP dynamic study with double dose Gd. Gadolinium 100-102 HCC Homo sapiens 47-50 11819809-3 2001 Hepatitis B and C viruses (HBV and HCV) and dietary aflatoxin intake remain the major causative factors of HCC. Aflatoxins 52-61 HCC Homo sapiens 107-110 11274643-9 2001 Finally, beta-Gal staining in nontumoral tissue was strongly correlated with the presence of HCC in the surrounding liver (P <.001). beta-D-galactose 9-17 HCC Homo sapiens 93-96 11286466-4 2001 To investigate whether pravastatin, a potent HMG-CoA reductase inhibitor, prolongs survival in patients with advanced HCC, this randomized controlled trial was conducted between February 1990 and February 1998 at Osaka University Hospital. Pravastatin 23-34 HCC Homo sapiens 118-121 11286466-16 2001 Pravastatin prolonged the survival of patients with advanced HCC, suggesting its value for adjuvant treatment. Pravastatin 0-11 HCC Homo sapiens 61-64 11012474-2 2000 AIM: To investigate serum retinol levels in patients with liver disease and hepatocellular carcinoma (HCC) and to assess its importance as a risk factor for the development of HCC. Vitamin A 26-33 HCC Homo sapiens 102-105 11012474-2 2000 AIM: To investigate serum retinol levels in patients with liver disease and hepatocellular carcinoma (HCC) and to assess its importance as a risk factor for the development of HCC. Vitamin A 26-33 HCC Homo sapiens 176-179 11012474-5 2000 in ng/mL, were 972.1 +/- 37.7 in the control group and 647 +/- 41.1 in patients with chronic hepatitis C. Serum retinol levels in patients with cirrhosis and HCC were lower than in patients with cirrhosis alone (365.8 +/- 43.1 vs. 438.9 +/- 22.1, P < 0.04). Vitamin A 112-119 HCC Homo sapiens 158-161 11012474-9 2000 Sixty percent of patients with Child-Pugh grade A cirrhosis/HCC had serum retinol levels below 350 ng/mL compared with only 18.4% of cirrhotics without HCC (chi 2-test, P=0.01). Vitamin A 74-81 HCC Homo sapiens 60-63 11012474-13 2000 Serum retinol levels may be a risk factor for the development of HCC. Vitamin A 6-13 HCC Homo sapiens 65-68 10838038-5 2000 Furthermore, we have shown that doxorubicin, when administered intravenously, is efficient in inhibiting the development of subcutaneous tumor but leads to the regression of the orthotopic human HCC. Doxorubicin 32-43 HCC Homo sapiens 195-198 11061618-1 2000 We describe a case of hepatocellular carcinoma (HCC) after long term tamoxifen therapy in a 71-year-old woman. Tamoxifen 69-78 HCC Homo sapiens 48-51 11061618-8 2000 An increased risk of HCC may not become apparent until after a decade or more of tamoxifen therapy. Tamoxifen 81-90 HCC Homo sapiens 21-24 11061618-9 2000 In addition, HCC in tamoxifen treated patients may be under-reported since there may be reluctance to biopsy liver tumours which are assumed to be secondary carcinoma of the breast. Tamoxifen 20-29 HCC Homo sapiens 13-16 11185536-12 2000 Dietary aflatoxin exposure is an important codeterminant of HCC risk in Africa and parts of Asia. Aflatoxins 8-17 HCC Homo sapiens 60-63 11185536-13 2000 In Canada and the United States, excessive alcohol intake, cigarette smoking and oral contraceptive use in women also are risk factors for HCC. Alcohols 43-50 HCC Homo sapiens 139-142 10694648-8 2000 TACE in patients with postresection recurrent HCC was associated with less morbidity, mortality, and a better survival outcome compared with patients with primary inoperable HCC, but this was largely related to smaller tumor size and better liver function in the former group at the time of TACE treatment. Chlorotrianisene 0-4 HCC Homo sapiens 46-49 10833253-2 2000 We evaluated the efficacy and clinical safety of using an Ethiodol-ethanol mixture as the embolizer for treatment of HCC and the possibility of a surgical approach for inoperable tumors after TAE. Ethiodized Oil 58-66 HCC Homo sapiens 117-120 10833253-2 2000 We evaluated the efficacy and clinical safety of using an Ethiodol-ethanol mixture as the embolizer for treatment of HCC and the possibility of a surgical approach for inoperable tumors after TAE. Ethanol 67-74 HCC Homo sapiens 117-120 10833253-12 2000 Transarterial Ethiodol and ethanol administration creating dual hepatic artery and portal vein embolization was a safe and efficacious method for treating HCC. Ethiodized Oil 14-22 HCC Homo sapiens 155-158 10833253-12 2000 Transarterial Ethiodol and ethanol administration creating dual hepatic artery and portal vein embolization was a safe and efficacious method for treating HCC. Ethanol 27-34 HCC Homo sapiens 155-158 9566688-1 1998 Aflatoxin B1 (AFB1) is a well-known mutagen and carcinogen which induces human hepatocellular carcinoma (HCC). Aflatoxin B1 0-12 HCC Homo sapiens 79-109 10654919-1 1999 This chapter reviews the data that have been accumulated implicating aflatoxin ingestion as an important risk factor in the aetiology of hepatocellular carcinoma (HCC). Aflatoxins 69-78 HCC Homo sapiens 163-166 10654919-2 1999 Numerous epidemiological studies have observed a correlation between areas of high aflatoxin exposure and a high incidence of HCC. Aflatoxins 83-92 HCC Homo sapiens 126-129 10405747-1 1999 PURPOSE: To determine whether the frequency of hepatocellular carcinoma (HCC) in patients with cirrhosis is affected by hepatic iron deposition as detected with magnetic resonance (MR) imaging. Iron 128-132 HCC Homo sapiens 73-76 10405747-6 1999 The frequency of HCC in patients with iron deposition in regenerative nodules (52% [37 of 71 patients]) was significantly higher (P = .015) than that in patients without iron in regenerative nodules (34% [43 of 125 patients]). Iron 38-42 HCC Homo sapiens 17-20 10405747-7 1999 CONCLUSION: The occurrence of HCC may be associated causally with iron deposition in regenerative nodules in patients with cirrhosis. Iron 66-70 HCC Homo sapiens 30-33 10405747-8 1999 MR imaging can enable detection of iron deposition in regenerative nodules as a possible risk factor for the development of HCC. Iron 35-39 HCC Homo sapiens 124-127 10346906-2 1999 Electron transfer in the physiological complex of yeast Cc (yCc) and CcP was studied using the Ru-39-Cc derivative, in which the H39C/C102T variant of yeast iso-1-cytochrome c is labeled at the single cysteine residue on the back surface with trisbipyridylruthenium(II). Ruthenium 95-97 HCC Homo sapiens 56-58 10346906-2 1999 Electron transfer in the physiological complex of yeast Cc (yCc) and CcP was studied using the Ru-39-Cc derivative, in which the H39C/C102T variant of yeast iso-1-cytochrome c is labeled at the single cysteine residue on the back surface with trisbipyridylruthenium(II). Ruthenium 95-97 HCC Homo sapiens 61-63 10346906-2 1999 Electron transfer in the physiological complex of yeast Cc (yCc) and CcP was studied using the Ru-39-Cc derivative, in which the H39C/C102T variant of yeast iso-1-cytochrome c is labeled at the single cysteine residue on the back surface with trisbipyridylruthenium(II). Cysteine 201-209 HCC Homo sapiens 56-58 10346906-2 1999 Electron transfer in the physiological complex of yeast Cc (yCc) and CcP was studied using the Ru-39-Cc derivative, in which the H39C/C102T variant of yeast iso-1-cytochrome c is labeled at the single cysteine residue on the back surface with trisbipyridylruthenium(II). trisbipyridylruthenium 243-265 HCC Homo sapiens 56-58 10346906-3 1999 Laser excitation of the 1:1 Ru-39-Cc-CcP compound I complex at low ionic strength results in rapid electron transfer from RuII to heme c FeIII, followed by electron transfer from heme c FeII to the Trp-191 indolyl radical cation with a rate constant keta of 2 x 10(6) s-1 at 20 degrees C. keta is not changed by increasing the viscosity up to 40 cP with glycerol and is independent of temperature. Heme 130-134 HCC Homo sapiens 34-36 10346906-3 1999 Laser excitation of the 1:1 Ru-39-Cc-CcP compound I complex at low ionic strength results in rapid electron transfer from RuII to heme c FeIII, followed by electron transfer from heme c FeII to the Trp-191 indolyl radical cation with a rate constant keta of 2 x 10(6) s-1 at 20 degrees C. keta is not changed by increasing the viscosity up to 40 cP with glycerol and is independent of temperature. Heme 179-183 HCC Homo sapiens 34-36 10346906-3 1999 Laser excitation of the 1:1 Ru-39-Cc-CcP compound I complex at low ionic strength results in rapid electron transfer from RuII to heme c FeIII, followed by electron transfer from heme c FeII to the Trp-191 indolyl radical cation with a rate constant keta of 2 x 10(6) s-1 at 20 degrees C. keta is not changed by increasing the viscosity up to 40 cP with glycerol and is independent of temperature. Tryptophan 198-201 HCC Homo sapiens 34-36 10346906-3 1999 Laser excitation of the 1:1 Ru-39-Cc-CcP compound I complex at low ionic strength results in rapid electron transfer from RuII to heme c FeIII, followed by electron transfer from heme c FeII to the Trp-191 indolyl radical cation with a rate constant keta of 2 x 10(6) s-1 at 20 degrees C. keta is not changed by increasing the viscosity up to 40 cP with glycerol and is independent of temperature. indolyl radical 206-221 HCC Homo sapiens 34-36 10346906-3 1999 Laser excitation of the 1:1 Ru-39-Cc-CcP compound I complex at low ionic strength results in rapid electron transfer from RuII to heme c FeIII, followed by electron transfer from heme c FeII to the Trp-191 indolyl radical cation with a rate constant keta of 2 x 10(6) s-1 at 20 degrees C. keta is not changed by increasing the viscosity up to 40 cP with glycerol and is independent of temperature. ibudilast 250-254 HCC Homo sapiens 34-36 10346906-3 1999 Laser excitation of the 1:1 Ru-39-Cc-CcP compound I complex at low ionic strength results in rapid electron transfer from RuII to heme c FeIII, followed by electron transfer from heme c FeII to the Trp-191 indolyl radical cation with a rate constant keta of 2 x 10(6) s-1 at 20 degrees C. keta is not changed by increasing the viscosity up to 40 cP with glycerol and is independent of temperature. ibudilast 289-293 HCC Homo sapiens 34-36 10346906-3 1999 Laser excitation of the 1:1 Ru-39-Cc-CcP compound I complex at low ionic strength results in rapid electron transfer from RuII to heme c FeIII, followed by electron transfer from heme c FeII to the Trp-191 indolyl radical cation with a rate constant keta of 2 x 10(6) s-1 at 20 degrees C. keta is not changed by increasing the viscosity up to 40 cP with glycerol and is independent of temperature. Glycerol 354-362 HCC Homo sapiens 34-36 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. Ruthenium 78-80 HCC Homo sapiens 42-44 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. Ruthenium 78-80 HCC Homo sapiens 46-49 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. Ruthenium 78-80 HCC Homo sapiens 47-49 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. Ruthenium 78-80 HCC Homo sapiens 97-100 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. trisbipyridylruthenium 117-139 HCC Homo sapiens 42-44 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. trisbipyridylruthenium 117-139 HCC Homo sapiens 46-49 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. trisbipyridylruthenium 117-139 HCC Homo sapiens 47-49 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. trisbipyridylruthenium 117-139 HCC Homo sapiens 97-100 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. Lysine 147-150 HCC Homo sapiens 42-44 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. Lysine 147-150 HCC Homo sapiens 46-49 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. Lysine 147-150 HCC Homo sapiens 47-49 10346906-7 1999 Electron transfer in the complex of horse Cc (hCc) and CcP was examined using Ru-27-Cc, in which hCc is labeled with trisbipyridylruthenium(II) at Lys-27. Lysine 147-150 HCC Homo sapiens 97-100 10346906-8 1999 Laser excitation of the Ru-27-Cc-CcP complex results in electron transfer from RuII to heme c FeII with a rate constant k1 of 2.3 x 10(7) s-1, followed by oxidation of the Trp-191 indole to a radical cation by RuIII with a rate constant k3 of 7 x 10(6) s-1. Heme 87-91 HCC Homo sapiens 30-32 10346906-8 1999 Laser excitation of the Ru-27-Cc-CcP complex results in electron transfer from RuII to heme c FeII with a rate constant k1 of 2.3 x 10(7) s-1, followed by oxidation of the Trp-191 indole to a radical cation by RuIII with a rate constant k3 of 7 x 10(6) s-1. Tryptophan 172-175 HCC Homo sapiens 30-32 10346906-11 1999 The results are consistent with a gating mechanism in which the Ru-27-Cc-CcP complex undergoes fluctuations between a major state A with the configuration of the hCc-CcP crystalline complex and a minor state B with the configuration of the yCc-CcP complex. ycc-ccp 240-247 HCC Homo sapiens 70-72 10346906-12 1999 The hCc-CcP complex, state A, has an inefficient pathway for electron transfer from heme c to the Trp-191 indolyl radical cation with a distance of 20.5 A and a predicted value of 5 x 10(2) s-1 for k4A. heme C 84-90 HCC Homo sapiens 4-7 10346906-12 1999 The hCc-CcP complex, state A, has an inefficient pathway for electron transfer from heme c to the Trp-191 indolyl radical cation with a distance of 20.5 A and a predicted value of 5 x 10(2) s-1 for k4A. Tryptophan 98-101 HCC Homo sapiens 4-7 10346906-12 1999 The hCc-CcP complex, state A, has an inefficient pathway for electron transfer from heme c to the Trp-191 indolyl radical cation with a distance of 20.5 A and a predicted value of 5 x 10(2) s-1 for k4A. indolyl radical 106-121 HCC Homo sapiens 4-7 11593648-3 1999 Selective internal radiation therapy using yttrium-90 (90 Y) microspheres has been shown to be an effective treatment for inoperable HCC in a phase I and II study. Yttrium-90 43-53 HCC Homo sapiens 133-136 10436243-1 1999 A 65-year-old man with multiple hepatocellular carcinoma (HCC) underwent intra-hepato-arterial chemotherapy (IHAC) through an implantable port over a period of 10 months after transcatheter arterial embolization (TAE) had been performed three times. ihac 109-113 HCC Homo sapiens 58-61 9885591-1 1999 PURPOSE: To investigate the relationship between the metal content of hepatocellular carcinoma (HCC) and the signal intensity pattern on magnetic resonance images. Metals 53-58 HCC Homo sapiens 70-100 9885591-6 1999 Multivariate analysis showed that the contrast-to-noise ratio between the HCC and surrounding hepatic parenchyma was affected by intratumoral copper content (P = .0338), zinc content of surrounding hepatic parenchyma (P = .0379), and the degree of histologic differentiation on T1-weighted (P = .0031) and T2-weighted (P = .0062) images. Copper 142-148 HCC Homo sapiens 74-77 9885591-7 1999 CONCLUSION: The signal intensity of HCC on T1-weighted images is related to the degree of histologic differentiation, intratumoral copper content, and zinc content of surrounding hepatic parenchyma, whereas the signal intensity on T2-weighted images is related to the degree of histologic differentiation. Copper 131-137 HCC Homo sapiens 36-39 9705539-5 1998 In nonsurgery, regional cancer therapy has been a new trend, which includes transcatheter arterial chemoembolization, percutaneous ethanol injection for small HCC, and others. Ethanol 131-138 HCC Homo sapiens 159-162 10639517-8 2000 RESULTS: The Ser-249 p53 mutation was detected in plasma DNA from 19 (36%) of the 53 patients with HCC, two (15%) of the 13 patients with cirrhosis, and three (6%) of the 53 control subjects. Serine 13-16 HCC Homo sapiens 99-102 10639517-11 2000 CONCLUSION: The Ser-249 p53 mutation in plasma DNA is strongly associated with HCC in Gambian patients. Serine 16-19 HCC Homo sapiens 79-82 10639517-13 2000 Use of the Ser-249 p53 mutation should facilitate further molecular epidemiologic studies on the development of HCC. Serine 11-14 HCC Homo sapiens 112-115 9142639-11 1997 As insulin is an essential factor for the metabolism of fatty acids, IGF-II may play an important role in both fatty degeneration and in the proliferation of HCC cells. Fatty Acids 56-67 HCC Homo sapiens 158-161 14966392-7 1997 Hepatic resection, liver transplantation and percutaneous ethanol injection are the options more frequently chosen for treating patients with HCC. Ethanol 58-65 HCC Homo sapiens 142-145 9151912-2 1997 One report showed intra-arterial administration of epirubicin to be effective in the treatment of nonresectable HCC. Epirubicin 51-61 HCC Homo sapiens 112-115 7648596-2 1995 The HFA was occluded by microcoils to prevent a possible toxic supraumbilical skin rash following chemoembolization of the HCC via the left hepatic artery. hfa 4-7 HCC Homo sapiens 123-126 8609152-4 1996 The results showed that the incidence of hepatocellular carcinoma (HCC) was significantly higher in the animals both infected with HBV and exposed to AFB1 (52.94%) than in those solely infected with HBV (11.11%) or exposed to AFB1 (12.50%). Aflatoxin B1 150-154 HCC Homo sapiens 67-70 8609152-4 1996 The results showed that the incidence of hepatocellular carcinoma (HCC) was significantly higher in the animals both infected with HBV and exposed to AFB1 (52.94%) than in those solely infected with HBV (11.11%) or exposed to AFB1 (12.50%). Aflatoxin B1 226-230 HCC Homo sapiens 67-70 9221576-10 1997 Toxins can be also important for the development of HCC (in particular aflatoxins, chlorinated hydrocarbons, pesticides). Hydrocarbons 95-107 HCC Homo sapiens 52-55 8854766-5 1996 It was suggested that the recurrence of HCC after resection might be inhibited by curative operation following preoperative