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Journal Cover Liver Cancer
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     ISSN (Print) 2235-1795 - ISSN (Online) 1664-5553
     Published by Karger Homepage  [104 journals]
  • Malignant Transformation of Hepatocellular Adenoma: How Frequently Does It
           Happen'
    • Abstract:
      Liver Cancer 2015;4:1-5
       
  • Yttrium-90 Microspheres: A Review of Its Emerging Clinical Indications
    • Abstract: Background: Many patients with liver malignancies are not candidates for resection, and systemic therapies are often not effective. Radioembolization (RE) is an alternative treatment for this group of patients. The safety and efficacy of RE with yttrium 90 (Y90) in patients with hepatocellular carcinoma (HCC) or metastatic colon cancer to the liver have been proven in several studies. However, fewer studies have focussed on the safety and efficacy of RE with Y90 in other extrahepatic primary and secondary liver cancers. The effect on outcomes of concomitant use of Y90 with a systemic therapy is still currently under investigation. Summary: A review of the published data on the use of RE as stand-alone, concomitant or sequential with other treatment modalities in HCC and other primary and secondary liver cancer is reported here. Key message: RE for the treatment of HCC and other extrahepatic, primary and secondary liver cancer has reasonable efficacy and acceptable toxicities. Definitive studies to establish the role of RE in the treatment of such malignancies are warranted.
      Liver Cancer 2015;4:6-15
       
  • Yttrium-90 Microsphere Radioembolization for Hepatocellular Carcinoma
    • Abstract: Yttrium-90 (Y90) radioembolization is an emerging strategy to treat liver malignancies, and clinical data supporting its use have accumulated in recent years. Y90-radioembolization has shown clinical effectiveness in intermediate and advanced hepatocellular carcinoma, with a favorable safety profile. Retrospective data show similar levels of effectiveness to transarterial chemoembolization in intermediate hepatocellular carcinoma, with some evidence of better tolerance. While phase 3 studies comparing Y90-radioembolization to chemoembolization in intermediate hepatocellular carcinoma would be difficult to conduct, studies comparing or combining Y90-radioembolization with sorafenib are under way. Questions also remain about the most suitable modalities for defining the dose to administer. Phase 3 studies are under way to clarify the place of Y90-radioembolization in the algorithm of HCC treatment.
      Liver Cancer 2015;4:16-25
       
  • JSH Consensus-Based Clinical Practice Guidelines for the Management of
           Hepatocellular Carcinoma: 2014 Update by the Liver Cancer Study Group of
           Japan
    • Abstract: The Clinical Practice Guidelines for the Management of Hepatocellular Carcinoma proposed by the Japan Society of Hepatology was updated in June 2014 at a consensus meeting of the Liver Cancer Study Group of Japan. Three important items have been updated: the surveillance and diagnostic algorithm, the treatment algorithm, and the definition of transarterial chemoembolization (TACE) failure/refractoriness. The most important update to the diagnostic algorithm is the inclusion of gadolinium-ethoxybenzyl-diethylenetriamine pentaacetic acid-enhanced magnetic resonance imaging as a first line surveillance/diagnostic tool. Another significant update concerns removal of the term “lipiodol” from the definition of TACE failure/refractoriness. © 2014 S. Karger AG, Basel
      Liver Cancer 2014;3:458-468
       