TAE with complete necrosis of tumor. tae 124-127 HCC Homo sapiens 40-43 8616754-2 1996 This Phase 11 study was designed to investigate the clinical activity and toxicity of flutamide in the treatment of patients with advanced HCC. Flutamide 86-95 HCC Homo sapiens 139-142 8659700-5 1996 In the AL group, the cumulative HCC occurrence rate was only 1% during the observation period of 3 years. Aluminum 7-9 HCC Homo sapiens 32-35 8659701-1 1996 Alcohol drinking has been reported to be an important factor that modulates the development and prognosis of chronic hepatitis B; however, little is known about an interrelationship between alcohol intake and the progression of chronic hepatitis C to liver cirrhosis (LC) and hepatocellular carcinoma (HCC). Alcohols 0-7 HCC Homo sapiens 302-305 8659701-5 1996 The period from transfusion to diagnosis in HCC patients with alcohol intake > or = 46 g/day and < 46 g/day were 26 +/- 6 and 31 +/- 9 years, respectively, resulting in a significant difference (p < 0.05). Alcohols 62-69 HCC Homo sapiens 44-47 8659701-8 1996 In conclusion, these data suggest that alcohol drinking might be an important factor that promotes an occurrence of HCC in patients with hepatitis C, and that hepatitis C virus infection in the elderly promotes development of liver disease via LC to HCC. Alcohols 39-46 HCC Homo sapiens 116-119 8032815-4 1994 In this communication, we report a case in which a patient with HCC has been successfully treated by TAE followed by limited-field radiotherapy. tae 101-104 HCC Homo sapiens 64-67 7656828-12 1995 Nearly 70% of the HCC+CC cases had intracytoplasmic glycogen in the HCC area. Glycogen 52-60 HCC Homo sapiens 18-21 7656828-12 1995 Nearly 70% of the HCC+CC cases had intracytoplasmic glycogen in the HCC area. Glycogen 52-60 HCC Homo sapiens 68-71 8682610-6 1995 HBV, consumption of aflatoxins, a genetic factor, and possibly a second hepatitis virus infection contribute to the risk of HCC. Aflatoxins 20-30 HCC Homo sapiens 124-127 2173494-2 1990 In this paper, we present MR image of the resected cases of HCC with the pathological findings, and assess MR image for the potential utility of demonstrating the pathologic features of HCC treated with TCE. Trichloroethylene 203-206 HCC Homo sapiens 186-189 8304302-10 1994 CONCLUSION: Our results showed that the efficacy of hepatectomy and the efficacy percutaneous ethanol injection therapy for small solitary HCC were similar. Ethanol 94-101 HCC Homo sapiens 139-142 7505994-1 1993 Reduced indocyanine green (ICG) uptake is one of the functional changes of human hepatocellular carcinoma (HCC). Indocyanine Green 8-25 HCC Homo sapiens 81-111 7505994-1 1993 Reduced indocyanine green (ICG) uptake is one of the functional changes of human hepatocellular carcinoma (HCC). Indocyanine Green 27-30 HCC Homo sapiens 81-111 7690345-7 1993 Alcohol drinking was associated with HCC and interacted with HBsAg positivity. Alcohols 0-7 HCC Homo sapiens 37-40 7690345-8 1993 Agricultural use of organophosphorous pesticides (30 liters/year or more) and military service in the south of Vietnam for 10 years or more were also associated with an increased risk of HCC. organophosphorous 20-37 HCC Homo sapiens 187-190 8440419-13 1993 Recent increase of HCC in alcoholic cirrhosis in Japan may be related to the increase of alcohol consumption, the increase of blood transfusions, and longer survival of cirrhosis patients. Alcohols 26-33 HCC Homo sapiens 19-22 7859834-2 1994 We carried out a hospital-based, case-control study to assess the association of both the Hepatitis B Virus (HBV) infection and the lifetime daily alcohol intake with the risk of developing hepatocellular carcinoma (HCC) in patients with liver cirrhosis (LC). Alcohols 147-154 HCC Homo sapiens 216-219 7859834-6 1994 HBV infection was associated with HCC development in cirrhotics (odds ratio = 6.8; 95% confidence interval = 1.4-32.3), whereas we observed a trend towards a decreased HCC risk at increased alcohol intake values (odds ratio from 1 for lifetime abstainers to 0.2 for drinkers of 175 g/day or more). Alcohols 190-197 HCC Homo sapiens 168-171 2538017-5 1989 HCC has a multifactorial etiology in which the most important factors are the Hepatitis B virus, cirrhosis and aflatoxin with alcohol as synergic co-carcinogen. Aflatoxins 111-120 HCC Homo sapiens 0-3 2170719-0 1990 [Portal perfusion defect after percutaneous ethanol injection therapy (PEIT) for hepatocellular carcinoma (HCC)]. Ethanol 44-51 HCC Homo sapiens 81-112 2554848-9 1989 Cholecystectomy should be performed during the elective hepatectomy for resectable HCC in patients who have received preoperative TAEs. taes 130-134 HCC Homo sapiens 83-86 34856322-18 2022 LAY SUMMARY: Patients with DAA-cured HCV-related liver cirrhosis without non-characterized liver nodules at SVR remain at risk of HCC development. daa 27-30 HCC Homo sapiens 130-133 34412596-1 2021 BACKGROUND: A hepatocellular carcinoma (HCC) prediction model (ASAP), including age, sex, and the biomarkers alpha-fetoprotein and prothrombin induced by vitamin K absence-II, showed potential clinical value in the early detection of HCC. vitamin k absence-ii 154-174 HCC Homo sapiens 40-43 34412596-1 2021 BACKGROUND: A hepatocellular carcinoma (HCC) prediction model (ASAP), including age, sex, and the biomarkers alpha-fetoprotein and prothrombin induced by vitamin K absence-II, showed potential clinical value in the early detection of HCC. vitamin k absence-ii 154-174 HCC Homo sapiens 234-237 2538017-5 1989 HCC has a multifactorial etiology in which the most important factors are the Hepatitis B virus, cirrhosis and aflatoxin with alcohol as synergic co-carcinogen. Alcohols 126-133 HCC Homo sapiens 0-3 2466073-1 1988 Lacking a treatment for nonresectable hepatocellular carcinoma (HCC), we have utilized the androgen antagonist properties of ketoconazole in treating eight patients, seven men and one woman, with HCC, which, in view of a higher prevalence of HCC in men, seems to be androgen dependent. Ketoconazole 125-137 HCC Homo sapiens 196-199 2466073-1 1988 Lacking a treatment for nonresectable hepatocellular carcinoma (HCC), we have utilized the androgen antagonist properties of ketoconazole in treating eight patients, seven men and one woman, with HCC, which, in view of a higher prevalence of HCC in men, seems to be androgen dependent. Ketoconazole 125-137 HCC Homo sapiens 196-199 2843119-1 1988 Transcatheter arterial embolization using lipiodol ultra-fluid (L-TAE) is frequently used for hepatocellular carcinoma (HCC). Ethiodized Oil 42-50 HCC Homo sapiens 120-123 2855054-1 1988 Fifty-three nude mice bearing human HCC were used for targeting study of HCC using 131I-antihuman HCC isoferritin IgG. Iodine-131 83-87 HCC Homo sapiens 73-76 2855054-1 1988 Fifty-three nude mice bearing human HCC were used for targeting study of HCC using 131I-antihuman HCC isoferritin IgG. Iodine-131 83-87 HCC Homo sapiens 73-76 2843119-1 1988 Transcatheter arterial embolization using lipiodol ultra-fluid (L-TAE) is frequently used for hepatocellular carcinoma (HCC). l-tae 64-69 HCC Homo sapiens 120-123 2843119-6 1988 Lipiodol remains long in the infarction area and interferes with the diagnosis of HCC. Ethiodized Oil 0-8 HCC Homo sapiens 82-85 2850594-4 1988 TAE should be considered the treatment of choice for ruptured HCC; however, long-term survival was limited to those patients without portal extension of HCC. tae 0-3 HCC Homo sapiens 62-65 2827880-2 1988 Both DTS and SS had a sensitivity of 96% and a specificity of 90.6% for HCC. dibenzyl trisulfide 5-8 HCC Homo sapiens 72-75 2827880-6 1988 In the clinical setting, when HCC is suspected (a situation in which tumors are usually larger than 2 cm and the pretest probability of disease is between 20% and 60%) the DTS and SS is an excellent test for the diagnosis or exclusion of HCC. dibenzyl trisulfide 172-175 HCC Homo sapiens 30-33 2827880-6 1988 In the clinical setting, when HCC is suspected (a situation in which tumors are usually larger than 2 cm and the pretest probability of disease is between 20% and 60%) the DTS and SS is an excellent test for the diagnosis or exclusion of HCC. dibenzyl trisulfide 172-175 HCC Homo sapiens 238-241 33374409-4 2020 Therefore, in this study, we describe an influence of membrane mimetic environment-mixed dodecylphosphocholine:sodium dodecyl sulfate (DPC:SDS) micelle (molar ratio 5:1)-on the effect of the hCC oligomerization. dodecylphosphocholine 89-110 HCC Homo sapiens 191-194 2827880-6 1988 In the clinical setting, when HCC is suspected (a situation in which tumors are usually larger than 2 cm and the pretest probability of disease is between 20% and 60%) the DTS and SS is an excellent test for the diagnosis or exclusion of HCC. H-SER-SER-OH 180-182 HCC Homo sapiens 30-33 6100289-5 1984 Studies in East Africa have shown a correlation between aflatoxin contamination and the incidence of HCC. Aflatoxins 56-65 HCC Homo sapiens 101-104 973599-1 1976 25-Hydroxycholecalciferol (25-HCC) levels were measured in 31 bedouin females and eight bedouin male tribesmen and compared with the levels in Jewish males and females in Beersheba. Calcifediol 0-25 HCC Homo sapiens 30-33 2981112-1 1985 This study assesses the diagnostic value of Lipiodol (iodized oil) and computed tomography (CT) in detecting hepatocellular carcinoma (HCC). Ethiodized Oil 44-52 HCC Homo sapiens 135-138 2981112-2 1985 Twenty-four patients who were suspected of having HCC received injections of a small amount of Lipiodol, along with an antitumor agent, in the hepatic artery following routine celiac angiography. Ethiodized Oil 95-103 HCC Homo sapiens 50-53 2981112-3 1985 CT scans obtained 7-10 days after Lipiodol administration demonstrated HCC in distinct contrast to the surrounding noncancerous parenchyma. Ethiodized Oil 34-42 HCC Homo sapiens 71-74 2981112-4 1985 In particular, the CT-Lipiodol procedure disclosed many small HCC lesions that were not shown by celiac angiography, scintigraphy, CT with and without contrast medium enhancement, and ultrasonography. Ethiodized Oil 22-30 HCC Homo sapiens 62-65 33710804-0 2021 SNORA23 inhibits HCC tumorigenesis by impairing the 2"-O-ribose methylation level of 28S rRNA. 2"-o-ribose 52-63 HCC Homo sapiens 17-20 33710804-13 2021 CONCLUSIONS: SNORA23 exhibited antitumor effects in HCC and together with rapamycin, provided a promising therapeutic strategy for HCC treatment. Sirolimus 74-83 HCC Homo sapiens 131-134 33374409-4 2020 Therefore, in this study, we describe an influence of membrane mimetic environment-mixed dodecylphosphocholine:sodium dodecyl sulfate (DPC:SDS) micelle (molar ratio 5:1)-on the effect of the hCC oligomerization. Sodium Dodecyl Sulfate 111-133 HCC Homo sapiens 191-194 33374409-4 2020 Therefore, in this study, we describe an influence of membrane mimetic environment-mixed dodecylphosphocholine:sodium dodecyl sulfate (DPC:SDS) micelle (molar ratio 5:1)-on the effect of the hCC oligomerization. di-2-pyridylketone 4-cyclohexyl-4-methyl-3-thiosemicarbazone 135-138 HCC Homo sapiens 191-194 33374409-4 2020 Therefore, in this study, we describe an influence of membrane mimetic environment-mixed dodecylphosphocholine:sodium dodecyl sulfate (DPC:SDS) micelle (molar ratio 5:1)-on the effect of the hCC oligomerization. Sodium Dodecyl Sulfate 139-142 HCC Homo sapiens 191-194 33374409-8 2020 Obtained data shows that the mixed DPC:SDS micelle does not accelerate the oligomerization of protein and even reverses the hCC dimerization process. di-2-pyridylketone 4-cyclohexyl-4-methyl-3-thiosemicarbazone 35-38 HCC Homo sapiens 124-127 33374409-8 2020 Obtained data shows that the mixed DPC:SDS micelle does not accelerate the oligomerization of protein and even reverses the hCC dimerization process. Sodium Dodecyl Sulfate 39-42 HCC Homo sapiens 124-127 32489260-12 2020 Sorafenib or lenvatinib are recommended for first-line systemic treatment of intermediate-stage hcc. Sorafenib 0-9 HCC Homo sapiens 96-99 33301499-0 2020 Low incidence of HCC in chronic hepatitis C patients with pretreatment liver stiffness measurements below 17.5 kilopascal who achieve SVR following DAAs. daas 148-152 HCC Homo sapiens 17-20 32314828-0 2020 HCC recurrence in HCV patients after liver transplantation: SiLVER Study reveals benefits of sirolimus in combination with CNIs. Sirolimus 93-102 HCC Homo sapiens 0-3 32314828-3 2020 METHODS: We performed a post-hoc analysis of 166 HCV+ SiLVER Study patients regarding HCC outcome after LTx. Silver 54-60 HCC Homo sapiens 86-89 32314828-3 2020 METHODS: We performed a post-hoc analysis of 166 HCV+ SiLVER Study patients regarding HCC outcome after LTx. Leukotriene C4 104-107 HCC Homo sapiens 86-89 32246992-4 2020 The expression of Nogo-B in TAMs of HCC patients is significantly increased, which correlated with the poor prognosis of the patients with HCC. tams 28-32 HCC Homo sapiens 36-39 32246992-4 2020 The expression of Nogo-B in TAMs of HCC patients is significantly increased, which correlated with the poor prognosis of the patients with HCC. tams 28-32 HCC Homo sapiens 139-142 32246992-10 2020 Nogo-B expression in macrophages facilitates tumor-associated macrophages M2 polarization and protumoral effects of TAMs in HCC. tams 116-120 HCC Homo sapiens 124-127 32489260-12 2020 Sorafenib or lenvatinib are recommended for first-line systemic treatment of intermediate-stage hcc. lenvatinib 13-23 HCC Homo sapiens 96-99 31850932-0 2020 Tenofovir for the Prevention of HCC in Patients With Cirrhosis. tfv 0-9 HCC Homo sapiens 32-35 31489034-1 2019 Background: Hepatocellular carcinoma (HCC) is the most common form of liver cancer and is generally caused by viral infections or consumption of mutagens, such as alcohol. Alcohols 163-170 HCC Homo sapiens 38-41 31730491-0 2019 Lipiodol retention pattern after TACE for HCC is a predictor for local progression in lesions with complete response. Ethiodized Oil 0-8 HCC Homo sapiens 42-45 31730491-1 2019 BACKGROUND: To evaluate the predictive value of the lipiodol retention pattern for local progression of HCC with a complete response (CR) on CT according to mRECIST criteria after a first session of conventional chemoembolization (cTACE). Ethiodized Oil 52-60 HCC Homo sapiens 104-107 31489034-9 2019 The MTH1 inhibitor Karonudib (TH1579) and siRNA effectively introduce toxic oxidized nucleotides into DNA, 8-oxoG, and kill HCC cell lines in vitro. karonudib 19-28 HCC Homo sapiens 124-127 31866520-2 2020 Recently, independent studies have indicated that some hepatitis viruses develop abilities to hijack autophagy for their replication, such as hepatitis B (HBV) and C (HCV); these two viruses are structurally unrelated, but both of them can cause hepatitis, liver cirrhosis, and even hepatocellular carcinoma (HCC). Carbon 164-165 HCC Homo sapiens 283-313 31338551-4 2019 MATERIALS AND METHODS: From January 2007 to January 2018, 86 octogenarians with HCC initially treated with TACE, who were treatment naive or had a recurrence after surgery and/or radiofrequency ablation, were enrolled in this study. Chlorotrianisene 107-111 HCC Homo sapiens 80-83 31489034-9 2019 The MTH1 inhibitor Karonudib (TH1579) and siRNA effectively introduce toxic oxidized nucleotides into DNA, 8-oxoG, and kill HCC cell lines in vitro. th1579 30-36 HCC Homo sapiens 124-127 31489034-10 2019 Furthermore, we demonstrate that HCC growth in a xenograft mouse model in vivo is efficiently suppressed by Karonudib. karonudib 108-117 HCC Homo sapiens 33-36 31188000-8 2019 These metabolites belong to TCA cycle, glycolysis, purines, and lipid metabolism and have been previously reported in liver metabolomic studies where high correlation with HCC progression is implied. Trichloroacetic Acid 28-31 HCC Homo sapiens 172-175 31188000-8 2019 These metabolites belong to TCA cycle, glycolysis, purines, and lipid metabolism and have been previously reported in liver metabolomic studies where high correlation with HCC progression is implied. Purines 51-58 HCC Homo sapiens 172-175 31384178-9 2019 Conclusions: These results demonstrated miR-125b-5p as a tumor suppressor in HCC through its inhibition of TXNRD1, thereby suggesting it as a potential target for the clinical treatment of HCC. mir-125b-5p 40-51 HCC Homo sapiens 189-192 31497746-9 2019 Tetracycline-inducible PTPN23 overexpression in human HCC cells resulted in significant inhibition in proliferation, migration, and invasion and in vivo tumorigenesis. Tetracycline 0-12 HCC Homo sapiens 54-57 31384178-3 2019 Methods: We detected miR-125b-5p levels in human HCC tissue samples through quantitative reverse transcription polymerase chain reaction (qRT-PCR), and in vitro experiments were employed to investigate the effect of miR-125b-5p on HCC cell proliferation, migration, and invasion. mir-125b-5p 21-32 HCC Homo sapiens 49-52 31384178-3 2019 Methods: We detected miR-125b-5p levels in human HCC tissue samples through quantitative reverse transcription polymerase chain reaction (qRT-PCR), and in vitro experiments were employed to investigate the effect of miR-125b-5p on HCC cell proliferation, migration, and invasion. mir-125b-5p 216-227 HCC Homo sapiens 231-234 31384178-8 2019 Moreover, dual luciferase-reporter assays revealed that miR-125b-5p targets TXNRD1 to directly regulate its expression, whereas TXNRD1 overexpression abolishes the inhibitory effect of miR-125b-5p on HCC cell proliferation, migration, and invasion. CHEMBL3740941 65-67 HCC Homo sapiens 200-203 31384178-9 2019 Conclusions: These results demonstrated miR-125b-5p as a tumor suppressor in HCC through its inhibition of TXNRD1, thereby suggesting it as a potential target for the clinical treatment of HCC. mir-125b-5p 40-51 HCC Homo sapiens 77-80 31234316-2 2019 Tremendous progress has been made over the past decade in the development of new agents for HCC, including small-molecule kinase inhibitors such as sorafenib, lenvatinib, cabozantinib, regorafenib, and monoclonal antibodies like ramucirumab, nivolumab, and pembrolizumab. Sorafenib 148-157 HCC Homo sapiens 92-95 31203490-5 2019 Here, we create a systematic kinase-inhibitor binding profile in a high-throughput manner by molecular docking and consensus scoring, where the kinases have been collected as therapeutic targets of hCC and the inhibitors are reversible, ATP-competitive and readily available. Adenosine Triphosphate 237-240 HCC Homo sapiens 198-201 31117479-4 2019 The formation of graphene is initiated by the breaking of acetylene (C2H2) molecules by collision into pieces such as H atoms, ethynyl (HC C ), and vinylidene (H2C C:) radicals. Graphite 17-25 HCC Homo sapiens 136-140 31142283-2 2019 However, the difference of effectiveness in reducing HCC occurrence between tenofovir (TDF) and enticavir (ETV), two first-line NAs drugs, is still little known. Tenofovir 76-85 HCC Homo sapiens 53-56 30898548-10 2019 The inhibition of HCC progression by miR-101 was counteracted by ZNF217 overexpression. mir-101 37-44 HCC Homo sapiens 18-21 31142283-2 2019 However, the difference of effectiveness in reducing HCC occurrence between tenofovir (TDF) and enticavir (ETV), two first-line NAs drugs, is still little known. enticavir 96-105 HCC Homo sapiens 53-56 31142283-3 2019 This meta analysis aims to assess the efficacy in reducing incidence of HCC comparing tenofovir monotherapy with entecavir monotherapy among chronic hepatitis B (CHB) patients by analyzing their long-term clinical outcomes. Tenofovir 86-95 HCC Homo sapiens 72-75 31142283-3 2019 This meta analysis aims to assess the efficacy in reducing incidence of HCC comparing tenofovir monotherapy with entecavir monotherapy among chronic hepatitis B (CHB) patients by analyzing their long-term clinical outcomes. entecavir 113-122 HCC Homo sapiens 72-75 31142283-9 2019 CONCLUSION: There is a better effect of tenofovir in reducing HCC incidence than entecavir, which indicates tenofovir should be used more widely while treating chronic hepatitis B patients. Tenofovir 40-49 HCC Homo sapiens 62-65 31142283-9 2019 CONCLUSION: There is a better effect of tenofovir in reducing HCC incidence than entecavir, which indicates tenofovir should be used more widely while treating chronic hepatitis B patients. Tenofovir 108-117 HCC Homo sapiens 62-65 30829008-7 2019 Accordingly, the newly developed miRNA restoration therapeutic strategy via biodegradable PEG-BCPVs as the carrier should be a promising modality for combating HCC. Polyethylene Glycols 90-93 HCC Homo sapiens 160-163 30600675-1 2019 Background/Aims: Sorafenib remains the only approved molecular targeted agent for hepatocellular carcinoma (HCC); however, reliable biomarkers that predict its efficacy are still lacking. Sorafenib 17-26 HCC Homo sapiens 82-113 31072375-2 2019 Cisplatinum, a well-known chemotherapeutic drug, has been widely used for treatment of numerous human cancers including HCC. Cisplatin 0-11 HCC Homo sapiens 120-123 31072375-3 2019 This study aimed to investigate the differential expressions of LncRNAs in HCC cells treated with cisplatinum and its underlying mechanism. Cisplatin 98-109 HCC Homo sapiens 75-78 31072375-4 2019 METHODS: The differential expressions of LncRNAs in HCC cells treated with cisplatinum were determined by RNA-seq. Cisplatin 75-86 HCC Homo sapiens 52-55 31072375-9 2019 RESULTS: LncRNA TPTEP1 was highly expressed in cisplatinum-treated HCC cells, which sensitizes hepatocellular carcinoma cell to cisplatinum-induced apoptosis. Cisplatin 47-58 HCC Homo sapiens 67-70 31072375-9 2019 RESULTS: LncRNA TPTEP1 was highly expressed in cisplatinum-treated HCC cells, which sensitizes hepatocellular carcinoma cell to cisplatinum-induced apoptosis. Cisplatin 128-139 HCC Homo sapiens 67-70 30684506-10 2019 Baseline liver function, alcohol intake and hepatic decompensation were associated with a higher risk of HCC. Alcohols 25-32 HCC Homo sapiens 105-108 30584071-9 2019 The newly identified HBx/GYS2/p53 axis is responsible for the deregulation of glycogen metabolism and represents a promising therapeutic target for the clinical management of HCC. Glycogen 78-86 HCC Homo sapiens 175-178 30874985-8 2019 In contrast, those who develop HCC in the setting of chronic HBV infection, treatment with nucleoside analogues (NAs) is recommended prior to treating HCC, to prevent further liver injury and reduce the risk for HCC recurrence. Nucleosides 91-101 HCC Homo sapiens 31-34 30765875-1 2019 BACKGROUND: Sorafenib is the first targeted agent proven to improve survival of patients with advanced hepatocellular carcinoma (HCC) and it has been used in first line treatments with heterogeneous response across patients. Sorafenib 12-21 HCC Homo sapiens 129-132 30765875-5 2019 The therapeutic potential of Notch3 inhibition combined with brivanib treatment was also demonstrated in a rat model of HCC and in cell lines derived from different human cancers. brivanib 61-69 HCC Homo sapiens 120-123 30765875-7 2019 CONCLUSION: We have demonstrated that regulation of the TCA cycle is a common mechanism in different human cancers, suggesting that Notch3 inhibitors combined with brivanib treatment may represent a strong formulation for the treatment of HCC as well as Notch3-driven cancers. Tricarboxylic Acids 56-59 HCC Homo sapiens 239-242 30765875-7 2019 CONCLUSION: We have demonstrated that regulation of the TCA cycle is a common mechanism in different human cancers, suggesting that Notch3 inhibitors combined with brivanib treatment may represent a strong formulation for the treatment of HCC as well as Notch3-driven cancers. brivanib 164-172 HCC Homo sapiens 239-242 31024205-4 2019 The Food and Drug Administration-approved Nexavar (sorafenib) is used in the treatment of patients with unresectable HCC. Sorafenib 42-49 HCC Homo sapiens 117-120 31024205-4 2019 The Food and Drug Administration-approved Nexavar (sorafenib) is used in the treatment of patients with unresectable HCC. Sorafenib 51-60 HCC Homo sapiens 117-120 31024205-5 2019 In 2017, Stivarga (regorafenib) and Opdivo (nivolumab) got approved for patients with HCC after being treated with sorafenib, and in 2018, Lenvima (lenvatinib) got approved for patients with unresectable HCC. Sorafenib 115-124 HCC Homo sapiens 86-89 31024205-8 2019 In this review, HCC etiology and new therapeutic strategies that include currently approved drugs and other potential candidates of HCC such as Milciclib, palbociclib, galunisertib, ipafricept, and ramucirumab are evaluated. Milciclib 144-153 HCC Homo sapiens 16-19 31024205-8 2019 In this review, HCC etiology and new therapeutic strategies that include currently approved drugs and other potential candidates of HCC such as Milciclib, palbociclib, galunisertib, ipafricept, and ramucirumab are evaluated. Milciclib 144-153 HCC Homo sapiens 132-135 31024205-8 2019 In this review, HCC etiology and new therapeutic strategies that include currently approved drugs and other potential candidates of HCC such as Milciclib, palbociclib, galunisertib, ipafricept, and ramucirumab are evaluated. palbociclib 155-166 HCC Homo sapiens 16-19 31024205-8 2019 In this review, HCC etiology and new therapeutic strategies that include currently approved drugs and other potential candidates of HCC such as Milciclib, palbociclib, galunisertib, ipafricept, and ramucirumab are evaluated. palbociclib 155-166 HCC Homo sapiens 132-135 31024205-8 2019 In this review, HCC etiology and new therapeutic strategies that include currently approved drugs and other potential candidates of HCC such as Milciclib, palbociclib, galunisertib, ipafricept, and ramucirumab are evaluated. LY-2157299 168-180 HCC Homo sapiens 16-19 31024205-8 2019 In this review, HCC etiology and new therapeutic strategies that include currently approved drugs and other potential candidates of HCC such as Milciclib, palbociclib, galunisertib, ipafricept, and ramucirumab are evaluated. LY-2157299 168-180 HCC Homo sapiens 132-135 31193326-4 2019 The American studies and some European studies clearly showed no relation, while the Japanese and Egyptian studies and the other European studies showed an increased risk of developing HCC after DAA exposure. daa 195-198 HCC Homo sapiens 185-188 31193326-6 2019 After reviewing the data from these different studies, it seems that some patients are at increased risk of developing HCC after DAA exposure. daa 129-132 HCC Homo sapiens 119-122 30774429-1 2019 Background: Sorafenib is the first regimen listed in the treatment algorithm for hepatocellular carcinoma (HCC) worldwide. Sorafenib 12-21 HCC Homo sapiens 107-110 30679943-10 2019 Conclusions: HBV DNA replication level is an independent risk factors for the formation of HCC MVI, and anti-hepatitis B virus treatment has an inhibitory effect on MVI formation. mogroside VI 95-98 HCC Homo sapiens 91-94 30774429-2 2019 This study aimed to assess the efficacy of sorafenib treatment for advanced HCC in a clinical practice using a nationwide population study. Sorafenib 43-52 HCC Homo sapiens 76-79 30774429-10 2019 Conclusion: The disease control rate of sorafenib in advanced HCC patients in this study seemed similarly poorer as what has been previously reported by clinical trials. Sorafenib 40-49 HCC Homo sapiens 62-65 30474170-1 2019 BACKGROUND: Occupational exposure to vinyl chloride monomer (VCM) has been established as a cause of hepatocellular carcinoma (HCC) and liver angiosarcoma (ASL). Vinyl Chloride 37-51 HCC Homo sapiens 127-130 31099615-2 2019 For more than a decade, the multikinase inhibitor sorafenib was the only U.S. Food and Drug Administration (FDA)-approved systemic therapy for HCC. Sorafenib 50-59 HCC Homo sapiens 143-146 30602007-3 2018 We systematically review this crucial topic by combining all the relevant articles to calculate the pooled HCC density after DAA treatment. daa 125-128 HCC Homo sapiens 107-110 30267080-3 2019 Objective: To compare entecavir and tenofovir in terms of the risk of HCC and death or liver transplant in patients with CHB infection. entecavir 22-31 HCC Homo sapiens 70-73 30267080-3 2019 Objective: To compare entecavir and tenofovir in terms of the risk of HCC and death or liver transplant in patients with CHB infection. Tenofovir 36-45 HCC Homo sapiens 70-73 30267080-10 2019 In the population cohort, the annual incidence rate of HCC was significantly lower in the tenofovir group (0.64 per 100 person-years [PY]) than in the entecavir group (1.06 per 100 PY). Tenofovir 90-99 HCC Homo sapiens 55-58 30267080-11 2019 By multivariable-adjusted analysis, tenofovir therapy was associated with a significantly lower risk of HCC (hazard ratio [HR], 0.61; 95% CI, 0.54-0.70) and all-cause mortality or transplant (HR, 0.77; 95% CI, 0.65-0.92) compared with entecavir. Tenofovir 36-45 HCC Homo sapiens 104-107 30267080-12 2019 The tenofovir group also showed a significantly lower risk of HCC in the 10 923-pair propensity score-matched population cohort (HR, 0.62; 95% CI, 0.54-0.70) and 869-pair propensity score-matched hospital cohort (HR, 0.68; 95% CI, 0.46-0.99) compared with the entecavir group. Tenofovir 4-13 HCC Homo sapiens 62-65 30267080-13 2019 Conclusions and Relevance: This study suggests that tenofovir treatment was associated with a significantly lower risk of HCC compared with entecavir treatment in a population-based cohort of adults with CHB; these findings were validated in a hospital cohort. Tenofovir 52-61 HCC Homo sapiens 122-125 30575322-7 2019 DNMT inhibitor decitabine treatment could increase the expression of DNAH17 in HCC cell lines. Decitabine 15-25 HCC Homo sapiens 79-82 30468662-2 2019 Aside from liver transplantation, the most effective and leading curative measure for HCC is the chemotherapeutic agent sorafenib, which is a multikinase inhibitor used for treating late-stage HCC. Sorafenib 120-129 HCC Homo sapiens 86-89 30468662-2 2019 Aside from liver transplantation, the most effective and leading curative measure for HCC is the chemotherapeutic agent sorafenib, which is a multikinase inhibitor used for treating late-stage HCC. Sorafenib 120-129 HCC Homo sapiens 193-196 30602007-10 2018 Furthermore, HCC occurrence rate following DAA-induced sustained virological response (SVR) was 2.1/100 py (95% CI: 1.4, 3.4); however, the rate in patients without SVR was 9.1/100 py (95% CI: 5.4, 15.3). daa 43-46 HCC Homo sapiens 13-16 30602007-11 2018 HCV cured after DAA therapy could induce a reduction of 78% in the risk of HCC occurrence compared with non-responders. daa 16-19 HCC Homo sapiens 75-78 30091371-1 2018 AIM: This multicenter field-practice study evaluates outcomes of long-term sorafenib in hepatocellular carcinoma (HCC) patients. Sorafenib 75-84 HCC Homo sapiens 114-117 30091371-2 2018 METHODS: Consecutive HCC patients on sorafenib were enrolled. Sorafenib 37-46 HCC Homo sapiens 21-24 30091371-10 2018 CONCLUSION: Sorafenib could result in long-term control of HCC in a relevant proportion of patients. Sorafenib 12-21 HCC Homo sapiens 59-62 30398482-3 2018 In particular, sorafenib was the only registered drug for the treatment of unresectable HCC until 2017. Sorafenib 15-24 HCC Homo sapiens 88-91 30364796-4 2018 With the introduction of multimodality imaging, combination of computed tomography with nuclear medicine imaging, particularly, 18F-fluorodeoxyglucose positron emission tomography fulfilled an unmet need and rapidly became a critical component of HCC management. Fluorodeoxyglucose F18 128-150 HCC Homo sapiens 247-250 30364796-5 2018 This review article will focus on the use of 18F-fluorodeoxyglucose positron emission tomography combined with computed tomography in the pre-transplant evaluation of HCC patients with special discussion on its ability to predict HCC recurrence after liver transplantation. Fluorodeoxyglucose F18 45-67 HCC Homo sapiens 167-170 30052303-1 2018 BACKGROUND & AIMS: The development of hepatocellular carcinoma (HCC) in patients with chronic hepatitis B (CHB) has decreased due to potent antiviral agents. Adenosine Monophosphate 12-15 HCC Homo sapiens 68-71 30052303-3 2018 This study aimed to compare the incidence of HCC within and beyond the first 5 years of entecavir (ETV) in treatment-naive Korean patients with CHB. entecavir 99-102 HCC Homo sapiens 45-48 30398482-6 2018 This paper deals with the most recent data concerning cabozantinib and ramucirumab, the two drugs that have recently demonstrated efficacy in phase III, randomized, controlled trials in HCC patients who failed previous treatment with sorafenib. cabozantinib 54-66 HCC Homo sapiens 186-189 29390939-1 2018 PURPOSE: To retrospectively investigate the efficacy of multipronged ethanol ablation with or without transarterial chemoembolization (TACE) in the treatment of intermediate hepatocellular carcinoma (HCC) (3.1-5.0 cm in diameter) at high-risk locations . Ethanol 69-76 HCC Homo sapiens 200-203 30505582-0 2018 Single institution experience of sorafenib for advanced HCC in a US tertiary care hospital. Sorafenib 33-42 HCC Homo sapiens 56-59 30505582-1 2018 Background: Sorafenib is first line chemotherapy for advanced hepatocellular carcinoma (HCC). Sorafenib 12-21 HCC Homo sapiens 88-91 30505582-3 2018 In this context, we present a single institution experience with sorafenib for HCC in a tertiary inner-city safety-net hospital of Chicago. Sorafenib 65-74 HCC Homo sapiens 79-82 30505582-4 2018 Methods: We retrospectively analyzed electronic medical records of patients with HCC (confirmed with radiographic criteria and/or biopsy) who received sorafenib from 2009 to 2016. Sorafenib 151-160 HCC Homo sapiens 81-84 30505582-9 2018 Alcohol was the leading cause of cirrhosis, 64% of them had Child-Turcotte-Pugh (CTP) class A cirrhosis or did not have cirrhosis and 73% had Barcelona stage C HCC at the time of sorafenib initiation. Alcohols 0-7 HCC Homo sapiens 160-163 30505582-12 2018 Conclusions: Overall survival of patients with HCC treated with sorafenib in US is lower than those observed in cohorts from Europe or Japan. Sorafenib 64-73 HCC Homo sapiens 47-50 30505582-13 2018 HCV infection could be a marker of benefit in those treated with sorafenib for HCC. Sorafenib 65-74 HCC Homo sapiens 79-82 29390939-6 2018 CONCLUSION: Multipronged ethanol ablation combined with TACE could improve local tumor control for patients with intermediate HCC at high-risk locations when compared with multipronged ethanol ablation alone, although the survival outcomes were comparable. Ethanol 25-32 HCC Homo sapiens 126-129 29958496-2 2018 Here, we present the use of acetylated polyethylenimine (PEI)-entrapped gold nanoparticles (Ac-PE-AuNPs) without antifouling modification for negative CT imaging of HCC. Polyethyleneimine 39-55 HCC Homo sapiens 165-168 30214375-3 2018 Moreover, various recent preclinical and clinical studies about the performances of "two efficient agents, sorafenib or natural killer (NK) cells", against HCC cells were investigated. Sorafenib 107-116 HCC Homo sapiens 156-159 30214375-4 2018 In addition, the focus this review was on the