  • Overexpression of Leucine-Rich Repeat-Containing G Protein-Coupled
           Receptor 5 (LGR5) Represents a Typical Wnt/β-Catenin
           Pathway-Activated Hepatocellular Carcinoma
    • Abstract: Background: Hepatocellular carcinoma (HCC) is one of the most common and most frequently lethal cancers worldwide. Although many advances have been made in the analysis of multistage hepatocarcinogenesis, we still lack information to guide adequate clinical management options for HCC. A large number of genetic alterations occur during hepatocarcinogenesis, and many genetic studies have indicated that one of the most frequently mutated oncogenes found in HCC is β-catenin. Summary: Molecular subclassification of HCC based on gene expression signatures has identified a typical hepatocyte-like subclass of HCC harboring β-catenin mutations; this subclass is characterized by better histological differentiation and a less aggressive nature. We previously identified overexpression of the leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5), also known as GPR49, in HCC with β-catenin mutations. LGR5 has been indicated as one of the downstream target genes of the Wnt signaling pathway; however, the functional role of LGR5 in cancer is largely unknown. We demonstrated that HCC cells transfected with LGR5 exhibited higher colony forming activity and were more resistant to a cytotoxic drug than the control HCC cells were. Overexpression of LGR5 also retarded cell migration. LGR5-transfected HCC cells formed nodule-type tumors in the livers of immunodeficient mice, whereas control cells formed more invasive tumors. Results of our recent research suggest that aberrant expression of LGR5 could regulate the epithelial cell phenotype and promotes HCC cell survival. HCC cells overexpressing LGR5 seem to represent a typical phenotype of a less aggressive HCC. Key messages: Recent efforts on the molecular classification of HCC have led us to new strategies for dealing with HCC. These specific signatures may predict the risk of recurrence or the patient survival rate, which affect the outlook and may suggest treatment strategies for HCC patients. © 2014 S. Karger AG, Basel
      Liver Cancer 2014;3:451-457
       
  • Using Modified RECIST and Alpha-Fetoprotein Levels to Assess Treatment
           Benefit in Hepatocellular Carcinoma
    • Abstract: Background and Aims: Assessing treatment responses in hepatocellular carcinoma (HCC) is challenging, and alternative radiologic methods of measuring treatment response are required. Modified Response Evaluation Criteria in Solid Tumors (mRECIST) for HCC and alpha-fetoprotein (AFP) levels were assessed in a post hoc analysis of a phase II study of brivanib, a selective dual inhibitor of fibroblast growth factor and vascular endothelial growth factor signaling. Methods: HCC patients were treated with first-line (cohort A; n = 55) or second-line (cohort B; n = 46) brivanib alaninate 800 mg once daily. Outcomes were compared between World Health Organization (WHO) criteria and (retrospectively by) mRECIST by independent review. The relationship between on-study AFP changes and outcome was analyzed in patients with elevated AFP at baseline. Results: Response rates were higher with mRECIST versus WHO criteria in cohorts A (25.5% vs. 7.3%) and B (10.9% vs. 4.3%). Progressive disease (PD) as assessed by mRECIST was associated with a very short median overall survival (OS; cohort A, 2.8 months; cohort B, 5.3 months); PD as assessed by WHO criteria reflected a mixed population of patients with better outcomes. mRECIST responders tended to have a>50% AFP decrease during therapy. In cohorts A and B pooled, an early AFP response (>20%or >50% decline from baseline within the first 4 weeks) was not associated with longer median OS. Conclusions: Tumor response as assessed by mRECIST differed from that by WHO criteria, with mRECIST possibly identifying true nonresponders with a poor prognosis. Many patients had AFP decreases correlating with tumor shrinkage, yet an association with long-term benefit was unclear. mRECIST and on-treatment AFP levels are being explored further with brivanib in HCC. © 2014 S. Karger AG, Basel
      Liver Cancer 2014;3:439-450
       
  • Management of Hepatocellular Carcinoma in Cirrhotic Patients with Portal
           Hypertension: Relevance of Hagen-Poiseuille's Law
    • Abstract: Background: Hepatic decompensation in cirrhosis heralds an accelerated course with poor survival. An increase in hepatic venous pressure gradient (HVPG), rather than surrogate tests of liver function, appears to be the sole predictor of decompensation after surgical resection. We propose that hepatic sinusoidal walls become less elastic as cirrhosis progresses. Decompensation signals the development of increased vessel wall rigidity. The pressure-flow characteristics then become subject to Hagen-Poiseuille's law, which applies only to rigid, cylindrical vessels. Thereafter, HVPG rises exponentially (by a factor inversely proportional to the fourth power of the net radius of functional sinusoidal vessels , 1/r4, at any given hepatic blood flow rate. This review attempts to correlate liver stiffness, risk of decompensation and outcomes from hepatocellular carcinoma (HCC) in patients with cirrhosis. Summary: We compare the complexity of autoregulation in the normal elastic liver, which has a unique dual blood supply, with that in the rigid cirrhotic liver. We also review, in the context of background liver cirrhosis, the management of HCC which is in essence, a solid mass of unorganized cells that exacerbates liver stiffness. We discuss the differential effects of various therapeutic modalities such as liver transplantation, loco-regional therapy and drugs on HCC outcomes, based on their effects on HVPG. Key Messages: Increased hepatic artery supply, or the hepatic artery buffer response, may be the only available method for autoregulation or maintenance of hepatic blood flow in the cirrhotic liver. In HCC, loco-regional therapies, including partial resection of the cirrhotic liver, can exacerbate portal hypertension by increasing blood flow within the remnant organ. We conclude that studies of HVPG reduction as part of HCC management may be beneficial and are warranted. © 2014 S. Karger AG, Basel
      Liver Cancer 2014;3:428-438
       