chemo-immunotherapy approach, correlation between sorafenib and NK cells and their effects on the performance of each other for better suppression of HCC. Sorafenib 96-105 HCC Homo sapiens 196-199 30214375-5 2018 Conclusion: It was concluded that combinational therapy with sorafenib and NK cells might improve the outcome of applied therapeutic approaches for HCC patients. Sorafenib 61-70 HCC Homo sapiens 148-151 30061739-4 2018 Sorafenib was the first systemic therapy approved for patients with advanced-stage HCC, after a landmark study revealed an improvement in median overall survival from 8 to 11 months. Sorafenib 0-9 HCC Homo sapiens 83-86 30181772-0 2018 Tenofovir disoproxil fumarate reduce incidence of HCC development in CHB-patients with compensated cirrhosis. Tenofovir 0-29 HCC Homo sapiens 50-53 30181772-2 2018 We aim to investigate whether CHB-related HCC patients receiving nucleoside analogue regimen or not have a different prognosis. Nucleosides 65-75 HCC Homo sapiens 42-45 30181772-9 2018 The cumulative probability of HCC development in TDF-contained group were significantly lower than it in non-TDF-contained group (p < 0.05). Tenofovir 49-52 HCC Homo sapiens 30-33 30181772-9 2018 The cumulative probability of HCC development in TDF-contained group were significantly lower than it in non-TDF-contained group (p < 0.05). Tenofovir 109-112 HCC Homo sapiens 30-33 29958496-2 2018 Here, we present the use of acetylated polyethylenimine (PEI)-entrapped gold nanoparticles (Ac-PE-AuNPs) without antifouling modification for negative CT imaging of HCC. Polyethyleneimine 57-60 HCC Homo sapiens 165-168 29958496-2 2018 Here, we present the use of acetylated polyethylenimine (PEI)-entrapped gold nanoparticles (Ac-PE-AuNPs) without antifouling modification for negative CT imaging of HCC. ac-pe 92-97 HCC Homo sapiens 165-168 29554896-4 2018 METHODS: The proliferation inhibition of ESC on HCC cells was measured with MTT assay. monooxyethylene trimethylolpropane tristearate 76-79 HCC Homo sapiens 48-51 29851093-2 2018 AIM: Characterize HCC recurrence patterns after DAA therapy. daa 48-51 HCC Homo sapiens 18-21 29851093-3 2018 METHODS: Two reviewers searched MEDLINE and SCOPUS from January 2015 to December 2017 and identified studies evaluating HCC recurrence patterns following DAA therapy. daa 154-157 HCC Homo sapiens 120-123 29851093-6 2018 RESULTS: Among 24 studies (n = 1820 patients), the proportion of patients with HCC recurrence following DAA therapy ranged from 0% to 59% (pooled estimate 24.4%; 95% CI: 18.4%-30.4%). daa 104-107 HCC Homo sapiens 79-82 29851093-13 2018 However, data characterising HCC recurrence after DAA therapy are of limited quality, highlighting the need for high quality prospective studies. daa 50-53 HCC Homo sapiens 29-32 29330919-2 2018 METHODS: An electronic search of reports published before August 2017 was carried out to identify comparative studies evaluating LH versus OH for HCC. Luteinizing Hormone 129-131 HCC Homo sapiens 146-149 29718963-1 2018 OBJECTIVE: The purpose of this study is to generate an ultrasonic nanobubble (NB)-mediated purine nucleoside phosphorylase (PNP)/fludarabine suicide gene system for the treatment of human hepatocellular carcinoma (HCC). fludarabine 129-140 HCC Homo sapiens 188-218 29718963-8 2018 The pcDNA3.1(+)/PNP plasmid was efficiently transfected into HCC cells using ultrasonic NBs. Niobium 88-91 HCC Homo sapiens 61-64 29718963-15 2018 The PNP/fludarabine suicide gene system inhibited the growth of HCC cells, induced HCC cell apoptosis, and caused a notable bystander effect at a low fludarabine concentration. fludarabine 8-19 HCC Homo sapiens 64-67 29718963-15 2018 The PNP/fludarabine suicide gene system inhibited the growth of HCC cells, induced HCC cell apoptosis, and caused a notable bystander effect at a low fludarabine concentration. fludarabine 8-19 HCC Homo sapiens 83-86 29924049-2 2018 Although sorafenib is currently recommended as standard treatment for advanced HCC, its treatment efficacy is limited. Sorafenib 9-18 HCC Homo sapiens 79-82 29924049-3 2018 Effective treatments for patients with advanced HCC that progresses on or after sorafenib treatment or patients who are intolerant of sorafenib remain an unmet medical need. Sorafenib 80-89 HCC Homo sapiens 48-51 29924049-4 2018 PATIENT CONCERNS: We report an advanced HCC patient with many lung metastases who failed sorafenib treatment. Sorafenib 89-98 HCC Homo sapiens 40-43 29924049-5 2018 DIAGNOSES: Sorafenib refractory HCC patient with a large number of lung metastases. Sorafenib 11-20 HCC Homo sapiens 32-35 29924049-9 2018 Finally, only a few lesions remained LESSONS:: Apatinib alone may be a good second-line therapy for advanced HCC patients who are refractory to sorafenib. apatinib 47-55 HCC Homo sapiens 109-112 29122695-2 2018 Non-alcoholic fatty liver disease (NAFLD) is becoming a major cause of HCC, with a steadily rising trend compared to viral or alcohol-induced chronic hepatitis. Alcohols 4-11 HCC Homo sapiens 71-74 29872724-5 2018 The HCC-associated inflammation can be initiated and propagated by extrinsic pathways through activation of pattern-recognition receptors (PRRs) by pathogen-associated molecule patterns (PAMPs) derived from gut microflora or damage-associated molecule patterns (DAMPs) released from dying liver cells. pamps 187-192 HCC Homo sapiens 4-7 29166610-3 2017 Cisd2 haploinsufficiency causes a low incidence (20%) of spontaneous HCC and promotes HBV-associated and DEN-induced HCC; conversely, 2-fold overexpression of Cisd2 suppresses HCC in these models. Diethylnitrosamine 105-108 HCC Homo sapiens 117-120 28823713-14 2017 CONCLUSIONS: EASL/mRECIST criteria and image subtraction have excellent diagnostic performance for predicting CPN in HCC treated with LRT, with image subtraction correlating best with pathologic degree of tumor necrosis. cpn 110-113 HCC Homo sapiens 117-120 29225478-6 2017 In this article, we look at approaches used to identify biomarkers of HCC using proton nuclear magnetic resonance (1H-NMR) spectroscopy of urine samples. Hydrogen 115-117 HCC Homo sapiens 70-73 29166610-3 2017 Cisd2 haploinsufficiency causes a low incidence (20%) of spontaneous HCC and promotes HBV-associated and DEN-induced HCC; conversely, 2-fold overexpression of Cisd2 suppresses HCC in these models. Diethylnitrosamine 105-108 HCC Homo sapiens 117-120 28651307-7 2017 The cumulative incidence rate of HCC was significantly higher in patients with higher LS values (>=10 kPa) than in those with lower LS values (<10 kPa) (p=0.001). leucylserine 86-88 HCC Homo sapiens 33-36 28651307-7 2017 The cumulative incidence rate of HCC was significantly higher in patients with higher LS values (>=10 kPa) than in those with lower LS values (<10 kPa) (p=0.001). leucylserine 135-137 HCC Homo sapiens 33-36 28532995-1 2017 BACKGROUND & AIMS: Our increasing understanding of hepatocellular carcinoma (HCC) biology holds promise for personalized care, however its translation into clinical practice requires a precise knowledge of its relationship to tumour phenotype. Adenosine Monophosphate 12-15 HCC Homo sapiens 81-84 28910823-3 2017 The current study focusses on camptothecin as a novel NRF2 inhibitor to sensitise HCC to chemotherapy. Camptothecin 30-42 HCC Homo sapiens 82-85 28815645-2 2017 advanced hepatocellular carcinoma (HCC) AIM: To explore potential biomarkers of lenalidomide efficacy as second-line therapy for HCC. Lenalidomide 80-92 HCC Homo sapiens 35-38 28815645-2 2017 advanced hepatocellular carcinoma (HCC) AIM: To explore potential biomarkers of lenalidomide efficacy as second-line therapy for HCC. Lenalidomide 80-92 HCC Homo sapiens 129-132 28815645-16 2017 CONCLUSIONS: Lenalidomide exhibited moderate activity as second-line therapy for advanced HCC. Lenalidomide 13-25 HCC Homo sapiens 90-93 29234637-1 2017 Aim/Background: After the introduction of sorafenib in the treatment of advanced hepatocellular carcinoma (HCC), different studies tried to evaluate whether other systemic therapies can improve survival. Sorafenib 42-51 HCC Homo sapiens 107-110 28609188-1 2017 OBJECTIVE: The purpose of this study is to evaluate the effect of subtraction images of gadoxetic acid-enhanced MRI on the image interpretation of focal hepatic lesions in patients at risk for hepatocellular carcinoma (HCC). gadolinium ethoxybenzyl DTPA 88-102 HCC Homo sapiens 219-222 28981732-4 2017 Methods: We had two patient cohorts, both comprising patients who received sorafenib-containing therapy as the first-line treatment for advanced HCC. Sorafenib 75-84 HCC Homo sapiens 145-148 28953220-2 2017 An ALS drug, Riluzole, has been shown to induce two different anticancer effects on hepatocellular carcinoma (HCC). Riluzole 13-21 HCC Homo sapiens 110-113 28946672-2 2017 Case-control studies from different countries report that chronic ethanol consumption is associated with an approximately 2-fold increased odds ratio for hepatocellular carcinoma (HCC). Ethanol 66-73 HCC Homo sapiens 154-184 28946672-3 2017 Despite the substantial epidemiologic data in humans demonstrating that chronic alcohol consumption is a major risk factor for HCC development, the pathways causing alcohol-induced liver cancer are poorly understood. Alcohols 80-87 HCC Homo sapiens 127-130 28562104-13 2017 CONCLUSIONS: LC with significant portal hypertension (varices or ascites), alcohol consumption, and older age at the time of starting antiviral therapy are independent predictors for future HCC development. Alcohols 75-82 HCC Homo sapiens 190-193 28542038-12 2017 mTOR inhibition can improve outcomes of doxorubicin treatment in HCC. Doxorubicin 40-51 HCC Homo sapiens 65-68 28389847-4 2017 A total of 40, 47, 29, and 33 N-glycan peaks were identified and annotated from HV, HB, HC, and HCC groups, respectively. n-glycan 30-38 HCC Homo sapiens 96-99 28839428-2 2017 The well-established causes of HCC are chronic liver infections such as hepatitis B virus or chronic hepatitis C virus, nonalcoholic fatty liver disease, consumption of aflatoxins and tobacco smocking. Aflatoxins 169-179 HCC Homo sapiens 31-34 28389847-7 2017 The proportion of fucosylated N-glycans was apparently increased in the HCC group (84.8%) than in any other group (73.1% +- 0.01), however, the proportion of sialylated N-glycans was decreased in HCC group (12.1%) than in any other group (17.23% +- 0.003). n-glycans 30-39 HCC Homo sapiens 72-75 28389847-7 2017 The proportion of fucosylated N-glycans was apparently increased in the HCC group (84.8%) than in any other group (73.1% +- 0.01), however, the proportion of sialylated N-glycans was decreased in HCC group (12.1%) than in any other group (17.23% +- 0.003). n-glycans 169-178 HCC Homo sapiens 72-75 28389847-7 2017 The proportion of fucosylated N-glycans was apparently increased in the HCC group (84.8%) than in any other group (73.1% +- 0.01), however, the proportion of sialylated N-glycans was decreased in HCC group (12.1%) than in any other group (17.23% +- 0.003). n-glycans 169-178 HCC Homo sapiens 196-199 28389847-8 2017 Our data provide pivotal information to distinguish between HBV-associated hepatitis, cirrhosis and HCC, and facilitate the discovery of biomarkers for HCC during its early stages based on precise alterations of N-linked glycans in saliva. n-linked glycans 212-228 HCC Homo sapiens 152-155 28627705-8 2017 Moreover, inactivation of NFkappaB blocked PD-L1/STAT3/DNMT1 pathway in sorafenib-resistant HCC cells. Sorafenib 72-81 HCC Homo sapiens 92-95 28627705-9 2017 Functionally, genetic or pharmacological disruption of PD-L1 or/and DNMT1 sensitize HCC resistance to sorafenib. Sorafenib 102-111 HCC Homo sapiens 84-87 28627705-1 2017 Molecule-targeted therapy, such as sorafenib, is one of the effectively therapeutic options for advanced hepatocellular carcinoma (HCC). Sorafenib 35-44 HCC Homo sapiens 131-134 28627705-10 2017 Importantly, dual inactivation of PD-L1 and DNMT1 by their inhibitor synergistically disrupts the colony formation of sorafenib-resistant HCC cells. Sorafenib 118-127 HCC Homo sapiens 138-141 28627705-2 2017 However, acquired resistance to sorafenib has been found in some HCC patients, resulting in poor prognosis. Sorafenib 32-41 HCC Homo sapiens 65-68 28627705-11 2017 These results demonstrate that targeting NFkappaB/PDL1/STAT3/DNMT1 axis is a new therapeutic strategy for preventing or overcoming the acquired resistance to sorafenib in HCC patients. Sorafenib 158-167 HCC Homo sapiens 171-174 28627705-4 2017 In this study, by inducing sorafenib-resistant HCC cell lines, we investigated their molecular and functional characteristics. Sorafenib 27-36 HCC Homo sapiens 47-50 28346420-9 2017 In keeping with this, loss of 5hmC was demonstrated in COX-2-induced HCC. 5-hydroxymethylcytosine 30-34 HCC Homo sapiens 69-72 28627705-5 2017 Our data indicated that highly upregulated DNMT1 was positively correlated with PD-L1 overexpression in sorafenib-resistant HCC cells. Sorafenib 104-113 HCC Homo sapiens 124-127 28744453-3 2017 Sorafenib is a treatment of choice for patients with performance status 1 or 2 and/or macrovascular invasion or extrahepatic spread, and regorafenib is the only systemic treatment found to provide survival benefit in HCC patients progressing on sorafenib treatment. regorafenib 137-148 HCC Homo sapiens 217-220 28638790-3 2017 Sorafenib, a multikinase inhibitor, is the only currently approved agent for systemic therapy in patients with advanced stage HCC and early stage liver disease. Sorafenib 0-9 HCC Homo sapiens 126-129 28370295-9 2017 In a diethylnitrosamine-induced murine model of HCC, genetic blocking of HMGB1 in hypoxic tumors resulted in a significant decrease in tumor growth. Diethylnitrosamine 5-23 HCC Homo sapiens 48-51 28437801-0 2017 [Regorafenib - a revolution in the systemic treatment options of HCC?] regorafenib 1-12 HCC Homo sapiens 65-69 28638790-7 2017 In this review our aim is to highlight in depth the current position of Sorafenib in the armamentarium against HCC and how that has evolved over time in its use either as a single agent or in combination with other therapies. Sorafenib 72-81 HCC Homo sapiens 111-114 28109738-2 2017 Here, we present the first case of genotype 2 HCV reactivation due to antiemetic steroid therapy during chemotherapy for hepatocellular carcinoma (HCC), which was verified by not only increased viral load but also pathological exacerbation of liver injury during HCV reactivation. Steroids 81-88 HCC Homo sapiens 147-150 28694740-4 2017 Chronic liver disease due to hepatitis B virus or hepatitis C virus and alcohol accounts for the majority of HCC cases. Alcohols 72-79 HCC Homo sapiens 109-112 28694740-8 2017 There is a significant role of both intrinsic genetic risk factors and extrinsic influences such as alcohol or viral infections that lead to the development of HCC. Alcohols 100-107 HCC Homo sapiens 160-163 28342103-2 2017 The aim of the present study was to report our experience with adjuvant use of 131I-lipiodol after curative treatment of HCC in terms of recurrence and survival in a large cohort of patients with a long follow-up. 131i-lipiodol 79-92 HCC Homo sapiens 121-124 28342103-3 2017 METHODS: All patients treated with 131I-lipiodol after curative treatment of HCC in two French centers from 1991 to 2009 were included in a retrospective cohort study. 131i-lipiodol 35-48 HCC Homo sapiens 77-80 28342103-11 2017 CONCLUSION: Our results suggest that the effect of 131I-lipiodol after curative treatment of HCC could be related to a beneficial impact on risk factors of early tumor recurrence. 131i-lipiodol 51-64 HCC Homo sapiens 93-96 28394358-7 2017 Finally, we showed that the proteasome inhibitor bortezomib mitigated the Warburg effect by inhibiting FBP1 degradation in HCC. Bortezomib 49-59 HCC Homo sapiens 123-126 28487602-6 2017 It remains controversial whether HBV and alcohol synergistically increase the incidence of HCC. Alcohols 41-48 HCC Homo sapiens 91-94 28480065-4 2017 Sorafenib remains the only drug approved for systemic treatment for advanced HCC. Sorafenib 0-9 HCC Homo sapiens 77-80 28219642-1 2017 Cisplatin is a main compound for human hepatocellular carcinoma (HCC) chemotherapies, but it has certain cytotoxicity during applications. Cisplatin 0-9 HCC Homo sapiens 39-69 28219642-4 2017 In order to investigate whether combination usage of RA and cisplatin can be priority to the later drug"s effect development and its toxicity reduction in HCC, both of two drugs were treated 24 h or 48 h in QGY-7703 cells for estimating their abilities in tumor cell proliferation inhibition. raddeanin A 53-55 HCC Homo sapiens 155-158 28219642-4 2017 In order to investigate whether combination usage of RA and cisplatin can be priority to the later drug"s effect development and its toxicity reduction in HCC, both of two drugs were treated 24 h or 48 h in QGY-7703 cells for estimating their abilities in tumor cell proliferation inhibition. Cisplatin 60-69 HCC Homo sapiens 155-158 28219642-9 2017 All these consequences reflect RA plays an important role in enhancing the therapeutic effect of cisplatin in HCC. raddeanin A 31-33 HCC Homo sapiens 110-113 28219642-9 2017 All these consequences reflect RA plays an important role in enhancing the therapeutic effect of cisplatin in HCC. Cisplatin 97-106 HCC Homo sapiens 110-113 28260092-1 2017 At advanced stages of hepatocellular carcinoma (HCC), the multikinase inhibitor sorafenib is the only effective treatment. Sorafenib 80-89 HCC Homo sapiens 48-51 28260092-5 2017 Sorafenib treatment effectively suppressed the expression of angiogenic factors and activation of the Raf/MEK/ERK pathway in HOXB9-expressing HCC cell lines. Sorafenib 0-9 HCC Homo sapiens 142-145 28260092-6 2017 Consistent with these findings, HCC patients, whose cancer expressed high levels of HOXB9, exhibited increased overall survival upon sorafenib treatment. Sorafenib 133-142 HCC Homo sapiens 32-35 28260092-7 2017 Collectively, these results suggest that HOXB9 expression in HCC could be a surrogate marker for a beneficial response to sorafenib treatment. Sorafenib 122-131 HCC Homo sapiens 61-64 28100026-4 2017 In this study, a rat model with liver cirrhosis and diffused HCC was established by administration of diethylnitrosamine. Diethylnitrosamine 102-120 HCC Homo sapiens 61-64 27911488-2 2017 The 2 well recognized HCC risk factors in thalassemia are iron overload and chronic viral infection with hepatitis C. The carcinogenicity of iron is related to its induction of oxidative damage, which results in genotoxicity, and to immunologic dysregulation, which attenuates cancer immune surveillance. Iron 58-62 HCC Homo sapiens 22-25 27911488-2 2017 The 2 well recognized HCC risk factors in thalassemia are iron overload and chronic viral infection with hepatitis C. The carcinogenicity of iron is related to its induction of oxidative damage, which results in genotoxicity, and to immunologic dysregulation, which attenuates cancer immune surveillance. Iron 141-145 HCC Homo sapiens 22-25 27911488-4 2017 Screening patients who have thalassemia using magnetic resonance imaging-based liver iron concentration measurement and liver ultrasound is recommended for early detection of iron overload and HCC, respectively. Iron 85-89 HCC Homo sapiens 193-196 27755152-8 2017 Safety and efficacy of sorafenib and other treatment modalities should be further studied and offered as deemed applicable to HIV patients diagnosed with HCC. Sorafenib 23-32 HCC Homo sapiens 154-157 28451419-2 2017 The actual reference standard systemic treatment for advanced HCC is represented by sorafenib, a multi-targeted orally active small-molecule tyrosine kinase inhibitor. Sorafenib 84-93 HCC Homo sapiens 62-65 28451419-5 2017 In the present study, the case of a patient with no known cardiovascular risk factors affected by highly enhancing advanced HCC in cirrhotic liver, who died during successful sorafenib monotherapy, is reported. Sorafenib 175-184 HCC Homo sapiens 124-127 27889576-1 2017 BACKGROUND & AIMS: The incidence and mortality of hepatocellular carcinoma (HCC) have been reported to be plateauing in the United States. Adenosine Monophosphate 12-15 HCC Homo sapiens 80-83 28243124-13 2017 These results revealed that miRNA-320a inhibits tumor proliferation and invasion by targeting c-Myc in HCC cells. mirna-320a 28-38 HCC Homo sapiens 103-106 27510230-3 2017 Chemotherapeutic agents such as doxorubicin are currently used as first-line agents for HCC therapy, but these are non-selective cytotoxic molecules with significant side effects. Doxorubicin 32-43 HCC Homo sapiens 88-91 27510230-4 2017 Sorafenib, a multi-targeted tyrosine kinase inhibitor, is the only approved targeted drug for HCC patients. Sorafenib 0-9 HCC Homo sapiens 94-97 28134936-0 2017 Hepatocyte-specific Smad7 deletion accelerates DEN-induced HCC via activation of STAT3 signaling in mice. Diethylnitrosamine 47-50 HCC Homo sapiens 59-62 27569777-1 2016 BACKGROUND & AIMS: This study evaluates trends in hepatocellular carcinoma (HCC) among people with hepatitis B virus (HBV) or hepatitis C virus (HCV) infection in New South Wales (NSW), Australia between 2000 and 2014. Adenosine Monophosphate 12-15 HCC Homo sapiens 80-83 30183165-5 2017 Using light and electronmicroscopy and flow cytometry, structural features of autophagy and apoptosis in HCC cells after their incubationwith various forms of lithium salts has been revealed. Lithium 159-166 HCC Homo sapiens 105-108 30183165-7 2017 At the same time, nanoscale lithiumcitrate mainly induced apoptosis, and nanosized form of lithium carbonate, along with apoptosis, inducedautophagic death of HCC-29cells. Lithium Carbonate 91-108 HCC Homo sapiens 159-162 28340971-2 2016 Animal models had shown glutathione species in plasma reflects liver glutathione state and it could be a surrogate for the detection of hepatocellular carcinoma (HCC). Glutathione 24-35 HCC Homo sapiens 162-165 28340971-3 2016 METHODS: The present study aimed to translate methods to the human and to explore the role of glutathione/metabolic prints in the progression of liver dysfunction and in the detection of HCC. Glutathione 94-105 HCC Homo sapiens 187-190 28340971-10 2016 CONCLUSIONS: Glutathione species and metabolic prints defined liver disease severity and may serve as surrogate for the detection of HCC in patients with established cirrhosis. Glutathione 13-24 HCC Homo sapiens 133-136 27320967-4 2016 However, hepatocellular carcinoma (HCC) developed about 20 months after the administration of danazol. Danazol 94-101 HCC Homo sapiens 35-38 27872682-10 2016 However, most patients with recurrent HCC considered for SLT are untransplantable cases due to HCC recurrence beyond MC or comorbidity. Methylcholanthrene 117-119 HCC Homo sapiens 38-41 27277188-7 2016 For the isolated NAbs, the epitopic fragments in hCC sequence were identified by MS-assisted proteolytic excision of the immune complex and compared with the ones predicted theoretically. nabs 17-21 HCC Homo sapiens 49-52 27277188-8 2016 The knowledge of hCC fragments binding to NAbs and other ligands may contribute to the search for new diagnostic methods for amyloidosis of different types and the search for their treatment. nabs 42-46 HCC Homo sapiens 17-20 27320967-5 2016 In humans, several cases of development of HCC after the administration of danazol have been reported. Danazol 75-82 HCC Homo sapiens 43-46 27320967-6 2016 The present report describes a case of HCC development in a dog after chronic administration of danazol in addition to other immunosuppressive drugs. Danazol 96-103 HCC Homo sapiens 39-42 27633066-6 2016 In vitro, it has been discovered that treatment of HCC cells with a miR-139-5p mimic lead to inhibition of cell growth and migration. mir-139-5p 68-78 HCC Homo sapiens 51-54 27803608-1 2016 BACKGROUND AND AIMS: In this pilot study, we assessed the safety and tolerability of combining sorafenib with 90Y radioembolization for the treatment of unresectable hepatocellular carcinoma (hcc). Sorafenib 95-104 HCC Homo sapiens 192-195 26961293-10 2016 These results suggest that the selenium and manganese content in primary HCC tissues could influence the response of the HCC cells to carboplatin and doxorubicin. Selenium 31-39 HCC Homo sapiens 73-76 26961293-10 2016 These results suggest that the selenium and manganese content in primary HCC tissues could influence the response of the HCC cells to carboplatin and doxorubicin. Selenium 31-39 HCC Homo sapiens 121-124 26961293-10 2016 These results suggest that the selenium and manganese content in primary HCC tissues could influence the response of the HCC cells to carboplatin and doxorubicin. Manganese 44-53 HCC Homo sapiens 73-76 26961293-10 2016 These results suggest that the selenium and manganese content in primary HCC tissues could influence the response of the HCC cells to carboplatin and doxorubicin. Manganese 44-53 HCC Homo sapiens 121-124 26961293-10 2016 These results suggest that the selenium and manganese content in primary HCC tissues could influence the response of the HCC cells to carboplatin and doxorubicin. Carboplatin 134-145 HCC Homo sapiens 73-76 27803608-15 2016 CONCLUSIONS: Preliminary results demonstrate the safety and tolerability of combining 90Y radioembolization and sorafenib for advanced hcc. Sorafenib 112-121 HCC Homo sapiens 135-138 26961293-10 2016 These results suggest that the selenium and manganese content in primary HCC tissues could influence the response of the HCC cells to carboplatin and doxorubicin. Carboplatin 134-145 HCC Homo sapiens 121-124 27699089-2 2016 We demonstrate systemic administration of a Cy5.5-labeled peptide specific for epidermal growth factor receptor (EGFR) to target HCC in vivo in a mouse xenograft model. CY5.5 cyanine dye 44-49 HCC Homo sapiens 129-132 26961293-10 2016 These results suggest that the selenium and manganese content in primary HCC tissues could influence the response of the HCC cells to carboplatin and doxorubicin. Doxorubicin 150-161 HCC Homo sapiens 73-76 26961293-10 2016 These results suggest that the selenium and manganese content in primary HCC tissues could influence the response of the HCC cells to carboplatin and doxorubicin. Doxorubicin 150-161 HCC Homo sapiens 121-124 27621761-2 2016 Sorafenib is proved to be effective for advanced HCC by two large randomized controlled trials in 2008 and 2009. Sorafenib 0-9 HCC Homo sapiens 49-52 27621761-3 2016 Therefore it stands to reason to expect that adjuvant sorafenib may improve post-surgery outcomes of patients with HCC. Sorafenib 54-63 HCC Homo sapiens 115-118 27621761-4 2016 However, many questions still exist about the value of sorafenib for patients with HCC after surgery or transarterial chemoembolization. Sorafenib 55-64 HCC Homo sapiens 83-86 27373617-1 2016 In this review we critically assess the literature to evaluate the level of risk posed by alcohol as both a primary etiology of hepatocellular carcinoma (HCC) and as a cofactor in its development. Alcohols 90-97 HCC Homo sapiens 128-158 27373617-2 2016 Although there have been conflicting findings, based on the body of evidence to date, it appears that the linkage between compensated alcoholic liver disease-associated cirrhosis and HCC is best characterized as medium-high risk, with the risk increasing with age and with quantity and duration of alcohol consumption and is more pronounced in females. Alcohols 134-141 HCC Homo sapiens 183-186 27373617-4 2016 Alcohol clearly interacts with other etiologies and conditions including viral hepatitis B and C, hereditary hemochromatosis, diabetes, and obesity to increase the risk for developing HCC, either synergistically or additively. Alcohols 0-7 HCC Homo sapiens 184-187 27158749-3 2016 The main risk factors for developing HCC are well known and include hepatitis B and C virus infection, alcohol intake and ingestion of the fungal metabolite aflatoxin B1. Alcohols 103-110 HCC Homo sapiens 37-40 27478537-5 2016 HCC that presents beyond MC initially can be downstaged with locoregional therapy (LRT). Methylcholanthrene 25-27 HCC Homo sapiens 0-3 27359325-9 2016 Multivariate Cox regression analysis showed that age > 65 years, low triglyceride levels and high gamma-glutamyl transferase levels were independently associated with an increased risk of HCC. Triglycerides 72-84 HCC Homo sapiens 191-194 26581909-6 2016 BDNF was then overexpressed in HepG2 and SNU-182 cells to evaluate its selective effect on miR-15a-5p in HCC modulation. mir-15a-5p 91-101 HCC Homo sapiens 105-108 26581909-7 2016 MiR-15a-5p is aberrantly downregulated in in vitro HCC cell lines and in vivo HCC clinical specimens. mir-15a-5p 0-10 HCC Homo sapiens 51-54 26581909-7 2016 MiR-15a-5p is aberrantly downregulated in in vitro HCC cell lines and in vivo HCC clinical specimens. mir-15a-5p 0-10 HCC Homo sapiens 78-81 26581909-9 2016 MiR-15a-5p selectively and negatively regulated BDNF at both gene and protein levels in HCC cells. mir-15a-5p 0-10 HCC Homo sapiens 88-91 26581909-11 2016 Our study demonstrated that miR-15a-5p is a tumor suppressor in HCC and its regulation is through BDNF in HCC. mir-15a-5p 28-38 HCC Homo sapiens 64-67 26581909-11 2016 Our study demonstrated that miR-15a-5p is a tumor suppressor in HCC and its regulation is through BDNF in HCC. mir-15a-5p 28-38 HCC Homo sapiens 106-109 27478537-2 2016 After initially dismal outcomes, the Milan criteria (MC) (single HCC <= 5 cm or up to 3 HCCs <= 3 cm) have been adopted worldwide to select HCC patients for LT, however cumulative experience has shown that MC can be too strict. Methylcholanthrene 53-55 HCC Homo sapiens 65-68 27128435-1 2016 BACKGROUND & AIMS: The fibrosis stage, which is evaluated by the distribution pattern of collagen fibers, is a major predictor for the development of hepatocellular carcinoma (HCC) for patients with hepatitis C. Meanwhile, the role of elastin fibers has not yet been elucidated. Adenosine Monophosphate 12-15 HCC Homo sapiens 180-183 27080032-6 2016 In the DEN-induced HCC mouse model, intravenous injection of sgp130 attenuated hepatic fibrosis at 16 weeks and reduced the initiation and progression of primary HCC at 36 weeks. Diethylnitrosamine 7-10 HCC Homo sapiens 19-22 27158749-3 2016 The main risk factors for developing HCC are well known and include hepatitis B and C virus infection, alcohol intake and ingestion of the fungal metabolite aflatoxin B1. Aflatoxin B1 157-169 HCC Homo sapiens 37-40 27158749-8 2016 At more developed stages, only chemoembolization (for intermediate HCC) and sorafenib (for advanced HCC) have shown survival benefits. Sorafenib 76-85 HCC Homo sapiens 100-103 26933996-2 2016 In the current study we assessed via mass spectrometry serum concentrations of sphingolipid metabolites in a series of 122 patients with hepatocellular carcinoma (HCC) compared to an age- and sex-matched series of 127 patients with cirrhosis. Sphingolipids 79-91 HCC Homo sapiens 163-166 26933996-3 2016 We observed a highly significant upregulation of long and very long chain ceramides (C16-C24) in the serum of patients with HCC as compared to patients with cirrhosis (P < 0.001). Ceramides 74-83 HCC Homo sapiens 124-127 26933996-4 2016 Accordingly, dihydro-ceramides, synthetic precursors of ceramides and notably sphingosine, sphingosine-1-phosphate (S1P) and sphinganine-1-phosphate (SA1P) were upregulated in patients with HCC (P < 0.001). dihydroceramide 13-30 HCC Homo sapiens 190-193 26933996-4 2016 Accordingly, dihydro-ceramides, synthetic precursors of ceramides and notably sphingosine, sphingosine-1-phosphate (S1P) and sphinganine-1-phosphate (SA1P) were upregulated in patients with HCC (P < 0.001). Ceramides 21-30 HCC Homo sapiens 190-193 26933996-4 2016 Accordingly, dihydro-ceramides, synthetic precursors of ceramides and notably sphingosine, sphingosine-1-phosphate (S1P) and sphinganine-1-phosphate (SA1P) were upregulated in patients with HCC (P < 0.001). Sphingosine 78-89 HCC Homo sapiens 190-193 26933996-4 2016 Accordingly, dihydro-ceramides, synthetic precursors of ceramides and notably sphingosine, sphingosine-1-phosphate (S1P) and sphinganine-1-phosphate (SA1P) were upregulated in patients with HCC (P < 0.001). sphingosine 1-phosphate 116-119 HCC Homo sapiens 190-193 26933996-4 2016 Accordingly, dihydro-ceramides, synthetic precursors of ceramides and notably sphingosine, sphingosine-1-phosphate (S1P) and sphinganine-1-phosphate (SA1P) were upregulated in patients with HCC (P < 0.001). dihydrosphingosine 1-phosphate 150-154 HCC Homo sapiens 190-193 26933996-6 2016 In conclusion, serum levels of sphingolipid metabolites show a significant upregulation in patients with HCC as compared to patients with cirrhosis. Sphingolipids 31-43 HCC Homo sapiens 105-108 26933996-7 2016 Particularly C16-ceramide and S1P may serve as novel diagnostic markers for the identification of HCC in patients with liver diseases. N-palmitoylsphingosine 13-25 HCC Homo sapiens 98-101 26933996-8 2016 Our data justify further investigations on the role of sphingolipids in HCC. Sphingolipids 55-68 HCC Homo sapiens 72-75 27022281-9 2016 We experimentally verified that one of these novel agents, prenylamine, induced HCC cell apoptosis using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, an acridine orange/ethidium bromide stain, and electron microscopy. Prenylamine 59-70 HCC Homo sapiens 80-83 26435297-13 2016 Chronic viral hepatitis and alcohol remain leading causes of cirrhosis and HCC. Alcohols 28-35 HCC Homo sapiens 75-78 27022281-9 2016 We experimentally verified that one of these novel agents, prenylamine, induced HCC cell apoptosis using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, an acridine orange/ethidium bromide stain, and electron microscopy. thiazolyl blue 105-165 HCC Homo sapiens 80-83 26752112-1 2016 BACKGROUND & AIMS: Many patients with hepatocellular carcinoma (HCC) have multiple lesions (primary tumors, intrahepatic metastases, multiple occurrences, satellite nodules, and tumor thrombi); these have been associated with a poor prognosis and tumor recurrence after surgery. Adenosine Monophosphate 12-15 HCC Homo sapiens 68-71 27028578-13 2016 Finally, in patients with advanced HCC with preserved liver function, sorafenib is the only approved systemic drug that has demonstrated a survival benefit and is the standard of care in this group of patients. Sorafenib 70-79 HCC Homo sapiens 35-38 26985932-1 2016 The purpose of this study was to investigate the effect of ST2825, an inhibitor of myeloid differentiation factor 88 (MyD88), on the proliferation and apoptosis of human hepatocellular carcinoma (HCC) cells as well as the potential mechanism and clinical significance of ST2825 in the treatment of HCC. ST2825 59-65 HCC Homo sapiens 298-301 27022281-9 2016 We experimentally verified that one of these novel agents, prenylamine, induced HCC cell apoptosis using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, an acridine orange/ethidium bromide