  • Biomarkers and Personalized Sorafenib Therapy
    • Abstract:
      Liver Cancer 2014;3:399-404
       
  • Multimodality Management for Barcelona Clinic Liver Cancer Stage C
           Hepatocellular Carcinoma
    • Abstract: This review summarizes the contents of a workshop on multimodality management for Barcelona Clinic Liver Cancer (BCLC) stage C hepatocellular carcinoma (HCC) held on July 6, 2013, under the auspices of the 4th Asia-Pacific Primary Liver Cancer Expert Meeting Scientific Advisory Committee. BCLC stage C HCC represents a varied disease spectrum and, therefore, further stratification of BCLC stage C should be explored. Although sorafenib is currently the standard treatment for BCLC stage C HCC, the survival benefits are modest and new treatment strategies are still needed. Based on the opinions of Asian experts, there are numerous alternative options aside from sorafenib for the treatment of BCLC stage C HCC, including surgical resection, hepatic arterial infusion chemotherapy, transarterial chemoembolization, and external radiotherapy. Moreover, there are several studies on the multimodality management of BCLC stage C HCC, mainly in the form of retrospective studies and a few phase I and II trials. Multimodality management with combinations of various locoregional therapies or locoregional therapies with systemic targeted therapy using sorafenib needs to be actively investigated. The Asia-Pacific clinical practice guidelines on multimodality management for BCLC stage C HCC need recommendations based on the level of evidence, the strength of the data, and the strength of recommendations of previously reported systems. © 2014 S. Karger AG, Basel
      Liver Cancer 2014;3:405-416
       
  • Alteration of Epigenetic Profile in Human Hepatocellular Carcinoma and Its
           Clinical Implications
    • Abstract: Hepatocellular carcinoma (HCC) is a common cancer worldwide and develops against a background of chronic liver damage. A variety of HCC-related genes are known to be altered by genetic and epigenetic mechanisms. Therefore, information regarding alteration of the genetic and epigenetic profiles in HCC is essential for understanding the biology of this type of tumor. Methylation at CpG sites in gene promoters is known to affect the transcription of the corresponding genes. Abnormal regional hypermethylation is observed in the 5′ region of several tumor suppressor genes (TSGs) in HCC, and this hypermethylation may promote carcinogenesis through the transcriptional inactivation of downstream TSGs. The DNA damage induced by oxidation is a trigger of abnormal DNA methylation and inactivation of TSGs through recruitment of the polycomb repressive complex to the promoter sequence. Thus, oxidative stress may be responsible for the emergence of HCC from chronic hepatitis and liver cirrhosis through the epigenetic alteration of TSGs. There have been several attempts to apply epigenetic information to the diagnosis and treatment of HCC. The predictive value of selected methylation events on survival in HCC patients has been reported, and the methylation profile of background liver could be associated with recurrence-free survival of HCC patients who have undergone hepatectomy. Another study detected methylated DNA from HCC cells in serum, and the circulating tumor DNA was regarded as a potential tumor marker. In addition, several trials of HCC therapy have targeted the epigenetic machinery and were based upon comprehensive analyses of DNA methylation of this type of tumor. Here, we present an overview of research regarding DNA methylation status in human HCC and describe the clinical application of epigenetic information to HCC. © 2014 S. Karger AG, Basel
      Liver Cancer 2014;3:417-427
       
 
 
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