stain, and electron microscopy. Acridine Orange 170-185 HCC Homo sapiens 80-83 27022281-9 2016 We experimentally verified that one of these novel agents, prenylamine, induced HCC cell apoptosis using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, an acridine orange/ethidium bromide stain, and electron microscopy. Ethidium 186-202 HCC Homo sapiens 80-83 26985932-8 2016 Compared with the control, ST2825 significantly inhibited the proliferation of and promoted the apoptosis of HCC cells. ST2825 27-33 HCC Homo sapiens 109-112 26985932-10 2016 ST2825 inhibits the proliferation of and promotes the apoptosis of HCC cells, thereby suggesting that ST2825 may be a new drug for HCC treatment. ST2825 0-6 HCC Homo sapiens 67-70 26985932-10 2016 ST2825 inhibits the proliferation of and promotes the apoptosis of HCC cells, thereby suggesting that ST2825 may be a new drug for HCC treatment. ST2825 0-6 HCC Homo sapiens 131-134 26985932-10 2016 ST2825 inhibits the proliferation of and promotes the apoptosis of HCC cells, thereby suggesting that ST2825 may be a new drug for HCC treatment. ST2825 102-108 HCC Homo sapiens 67-70 26985932-10 2016 ST2825 inhibits the proliferation of and promotes the apoptosis of HCC cells, thereby suggesting that ST2825 may be a new drug for HCC treatment. ST2825 102-108 HCC Homo sapiens 131-134 26754678-2 2016 This prospective multicenter trial assessed the efficacy of hepatic arterial infusion chemoembolization therapy with cisplatin suspended in lipiodol combined with 5-fluorouracil for HCC patients with portal vein tumor thrombosis. Cisplatin 117-126 HCC Homo sapiens 182-185 26733159-3 2016 HCC was induced in rats using thioacetamide (200 mg/kg). Thioacetamide 30-43 HCC Homo sapiens 0-3 26825459-3 2016 Here, we demonstrated that high glucose (HG), one of the main characteristics of diabetes, was capable of accelerating tumorigenesis in HCC cells. Glucose 32-39 HCC Homo sapiens 136-139 26825459-9 2016 Finally, we found that AG490, an inhibitor of Janus kinase, has the ability to impair AGER expression and its functions in HCC cells. alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide 23-28 HCC Homo sapiens 123-126 26929917-9 2016 An important step in the treatment of advanced HCC has been the introduction of sorafenib, the first oral, systemic drug that has provided significant improvement in survival. Sorafenib 80-89 HCC Homo sapiens 47-50 26859293-6 2016 Inhibition of autophagy by inhibitors or knockdown of Atg5 cancels galectin-1-induced cisplatin resistance in HCC cells. Cisplatin 86-95 HCC Homo sapiens 110-113 26859293-8 2016 Finally, using an in situ hepatoma mouse model, we clearly demonstrated that inhibition of galectin-1 by thiodigalactoside could significantly augment the anti-HCC effect of cisplatin. thiodigalactoside 105-122 HCC Homo sapiens 160-163 26859293-8 2016 Finally, using an in situ hepatoma mouse model, we clearly demonstrated that inhibition of galectin-1 by thiodigalactoside could significantly augment the anti-HCC effect of cisplatin. Cisplatin 174-183 HCC Homo sapiens 160-163 26859293-9 2016 Taken together, our findings offer a new insight into the chemoresistance galectin-1 causes against cisplatin treatment, and points to a potential approach to improve the efficacy of cisplatin in the treatment of HCC patients. Cisplatin 183-192 HCC Homo sapiens 213-216 26352789-1 2016 BACKGROUND & AIMS: There has been remarkable progress in the management of hepatocellular carcinoma (HCC) during the last several decades, but its effect on the prognosis of HCC patient needs clarification. Adenosine Monophosphate 12-15 HCC Homo sapiens 79-109 26352789-1 2016 BACKGROUND & AIMS: There has been remarkable progress in the management of hepatocellular carcinoma (HCC) during the last several decades, but its effect on the prognosis of HCC patient needs clarification. Adenosine Monophosphate 12-15 HCC Homo sapiens 105-108 26754678-12 2016 CONCLUSIONS: Hepatic arterial infusion chemoembolization therapy with cisplatin suspension in lipiodol combined with 5-fluorouracil is effective treatment for unresectable HCC with portal vein tumor thrombosis. Cisplatin 70-79 HCC Homo sapiens 172-175 26754678-12 2016 CONCLUSIONS: Hepatic arterial infusion chemoembolization therapy with cisplatin suspension in lipiodol combined with 5-fluorouracil is effective treatment for unresectable HCC with portal vein tumor thrombosis. Ethiodized Oil 94-102 HCC Homo sapiens 172-175 26754678-12 2016 CONCLUSIONS: Hepatic arterial infusion chemoembolization therapy with cisplatin suspension in lipiodol combined with 5-fluorouracil is effective treatment for unresectable HCC with portal vein tumor thrombosis. Fluorouracil 117-131 HCC Homo sapiens 172-175 27457348-7 2016 Sorafenib (SOR) is still the only drug approved as systemic therapy in patients with HCC, whereas immunotherapy represents a promising approach for the treatment of HCC. Sorafenib 0-9 HCC Homo sapiens 85-88 24786484-8 2016 The uptake of LA-LP and uncoupled liposomes by BEL7402 HCC cell lines was visualized using fluorescence microscopy that revealed the dependence of liposomal recognition and higher uptake of the LA-LP. la-lp 14-19 HCC Homo sapiens 55-58 26507276-3 2016 MATERIALS AND METHODS: A nationwide, retrospective cohort study of HCC patients treated with first-line TACE or TAE within the Veterans Affairs health care system (2005-2012) was performed. Chlorotrianisene 104-108 HCC Homo sapiens 67-70 26507276-3 2016 MATERIALS AND METHODS: A nationwide, retrospective cohort study of HCC patients treated with first-line TACE or TAE within the Veterans Affairs health care system (2005-2012) was performed. tae 112-115 HCC Homo sapiens 67-70 27186420-0 2016 Over expression of hyaluronan promotes progression of HCC via CD44-mediated pyruvate kinase M2 nuclear translocation. Hyaluronic Acid 19-29 HCC Homo sapiens 54-57 27186420-1 2016 Hyaluronan is expressed in hepatocellular carcinoma (HCC) as HCC generally arises from a cirrhotic liver in which excessive production and accumulation of HA leads to developing cirrhosis. Hyaluronic Acid 0-10 HCC Homo sapiens 53-56 27186420-1 2016 Hyaluronan is expressed in hepatocellular carcinoma (HCC) as HCC generally arises from a cirrhotic liver in which excessive production and accumulation of HA leads to developing cirrhosis. Hyaluronic Acid 0-10 HCC Homo sapiens 61-64 26916922-4 2016 To determine the effects of DNE on the migration and invasion in HCC cells we used a wound healing model, Boyden chamber assays, gelatin/casein zymography and Western blotting. dne 28-31 HCC Homo sapiens 65-68 26092946-1 2015 BACKGROUND: Sorafenib-everolimus combination therapy may be more effective than sorafenib monotherapy for hepatocellular carcinoma (HCC). Sorafenib 12-21 HCC Homo sapiens 106-136 26394136-1 2015 BACKGROUND/PURPOSE: Laparoscopic hepatic resection (LH) for hepatocellular carcinoma (HCC) has gradually gained ground as a safe and minimally invasive treatment, although LH for cirrhotic patients remains challenging. Luteinizing Hormone 52-54 HCC Homo sapiens 60-90 26632544-4 2015 According to the results of SHARP and ORIENTAL study, sorafenib became the standard first-line therapy since 2008 because of nearly three months of survival improvement in patients with advanced HCC. Sorafenib 54-63 HCC Homo sapiens 195-198 26632544-7 2015 Randomized controlled EACH study and retrospective AGEO study for systemic chemotherapy showed that oxaliplatin-based or gemcitabine-based regimen was effective for advanced HCC patients. Oxaliplatin 100-111 HCC Homo sapiens 174-177 26632544-7 2015 Randomized controlled EACH study and retrospective AGEO study for systemic chemotherapy showed that oxaliplatin-based or gemcitabine-based regimen was effective for advanced HCC patients. gemcitabine 121-132 HCC Homo sapiens 174-177 26632544-8 2015 Randomized controlled trial for adjuvant chemotherapy in China showed that capecitabine could reduce the risk of recurrence and improve postoperative survival of HCC. Capecitabine 75-87 HCC Homo sapiens 162-165 26146882-4 2015 Using this distinct fluorescence measure, we found that poorly differentiated hepatocellular carcinoma (HCC) tissues on average showed 3.7 times lower concentration of bilirubins than the corresponding nontumor parts. Bilirubin 168-178 HCC Homo sapiens 104-107 26814101-3 2015 RESULTS: The identified 52 studies involving 14 922 patients that investigated the use of hepatic resection for large/multinodular HCC, and 25 studies with 4 412 patients that investigated hepatic resection for HCC with MVI. mogroside VI 220-223 HCC Homo sapiens 211-214 26173501-8 2015 Moreover, upregulation of FSCN1 and downregulation of miR-145 and miR-133a co-existed in HCC. mir-133a 66-74 HCC Homo sapiens 89-92 26319021-7 2015 The education intervention significantly increased the participants" knowledge on HCC and its risk factors, particularly regarding the use of pesticides at home and aflatoxin contaminated foods (both p < 0.05). Aflatoxins 165-174 HCC Homo sapiens 82-85 26245668-2 2015 We previously reported the cytotoxicity of a series of synthetic phenyl-substituted polyoxygenated xanthone derivatives against human HCC. xanthone 99-107 HCC Homo sapiens 134-137 26092946-1 2015 BACKGROUND: Sorafenib-everolimus combination therapy may be more effective than sorafenib monotherapy for hepatocellular carcinoma (HCC). Everolimus 22-32 HCC Homo sapiens 106-136 26085911-9 2015 Sorafenib is a viable option for advanced HCC in elderly provided that a careful evaluation of concomitant comorbidities, particularly cardiovascular ones, is taken into account. Sorafenib 0-9 HCC Homo sapiens 42-45 25866604-7 2015 There is currently no effective systemic chemotherapy, immunologic, or hormonal therapy for HCC, and sorafenib is the only approved molecular-targeted treatment for advanced HCC. Sorafenib 101-110 HCC Homo sapiens 174-177 25749785-1 2015 Sorafenib is an oral multikinase inhibitor with clinical activity against hepatocellular carcinoma (HCC) and renal cell carcinoma. Sorafenib 0-9 HCC Homo sapiens 100-103 25749785-6 2015 The first case was a 47-year female had targetoid erythematous rashes on her arms 12 days after starting sorafenib for HCC. Sorafenib 105-114 HCC Homo sapiens 119-122 25749785-9 2015 The second case was an 81-year-old male had maculopapular eruptions with multiple targetoid lesions on the trunk, arms, and legs 10 days after starting sorafenib for his HCC. Sorafenib 152-161 HCC Homo sapiens 170-173 25749785-12 2015 The last one was a 20-year-old female developed generalized maculopapular eruptions in the whole body 10 days after starting sorafenib for the treatment of HCC. Sorafenib 125-134 HCC Homo sapiens 156-159 25921671-2 2015 Sorafenib remains the only approved, targeted molecule for the treatment of advanced HCC. Sorafenib 0-9 HCC Homo sapiens 85-88 25838254-4 2015 The evidence-based therapy for advanced HCC that is unsuitable for locoregional treatment is limited to sorafenib, with no second-line option available. Sorafenib 104-113 HCC Homo sapiens 40-43 25838254-5 2015 This article focuses on the development of the MET inhibitor tivantinib in HCC as a promising treatment option for patients who failed sorafenib. ARQ 197 61-71 HCC Homo sapiens 75-78 25838254-5 2015 This article focuses on the development of the MET inhibitor tivantinib in HCC as a promising treatment option for patients who failed sorafenib. Sorafenib 135-144 HCC Homo sapiens 75-78 25838254-7 2015 Based on these results, the METIV-HCC phase III study in second-line treatment for MET-high patients was initiated to demonstrate the survival advantage of tivantinib compared to placebo. ARQ 197 156-166 HCC Homo sapiens 34-37 25549355-6 2014 miR-150-5p expression is also decreased in metastatic cancer tissues compared with pair primary tissues, indicating that miR-150-5p may be involved in HCC metastasis. mir-150-5p 0-10 HCC Homo sapiens 151-154 25542894-7 2015 Also, GPC3 expression positively correlated with mRNA expression of HCC-related genes in the qRT-PCR and GSEA evaluations. gsea 105-109 HCC Homo sapiens 68-71 26225676-0 2015 Increased Oxidative Stress and RUNX3 Hypermethylation in Patients with Hepatitis B Virus-Associated Hepatocellular Carcinoma (HCC) and Induction of RUNX3 Hypermethylation by Reactive Oxygen Species in HCC Cells. Reactive Oxygen Species 174-197 HCC Homo sapiens 201-204 26225676-6 2015 Effect of reactive oxygen species (ROS) on induction of RUNX3 hypermethylation in HCC cells was investigated. Reactive Oxygen Species 10-33 HCC Homo sapiens 82-85 26225676-6 2015 Effect of reactive oxygen species (ROS) on induction of RUNX3 hypermethylation in HCC cells was investigated. Reactive Oxygen Species 35-38 HCC Homo sapiens 82-85 25477009-1 2015 PURPOSE: Sorafenib is the standard of care for advanced hepatocellular carcinoma (HCC). Sorafenib 9-18 HCC Homo sapiens 82-85 25477009-4 2015 METHODS: We retrospectively reviewed data from patients treated with sorafenib for HCC at our institution. Sorafenib 69-78 HCC Homo sapiens 83-86 25477009-12 2015 CONCLUSION: Sorafenib showed similar results in terms of safety and efficacy in the elderly and younger HCC populations. Sorafenib 12-21 HCC Homo sapiens 104-107 26788381-3 2015 We report a case of 62-year-old male with long history of CD treated with azathioprine (AZA) and aminosalicylic acid (ASA) who was incidentally diagnosed with HCC, for which left hepatectomy was done. Azathioprine 74-86 HCC Homo sapiens 159-162 26788381-3 2015 We report a case of 62-year-old male with long history of CD treated with azathioprine (AZA) and aminosalicylic acid (ASA) who was incidentally diagnosed with HCC, for which left hepatectomy was done. Azathioprine 88-91 HCC Homo sapiens 159-162 26788381-3 2015 We report a case of 62-year-old male with long history of CD treated with azathioprine (AZA) and aminosalicylic acid (ASA) who was incidentally diagnosed with HCC, for which left hepatectomy was done. Aminosalicylic Acid 97-116 HCC Homo sapiens 159-162 26788381-3 2015 We report a case of 62-year-old male with long history of CD treated with azathioprine (AZA) and aminosalicylic acid (ASA) who was incidentally diagnosed with HCC, for which left hepatectomy was done. Aminosalicylic Acid 118-121 HCC Homo sapiens 159-162 26788381-6 2015 AZA was reported in all case reports of CD that developed HCC. Azathioprine 0-3 HCC Homo sapiens 58-61 25941903-7 2015 In conclusion, THIAA and HHIAA show antitumor properties in vitro in human HCC cell lines as well as in vivo in a chemically induced animal model of HCC. thiaa 15-20 HCC Homo sapiens 75-78 25941903-7 2015 In conclusion, THIAA and HHIAA show antitumor properties in vitro in human HCC cell lines as well as in vivo in a chemically induced animal model of HCC. thiaa 15-20 HCC Homo sapiens 149-152 25941903-7 2015 In conclusion, THIAA and HHIAA show antitumor properties in vitro in human HCC cell lines as well as in vivo in a chemically induced animal model of HCC. hhiaa 25-30 HCC Homo sapiens 75-78 25941903-7 2015 In conclusion, THIAA and HHIAA show antitumor properties in vitro in human HCC cell lines as well as in vivo in a chemically induced animal model of HCC. hhiaa 25-30 HCC Homo sapiens 149-152 25549355-6 2014 miR-150-5p expression is also decreased in metastatic cancer tissues compared with pair primary tissues, indicating that miR-150-5p may be involved in HCC metastasis. mir-150-5p 121-131 HCC Homo sapiens 151-154 25429315-3 2014 Sorafenib, a multi-targeted kinase inhibitor, is the only available systemic agent for treatment of HCC that improves overall survival for patients with advanced stage disease; unfortunately, an effective second-line agent for the treatment of progressive or sorafenib-resistant HCC has yet to be identified. Sorafenib 0-9 HCC Homo sapiens 100-103 25544869-8 2014 Sorafenib is an oral multikinase inhibitor with anti-proliferative and anti-angiogenic effects and is the first molecular target drug approved for the treatment of advanced HCC. Sorafenib 0-9 HCC Homo sapiens 173-176 25544869-11 2014 Therefore, understanding the mechanism(s) underlying sorafenib resistance of cancer cells is highlighted for efficiently treating HCC. Sorafenib 53-62 HCC Homo sapiens 130-133 25262955-1 2014 RATIONALE AND OBJECTIVES: To determine the accuracy of magnetic resonance imaging (MRI) with gadoxetic acid disodium for the detection of hepatocellular carcinoma (HCC). gadolinium ethoxybenzyl DTPA 93-116 HCC Homo sapiens 164-167 25262955-11 2014 CONCLUSIONS: MRI with gadoxetic acid disodium is a noninvasive and no radiation exposure imaging modality with high sensitivity and specificity for the detection of HCC. gadolinium ethoxybenzyl DTPA 22-45 HCC Homo sapiens 165-168 25429315-3 2014 Sorafenib, a multi-targeted kinase inhibitor, is the only available systemic agent for treatment of HCC that improves overall survival for patients with advanced stage disease; unfortunately, an effective second-line agent for the treatment of progressive or sorafenib-resistant HCC has yet to be identified. Sorafenib 0-9 HCC Homo sapiens 279-282 25294808-8 2014 HCC-HCV/EtOH methylomes overlap highly with cryptogenic HCC, suggesting shared epigenetically deregulated pathways for hepatocarcinogenesis. Ethanol 8-12 HCC Homo sapiens 56-59 24644045-1 2014 UNLABELLED: The association between vitamin D status and hepatocellular carcinoma (HCC) has not been well investigated, despite experimental evidence supporting an important role of vitamin D in liver pathophysiology. Vitamin D 36-45 HCC Homo sapiens 83-86 24644045-2 2014 Our objective was to investigate the association between prediagnostic circulating 25-hydroxyvitamin D [25(OH)D] serum levels and the risk of HCC in a prospective, nested case-control study among 520,000 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. 25-hydroxyvitamin D 83-102 HCC Homo sapiens 142-145 24644045-2 2014 Our objective was to investigate the association between prediagnostic circulating 25-hydroxyvitamin D [25(OH)D] serum levels and the risk of HCC in a prospective, nested case-control study among 520,000 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. 25(oh)d 104-111 HCC Homo sapiens 142-145 24297598-1 2014 PURPOSE: The aim of our study was to evaluate the diagnostic accuracy of gadoxetic acid-enhanced magnetic resonance (MR) imaging both in the detection of hepatocellular carcinoma (HCC) and precancerous lesions and in the assessment of their evolution. gadolinium ethoxybenzyl DTPA 73-87 HCC Homo sapiens 180-183 24903383-4 2014 Among women group, individuals with TC or CC alleles of TIMP-3 -1296 T>C gene polymorphism protected against HCC (AOR = 0.35, 95% confidence interval (CI) = 0.12-0.97; p = 0.04) compared to individuals with TT alleles, after adjusting for other confounders. Technetium 36-38 HCC Homo sapiens 112-115 24476004-8 2014 A diethylnitrosamine (DEN)-induced HCC mouse model was assessed with or without injection of NSC 74859, a STAT3 inhibitor, to show accompanied changes among the expressions of STAT3, SOCS3, c-myc, MMP-2, and MMP-9. Diethylnitrosamine 2-20 HCC Homo sapiens 35-38 24476004-8 2014 A diethylnitrosamine (DEN)-induced HCC mouse model was assessed with or without injection of NSC 74859, a STAT3 inhibitor, to show accompanied changes among the expressions of STAT3, SOCS3, c-myc, MMP-2, and MMP-9. Diethylnitrosamine 22-25 HCC Homo sapiens 35-38 24283268-8 2014 Finally, everolimus treatment reduced the load of tumoral myofibroblasts in a rat model of HCC. Everolimus 9-19 HCC Homo sapiens 91-94 24283268-9 2014 These data suggest that everolimus targets multiple mechanisms, making it a potent blocker of the progression of HCC from liver fibrosis. Everolimus 24-34 HCC Homo sapiens 113-116 24297598-10 2014 CONCLUSIONS: Gadoxetic acid-enhanced MR imaging is useful for detecting HCC as well as hypovascular nodules with potential progression to HCC. gadolinium ethoxybenzyl DTPA 13-27 HCC Homo sapiens 72-75 24297598-10 2014 CONCLUSIONS: Gadoxetic acid-enhanced MR imaging is useful for detecting HCC as well as hypovascular nodules with potential progression to HCC. gadolinium ethoxybenzyl DTPA 13-27 HCC Homo sapiens 138-141 24151232-0 2014 BRCA1-mediated inflammation and growth activated & inhibited transition mechanisms between no-tumor hepatitis/cirrhotic tissues and HCC. Adenosine Monophosphate 50-53 HCC Homo sapiens 136-139 24764653-1 2014 The kinase inhibitor sorafenib is the only systemic therapy proven to have a positive effect on survival of patients with advanced hepatocellular carcinoma (HCC). Sorafenib 21-30 HCC Homo sapiens 157-160 24764653-6 2014 In addition, effectiveness of the expanded application of sorafenib is still controversial, although a few studies have shed some light on combinational treatment with sorafenib for intermediate-stage HCC. Sorafenib 168-177 HCC Homo sapiens 201-204 24336935-11 2014 In order to generate B-H H-C(c) dihydrogen bonds the H-C(c) from the carborane cluster is needed. carborane 71-80 HCC Homo sapiens 27-33 24336935-11 2014 In order to generate B-H H-C(c) dihydrogen bonds the H-C(c) from the carborane cluster is needed. carborane 71-80 HCC Homo sapiens 55-61 24764717-7 2014 Here, we report a case of a large hcc presenting in a patient with metabolic syndrome without significant alcohol history or biochemical liver dysfunction. Alcohols 106-113 HCC Homo sapiens 34-37 23819582-7 2014 We review the clinical significance of therapy using BCAA granules in patients receiving different treatment approaches for cirrhosis and HCC based on the published work as well as our own data. Amino Acids, Branched-Chain 53-57 HCC Homo sapiens 138-141 27508172-4 2014 Targeted molecular therapies, such as the multikinase inhibitor sorafenib, provide a modest increase in survival for advanced HCC patients and display significant toxicity. Sorafenib 64-73 HCC Homo sapiens 126-129 24672518-12 2014 Future validation for all of these miRNAs will be needed to assess their prognostic significance and confirm their relationship with the induction of HCC due to aflatoxin exposure. Aflatoxins 161-170 HCC Homo sapiens 150-153 24698672-1 2014 OBJECTIVE: To explore the efficacy and safty of sorafenib in Child-Pugh class B to class C hepatocellular carcinoma (HCC). Sorafenib 48-57 HCC Homo sapiens 117-120 24698672-9 2014 CONCLUSIONS: Sorafenib is safe in patients with liver function impaired advanced HCC. Sorafenib 13-22 HCC Homo sapiens 81-84 24924566-1 2014 OBJECTIVE: To evaluate the influence of sirolimus on the long-term survival of patients after orthotopic liver transplantation (OLT) for hepatocellular carcinoma (HCC). Sirolimus 40-49 HCC Homo sapiens 137-167 24924566-10 2014 CONCLUSION: The sirolimus-based immunosuppressive protocol reduce long-term postoperative recurrence rate and improve the survival rate of patients after OLT for HCC significantly (especially early-mid HCC). Sirolimus 16-25 HCC Homo sapiens 162-165 24924566-10 2014 CONCLUSION: The sirolimus-based immunosuppressive protocol reduce long-term postoperative recurrence rate and improve the survival rate of patients after OLT for HCC significantly (especially early-mid HCC). Sirolimus 16-25 HCC Homo sapiens 202-205 24716227-4 2014 Therefore, identification of genes involved in sorafenib resistance is important to effectively treat advanced HCC. Sorafenib 47-56 HCC Homo sapiens 111-114 24716227-5 2014 METHODS: We performed a genomic screening with a short-hairpin RNA library cassette on HCC cell lines to find genes relating resistance to sorafenib. Sorafenib 139-148 HCC Homo sapiens 87-90 24716227-7 2014 The inhibition of ZMYM2 resulted in sorafenib-resistance in formerly sensitive HCC cell lines. Sorafenib 36-45 HCC Homo sapiens 79-82 24048683-8 2014 Iron homeostasis is known to be perturbed in HCC and we observed downregulation of genes in this pathway. Iron 0-4 HCC Homo sapiens 45-48 24048683-9 2014 In the metabolomics analysis of hepatic NAFLD samples, several changes were opposite to what has been reported in plasma of HCC patients (lysine, phenylalanine, citrulline, creatine, creatinine, glycodeoxycholic acid, inosine, and alpha-ketoglutarate). Lysine 138-144 HCC Homo sapiens 124-127 24048683-9 2014 In the metabolomics analysis of hepatic NAFLD samples, several changes were opposite to what has been reported in plasma of HCC patients (lysine, phenylalanine, citrulline, creatine, creatinine, glycodeoxycholic acid, inosine, and alpha-ketoglutarate). Inosine 218-225 HCC Homo sapiens 124-127 24048683-9 2014 In the metabolomics analysis of hepatic NAFLD samples, several changes were opposite to what has been reported in plasma of HCC patients (lysine, phenylalanine, citrulline, creatine, creatinine, glycodeoxycholic acid, inosine, and alpha-ketoglutarate). Ketoglutaric Acids 231-250 HCC Homo sapiens 124-127 24048683-10 2014 In contrast, multiple acyl-lyso-phosphatidylcholine metabolites were downregulated in NASH livers, consistent with observations in HCC patient plasma. acyl-lyso-phosphatidylcholine 22-51 HCC Homo sapiens 131-134 29147365-8 2013 It demonstrated the importance of early detection and initiation of treatment of iron overload in preventing HCC in MDS patients, even among Asian population. Iron 81-85 HCC Homo sapiens 109-112 30190939-5 2014 Utilization of doxorubicin-eluting bead embolization may offer safer treatment in eligible HCC patients. Doxorubicin 15-26 HCC Homo sapiens 91-94 24224926-6 2013 The aim of this brief review is to highlight the main concerns, pitfalls and warnings regarding the management of HCC in elderly patients, with particular focus on systemic therapy with sorafenib. Sorafenib 186-195 HCC Homo sapiens 114-117 24132648-1 2013 PURPOSE: Sorafenib is the reference therapy for advanced hepatocellular carcinoma (HCC). Sorafenib 9-18 HCC Homo sapiens 83-86 25011557-2 2014 Traditional dried food was suggested as the major reason for high HCC numbers, due to possible aflatoxin contamination during manufacturing. Aflatoxins 95-104 HCC Homo sapiens 66-69 24818010-15 2014 Adjuvant use of sorafenib is safe and decreases risk of HCC recurrence in high-risk LT recipients. Sorafenib 16-25 HCC Homo sapiens 56-59 25427741-1 2014 BACKGROUND: Little data are available on the long-term survival of patients treated with sorafenib for advanced hepatocellular carcinoma (HCC). Sorafenib 89-98 HCC Homo sapiens 138-141 25427741-6 2014 CONCLUSION: The overview obtained from the workshop reflects the pattern of management in practice for long-term survivors following sorafenib treatment for HCC in Japan and may also provide valuable information for other countries. Sorafenib 133-142 HCC Homo sapiens 157-160 24222107-3 2013 The remarkable inhibitory effects of DMTreCn on the growth of human hepatocellular carcinoma (HCC) (Hep-G2 and HuH-7) cells were obtained along with apoptosis, without affecting the growth of normal cells. dmtrecn 37-44 HCC Homo sapiens 68-98 24266510-6 2013 Most common drugs like sorafenib, doxorubicin and daunorubicin have been used widely for treatment of HCC. Sorafenib 23-32 HCC Homo sapiens 102-105 24266510-6 2013 Most common drugs like sorafenib, doxorubicin and daunorubicin have been used widely for treatment of HCC. Doxorubicin 34-45 HCC Homo sapiens 102-105 24266510-6 2013 Most common drugs like sorafenib, doxorubicin and daunorubicin have been used widely for treatment of HCC. Daunorubicin 50-62 HCC Homo sapiens 102-105 24222107-6 2013 It is noteworthy that the remarkable inhibitory effects of DMTreCn on the growth of human HCC cells were obtained along with apoptosis for the first time. dmtrecn 59-66 HCC Homo sapiens 90-93 23389810-11 2013 CONCLUSION: Entecavir therapy reduces the risks of hepatic events, HCC, liver-related and all-cause mortality of CHB patients with liver cirrhosis in 5 years, particularly among those who had maintained viral suppression. entecavir 12-21 HCC Homo sapiens 67-70 24013415-1 2013 A series of novel derivatives of phenyl substituted tetramethoxy xanthone were synthesized and evaluated for their in vitro cytotoxicity against human hepatocellular carcinoma (HCC) and non-tumor hepatic cells. phenyl substituted tetramethoxy xanthone 33-73 HCC Homo sapiens 151-181 24013415-5 2013 Our findings suggested that these phenylxanthone derivatives may hold promise as chemotherapeutic agents for the treatment of human HCC. phenylxanthone 34-48 HCC Homo sapiens 132-135 23591326-1 2013 Currently, only one drug, sorafenib, is FDA approved for the treatment of advanced hepatocellular carcinoma (HCC), achieving modest objective response rates while still conferring an overall survival benefit. Sorafenib 26-35 HCC Homo sapiens 109-112 23970349-3 2013 In this study, we aimed to isolate and characterize a small population of CD133+ cells that existed in the HCC cell line SMMC-7721 by MACS and investigated the possible roles of 8-bromo-7-methoxychrysin (BrMC), a synthetic analogue of chrysin, in inhibiting the properties of CD133+ sphere-forming cells (SFCs) derived from the HCC cell line SMMC-7721, namely liver cancer stem cells (LCSCs). smmc 121-125 HCC Homo sapiens 107-110 24097332-5 2013 Sorafenib was demonstrated to significantly increase the survival of patients with advanced HCC in two prospective, randomized, placebo-controlled trials. Sorafenib 0-9 HCC Homo sapiens 92-95 24097332-6 2013 Subsequently, a number of retrospective or prospective studies have indicated that the effectiveness of sorafenib therapy in the treatment of HCC is similar in elderly and non-elderly patients. Sorafenib 104-113 HCC Homo sapiens 142-145 24097332-7 2013 The aim of this review is to describe the impact of age on the effects of sorafenib-targeted therapy in patients with HCC, and the next treatment options with new targeted agents (everolimus, tivantinib, linifanib, etc. Sorafenib 74-83 HCC Homo sapiens 118-121 23970349-6 2013 This study not only provides an important experimental and theoretical basis for investigation of BrMC in LCSCs, but also helps in the development of effective therapeutic medicine for HCC. 8-bromo-7-methoxychrysin 98-102 HCC Homo sapiens 185-188 24115810-5 2013 The introduction of sorafenib as the standard systemic therapy has unveiled a new direction for future research regarding HCC treatment. Sorafenib 20-29 HCC Homo sapiens 122-125 23534992-3 2013 There are no other reports about erlotinib-induced leukocytoclastic vasculitis (LV) in the erlotinib-bevacizumab regimen for bone metastasis, from a relapsed hepatocellular carcinoma (HCC) in liver-transplanted patients. Erlotinib Hydrochloride 33-42 HCC Homo sapiens 184-187 23720072-10 2013 CONCLUSIONS: This study emphasizes the 3-cm size, and possibly the 6-cm size, as informative predictive thresholds when ablating HCC, because variability of DSS occurred specifically at these tumor sizes. dss 157-160 HCC Homo sapiens 129-132 23845776-5 2013 Hemochromatosis gene (HFE) mutations namely C282Y and H63D may cause hepatic iron overload, thus increasing the risk of HCC in HCV patients. Iron 77-81 HCC Homo sapiens 120-123 23933933-1 2013 UNLABELLED: BACKROUND-AIMS: To determine long term outcomes, regarding recurrence and survival, in patients with HCC that achieved complete response after initial treatment with drug eluting beads (DEB) using DC Bead loaded with doxorubicin (DEB-DOX). Doxorubicin 229-240 HCC Homo sapiens 113-116 23836469-8 2013 The idea is corroborated by the fact that the most important residues in the hCC sequence are Ser-98 and Tyr-102; these residues are able to form hydrogen bonds via their hydroxyl groups. Serine 94-97 HCC Homo sapiens 77-80 23836469-8 2013 The idea is corroborated by the fact that the most important residues in the hCC sequence are Ser-98 and Tyr-102; these residues are able to form hydrogen bonds via their hydroxyl groups. Tyrosine 105-108 HCC Homo sapiens 77-80 23836469-8 2013 The idea is corroborated by the fact that the most important residues in the hCC sequence are Ser-98 and Tyr-102; these residues are able to form hydrogen bonds via their hydroxyl groups. Hydrogen 146-154 HCC Homo sapiens 77-80 23933933-1 2013 UNLABELLED: BACKROUND-AIMS: To determine long term outcomes, regarding recurrence and survival, in patients with HCC that achieved complete response after initial treatment with drug eluting beads (DEB) using DC Bead loaded with doxorubicin (DEB-DOX). deb-dox 242-249 HCC Homo sapiens 113-116 23751800-1 2013 Despite the successful FDA approval of sorafenib as the standard of care therapy in patients with advanced hepatocellular carcinoma (HCC), its clinical benefits have been modest. Sorafenib 39-48 HCC Homo sapiens 133-136 23983424-8 2013 Iron overload occurs in several liver diseases associated with the development of HCC including Hepatitis C infection and the importance of miRNAs in iron homeostasis and hepatic iron overload is well characterised. Iron 0-4 HCC Homo sapiens 82-85 23751800-3 2013 The exact mechanism of sorafenib in the treatment of HCC and its resistance at the molecular levels are largely unknown. Sorafenib 23-32 HCC Homo sapiens 53-56 23881427-11 2013 The multikinase inhibitor sorafenib is the only treatment option approved for patients with advanced-stage HCC. Sorafenib 26-35 HCC Homo sapiens 107-110 23628963-3 2013 Among several risk factors for HCC, the most common are cirrhosis because of chronic hepatitis B virus or hepatitis C virus infection and alcohol consumption, obesity, and diabetes. Alcohols 138-145 HCC Homo sapiens 31-34 23628963-9 2013 The multikinase inhibitor sorafenib is the only approved targeted agent for advanced HCC, although promising results have been obtained with other targeted agents and combinations, and the results of ongoing trials are eagerly awaited. Sorafenib 26-35 HCC Homo sapiens 85-88 24872793-11 2013 The multikinase inhibitor sorafenib is the only treatment option approved for patients with advanced-stage HCC. Sorafenib 26-35 HCC Homo sapiens 107-110 23389758-11 2013 CONCLUSION: Postoperative pegylated interferon plus ribavirin is associated with reduced recurrence of HCC in patients with HCV infection. Ribavirin 52-61 HCC Homo sapiens 103-106 23667593-3 2013 In our previous study, we successfully isolated CAFs from hepatocellular carcinoma (HCC) (H-CAFs) and proved that H-CAFs suppressed the activation of NK cells and thereby created favorable conditions for HCC progression. h-cafs 90-96 HCC Homo sapiens 58-88 23667593-3 2013 In our previous study, we successfully isolated CAFs from hepatocellular carcinoma (HCC) (H-CAFs) and proved that H-CAFs suppressed the activation of NK cells and thereby created favorable conditions for HCC progression. h-cafs 90-96 HCC Homo sapiens 84-87 23667593-3 2013 In our previous study, we successfully isolated CAFs from hepatocellular carcinoma (HCC) (H-CAFs) and proved that H-CAFs suppressed the activation of NK cells and thereby created favorable conditions for HCC progression. h-cafs 114-120 HCC Homo sapiens 58-88 23667593-3 2013 In our previous study, we successfully isolated CAFs from hepatocellular carcinoma (HCC) (H-CAFs) and proved that H-CAFs suppressed the activation of NK cells and thereby created favorable conditions for HCC progression. h-cafs 114-120 HCC Homo sapiens 84-87 23667593-9 2013 These results indicate that H-CAFs are an important factor for promoting the growth of HCC in vitro and in vivo, and that HGF plays a key role in HCC proliferation induced by H-CAFs. h-cafs 28-34 HCC Homo sapiens 87-90 23667593-9 2013 These results indicate that H-CAFs are an important factor for promoting the growth of HCC in vitro and in vivo, and that HGF plays a key role in HCC proliferation induced by H-CAFs. h-cafs 175-181 HCC Homo sapiens 146-149 23333348-1 2013 BACKGROUND & AIMS: Cirrhosis affects 1% to 2% of the world population and is the major risk factor for hepatocellular carcinoma (HCC). Adenosine Monophosphate 12-15 HCC Homo sapiens 133-136 23704814-6 2013 Total bilirubin was higher in HCC compared with cirrhosis (p<0.01). Bilirubin 6-15 HCC Homo sapiens 30-33 23307533-3 2013 Conversely, higher folate intake has been inversely associated with liver damage and HCC. Folic Acid 19-25 HCC Homo sapiens 85-88 23497349-14 2013 CONCLUSIONS: We report the first clinical results of patients with HCC undergoing carbon ion therapy using the rasterscanning technique at our institution. Carbon 82-88 HCC Homo sapiens 67-70 23307533-4 2013 In the current study, we investigate the effect of alcohol consumption and folate intake on HCC incidence and liver disease mortality in the NIH-American Association of Retired Persons Diet and Health Study. Folic Acid 75-81 HCC Homo sapiens 92-95 23307533-9 2013 Folate, however, modified the relationship between alcohol and HCC incidence (Pinteraction = 0.03), but had no effect on the relationship between alcohol and liver disease mortality (Pinteraction = 0.54). Folic Acid 0-6 HCC Homo sapiens 63-66 23307533-9 2013 Folate, however, modified the relationship between alcohol and HCC incidence (Pinteraction = 0.03), but had no effect on the relationship between alcohol and liver disease mortality (Pinteraction = 0.54). Alcohols 51-58 HCC Homo sapiens 63-66 23307533-10 2013 CONCLUSIONS: These results suggest that higher folate intake may ameliorate the effect of alcohol consumption on the development of HCC. Folic Acid 47-53 HCC Homo sapiens 132-135 23307533-10 2013 CONCLUSIONS: These results suggest that higher folate intake may ameliorate the effect of alcohol consumption on the development of HCC. Alcohols 90-97 HCC Homo sapiens 132-135 23307533-11 2013 IMPACT: Folate intake may be beneficial in the prevention of alcohol-associated HCC. Folic Acid 8-14 HCC Homo sapiens 80-83 23307533-11 2013 IMPACT: Folate intake may be beneficial in the prevention of alcohol-associated HCC. Alcohols 61-68 HCC Homo sapiens 80-83 23112096-8 2013 CONCLUSION: This analysis of both randomized and nonrandomized studies evaluating an antiangiogenic agent in HCC showed that whereas the use of sorafenib was associated with an increased risk of bleeding in HCC, this was primarily for lower-grade events and similar in magnitude to the risk encountered in RCC. Sorafenib 144-153 HCC Homo sapiens 109-112 23112096-8 2013 CONCLUSION: This analysis of both randomized and nonrandomized studies evaluating an antiangiogenic agent in HCC showed that whereas the use of sorafenib was associated with an increased risk of bleeding in HCC, this was primarily for lower-grade events and similar in magnitude to the risk encountered in RCC. Sorafenib 144-153 HCC Homo sapiens 207-210 24159587-11 2012 Sorafenib, the only agent specifically approved for HCC treatment, is of limited efficacy in this setting. Sorafenib 0-9 HCC Homo sapiens 52-55 23426789-1 2013 The multikinase inhibitor sorafenib has demonstrated an overall survival benefit in phase III hepatocellular carcinoma (HCC) trials and has become the new standard of care for advanced stages of this disease. Sorafenib 26-35 HCC Homo sapiens 120-123 23426789-4 2013 We report a case of 4-year sorafenib treatment in a patient with an advanced hepatitis C virus (HCV)-related HCC with extensive infiltration of the inferior vena cava. Sorafenib 27-36 HCC Homo sapiens 109-112 23426789-7 2013 Thus, it is likely that a subgroup of human HCC may be highly sensitive to sorafenib; new molecular determinants are required to select those patients who may benefit from this therapy. Sorafenib 75-84 HCC Homo sapiens 44-47 23063418-1 2013 BACKGROUND & AIMS: Early treatment has been recommended for hepatocellular carcinoma (HCC) due to its high cure rate. Adenosine Monophosphate 12-15 HCC Homo sapiens 64-94 23143027-3 2013 Analysis was performed retrospectively on 50 targeted HCC lesions in 29 patients (16 men, 13 women; mean age, 61.9 years +- 10.7) treated with TACE with drug-eluting beads. Chlorotrianisene 143-147 HCC Homo sapiens 54-57 23010890-3 2013 Although several experimental lines of research support a direct role for hepatitis C virus (HCV) in cancer promotion, cirrhosis is the main risk factor for this tumor, whereas other factors like alcohol and tobacco smoking are clearly able to accelerate HCC development. Alcohols 196-203 HCC Homo sapiens 255-258 22147505-7 2012 Another 91 paraffin-embedded HCC tissues were examined by immunohistochemistry. Paraffin 11-19 HCC Homo sapiens 29-32 22187145-1 2012 PURPOSE: To evaluate the efficacy and safety of ultrasound (US)-guided percutaneous argon-helium cryoablation for hepatocellular carcinoma (HCC) and determine appropriate indications. Argon 84-89 HCC Homo sapiens 114-144 22187145-1 2012 PURPOSE: To evaluate the efficacy and safety of ultrasound (US)-guided percutaneous argon-helium cryoablation for hepatocellular carcinoma (HCC) and determine appropriate indications. Helium 90-96 HCC Homo sapiens 114-144 23076705-0 2012 Unexpected remission of hepatocellular carcinoma (HCC) with lung metastasis to the combination therapy of thalidomide and cyproheptadine: report of two cases and a preliminary HCC cell line study. Thalidomide 106-117 HCC Homo sapiens 50-53 23146514-2 2012 We herein report our experience with sorafenib treatment for HCC recurrence post-OLT. Sorafenib 37-46 HCC Homo sapiens 61-64 23146514-3 2012 PATIENTS AND METHODS: We reviewed data on transplanted HCC patients receiving sorafenib for HCC recurrence. Sorafenib 78-87 HCC Homo sapiens 55-58 23146514-3 2012 PATIENTS AND METHODS: We reviewed data on transplanted HCC patients receiving sorafenib for HCC recurrence. Sorafenib 78-87 HCC Homo sapiens 92-95 23146514-12 2012 CONCLUSION: Sorafenib treatment for HCC recurrence in transplant recipients represents a challenging oncologic approach that requires further validation in prospective, multicenter studies. Sorafenib 12-21 HCC Homo sapiens 36-39 23076705-0 2012 Unexpected remission of hepatocellular carcinoma (HCC) with lung metastasis to the combination therapy of thalidomide and cyproheptadine: report of two cases and a preliminary HCC cell line study. Thalidomide 106-117 HCC Homo sapiens 176-179 23076705-0 2012 Unexpected remission of hepatocellular carcinoma (HCC) with lung metastasis to the combination therapy of thalidomide and cyproheptadine: report of two cases and a preliminary HCC cell line study. Cyproheptadine 122-136 HCC Homo sapiens 50-53 23076705-0 2012 Unexpected remission of hepatocellular carcinoma (HCC) with lung metastasis to the combination therapy of thalidomide and cyproheptadine: report of two cases and a preliminary HCC cell line study. Cyproheptadine 122-136 HCC Homo sapiens 176-179 23076705-1 2012 We reported two cases of hepatocellular carcinoma (HCC) with lung metastases who were treated with a combination of thalidomide and cyproheptadine. Thalidomide 116-127 HCC Homo sapiens 51-54 23076705-1 2012 We reported two cases of hepatocellular carcinoma (HCC) with lung metastases who were treated with a combination of thalidomide and cyproheptadine. Cyproheptadine 132-146 HCC Homo sapiens 51-54 23076705-4 2012 A following experimental cell line study demonstrated that cyproheptadine effectively reduced the viability of two HCC cell lines. Cyproheptadine 59-73 HCC Homo sapiens 115-118 23162763-2 2012 Using non-inflammatory diethylnitrosamine (DEN)-induced liver cancer in mice, we demonstrate that distinct axes of the adaptive immune system, which are also prognostic in human HCC, actively suppress hepatocarcinogenesis by controlling tumor formation and progression. Diethylnitrosamine 23-41 HCC Homo sapiens 178-181 22674847-5 2012 On the basis of the obtained results we can conclude that proline residue at the hinge region makes cystatin C structure more flexible and dynamic, what probably facilitates the dimerization process of this hCC variant. Proline 58-65 HCC Homo sapiens 207-210 23162763-2 2012 Using non-inflammatory diethylnitrosamine (DEN)-induced liver cancer in mice, we demonstrate that distinct axes of the adaptive immune system, which are also prognostic in human HCC, actively suppress hepatocarcinogenesis by controlling tumor formation and progression. Diethylnitrosamine 43-46 HCC Homo sapiens 178-181 22490318-2 2012 In the case of primary hepatocellular carcinoma (HCC), one alteration that has often been associated is increased amounts of fucose attached to the N-glycans of serum proteins secreted by the liver. Fucose 125-131 HCC Homo sapiens 49-52 22846865-3 2012 In 2008, phase III clinical trials revealed anti-angiogenic agent "sorafenib" as the first drug that demonstrated an improved overall survival in patients with advanced HCC. Sorafenib 67-76 HCC Homo sapiens 169-172 22391979-10 2012 The LHM and the hilar Glissonean pedicle approach proved effective for resolving the difficulties of performing surgery in a mirror image for HCC in a patient with situs inversus totalis. glissonean 22-32 HCC Homo sapiens 142-145 22490318-2 2012 In the case of primary hepatocellular carcinoma (HCC), one alteration that has often been associated is increased amounts of fucose attached to the N-glycans of serum proteins secreted by the liver. n-glycans 148-157 HCC Homo sapiens 49-52 22490318-5 2012 On the other hand, increased levels of a tetra-antennary glycan were observed in the HCC tissue as compared with the surrounding tissue or to the nondiseased livers. Polysaccharides 57-63 HCC Homo sapiens 85-88 22490318-7 2012 IMPACT: The identification of increased levels of tetra-antennary glycan on liver tumor tissue, as opposed to adjacent or nondiseased tissue may lead to improved detection of HCC. Polysaccharides 66-72 HCC Homo sapiens 175-178 22745587-4 2012 Inhibition of Plk1 by an adenovirus encoding for a short hairpin RNA against Plk1 or by the small-molecule inhibitor BI 2536 reduced the viability of HCC cell lines and inhibited HCC xenograft progression in nude mice. BI 2536 117-124 HCC Homo sapiens 150-153 22434314-1 2012 The positive results of sorafenib have unveiled a new direction of research in the management of hepatocellular carcinoma (HCC). Sorafenib 24-33 HCC Homo sapiens 123-126 23044206-7 2012 However, after adjusting by multivariate logistic regression, the odds ratio (OR) of HCC for the G allele (CG + GG genotypes) carriers was 1.31 (95% confidence interval (CI): 1.00 - 1.71) compared with the CC genotype. cysteinylglycine 107-109 HCC Homo sapiens 85-88 22270142-8 2012 CONCLUSION: Contrast-enhanced ultrasound yields a significantly higher AUC value than gadoxetate disodium-enhanced MR imaging in the assessment of arterial hypervascularity of HCC and DN. gadolinium ethoxybenzyl DTPA 86-105 HCC Homo sapiens 176-179 22707881-10 2012 The mortality from liver cirrhosis and HCC in Mongolia may be reduced by implementation of antiviral therapy program and control of alcohol consumption. Alcohols 132-139 HCC Homo sapiens 39-42 22510407-5 2012 However, HBx inhibited the upregulation of Mfn2 in HBx-transfected HCC cells simultaneously treated with doxorubicin or cotransfected with p53 plasmid, as evidenced by Western Blot and real-time PCR. Doxorubicin 105-116 HCC Homo sapiens 67-70 22510407-8 2012 These results indicate that HBx impacts p53-mediated transcription of Mfn2, providing insight into the negative effect of HBx against p53-dependent chemotherapeutic agents, such as doxorubicin, used in the treatment of HCC. Doxorubicin 181-192 HCC Homo sapiens 219-222 22745587-4 2012 Inhibition of Plk1 by an adenovirus encoding for a short hairpin RNA against Plk1 or by the small-molecule inhibitor BI 2536 reduced the viability of HCC cell lines and inhibited HCC xenograft progression in nude mice. BI 2536 117-124 HCC Homo sapiens 179-182 22745587-7 2012 Measurement of BI 2536 by mass spectrometry revealed considerably lower BI 2536 levels in HCC compared with the adjacent normal liver tissue. Bismuth 15-17 HCC Homo sapiens 90-93 22745587-7 2012 Measurement of BI 2536 by mass spectrometry revealed considerably lower BI 2536 levels in HCC compared with the adjacent normal liver tissue. Bismuth 72-74 HCC Homo sapiens 90-93 22285185-2 2012 Sorafenib is the first effective drug approved for the treatment of HCC. Sorafenib 0-9 HCC Homo sapiens 68-71 22285185-3 2012 Although it is known that sorafenib promotes apoptosis of HCC cells, the underlying mechanism remains largely obscure. Sorafenib 26-35 HCC Homo sapiens 58-61 22285185-4 2012 Here we report that sorafenib down-regulates protein expression of the anti-apoptotic protein c-IAP1 in a time- and dose-dependent manner in HCC cells in vitro and in vivo. Sorafenib 20-29 HCC Homo sapiens 141-144 22285185-8 2012 In conclusion, our data highlight a previously unidentified pathway that contributes to sorafenib mediated HCC cell apoptosis and as such provide novel mechanistic insight into the rational use of sorafenib in treating HCC. Sorafenib 88-97 HCC Homo sapiens 107-110 22285185-8 2012 In conclusion, our data highlight a previously unidentified pathway that contributes to sorafenib mediated HCC cell apoptosis and as such provide novel mechanistic insight into the rational use of sorafenib in treating HCC. Sorafenib 88-97 HCC Homo sapiens 219-222 22285185-8 2012 In conclusion, our data highlight a previously unidentified pathway that contributes to sorafenib mediated HCC cell apoptosis and as such provide novel mechanistic insight into the rational use of sorafenib in treating HCC. Sorafenib 197-206 HCC Homo sapiens 107-110 22285185-8 2012 In conclusion, our data highlight a previously unidentified pathway that contributes to sorafenib mediated HCC cell apoptosis and as such provide novel mechanistic insight into the rational use of sorafenib in treating HCC. Sorafenib 197-206 HCC Homo sapiens 219-222 22518301-0 2012 (188)Re-SSS/Lipiodol: Development of a Potential Treatment for HCC from Bench to Bedside. Ethiodized Oil 12-20 HCC Homo sapiens 63-66 22375182-1 2012 We report a case of a man who developed duodenal bleeding caused by direct hepatocellular carcinoma (HCC) invasion, which was successfully treated with endoscopic ethanol injection. Ethanol 163-170 HCC Homo sapiens 101-104 22375182-9 2012 In conclusion, Endoscopic ethanol injection can be used as a significantly effective and safe therapeutic tool in gastrointestinal tract bleeding caused by HCC invasion. Ethanol 26-33 HCC Homo sapiens 156-159 21920517-1 2012 AIM: To compare the diagnostic performances of gadoxetic acid-enhanced magnetic resonance imaging (MRI) and multiphasic multidetector computed tomography (MDCT) in the detection of hepatocellular carcinoma (HCC) in patients with chronic liver disease. gadolinium ethoxybenzyl DTPA 47-61 HCC Homo sapiens 207-210 21920517-11 2012 CONCLUSION: Gadoxetic acid-enhanced MRI and MDCT show similar diagnostic performances for the detection of HCC in patients with chronic liver disease. gadolinium ethoxybenzyl DTPA 12-26 HCC Homo sapiens 107-110 22518301-3 2012 The Comprehensive Cancer Centre Eugene Marquis and the National Graduate School of Chemistry of Rennes (ENSCR) have jointly developed a stable and efficient labelling of Lipiodol with rhenium-188 (E(betamax) = 2.1 MeV) for the treatment of HCC. Ethiodized Oil 170-178 HCC Homo sapiens 240-243 22518301-3 2012 The Comprehensive Cancer Centre Eugene Marquis and the National Graduate School of Chemistry of Rennes (ENSCR) have jointly developed a stable and efficient labelling of Lipiodol with rhenium-188 (E(betamax) = 2.1 MeV) for the treatment of HCC. Rhenium-188 184-195 HCC Homo sapiens 240-243 23284992-3 2012 The current study demonstrated that combining ABT-737 and Celastrol synergistically suppressed HCC cell proliferation, and induced apoptosis which was accompanied with the activation of caspase cascade and release of cytochrome c from mitochondria. ABT-737 46-53 HCC Homo sapiens 95-98 23284992-3 2012 The current study demonstrated that combining ABT-737 and Celastrol synergistically suppressed HCC cell proliferation, and induced apoptosis which was accompanied with the activation of caspase cascade and release of cytochrome c from mitochondria. celastrol 58-67 HCC Homo sapiens 95-98 23284992-4 2012 Further study revealed that the enhanced Noxa caused by Celastrol was the key factor for the synergy, since small interfering RNA-mediated knockdown of Noxa expression in HCC cells resulted in decreased apoptosis and attenuated anti-proliferative effects of the combination. celastrol 56-65 HCC Homo sapiens 171-174 21624052-4 2011 In recent years, the ganglioside-binding sites of all seven BoNT serotypes have been allocated to the H(CC) domain. Gangliosides 21-32 HCC Homo sapiens 102-107