Disease relevance of HCC

• The results in this study also showed that the frequency of antibodies to p16 is relatively higher in nasopharyngeal cancer (28.6%), breast cancer (17.1%) and hepatocellular carcinoma (HCC, 21.4%) [1].
• Increased frequencies at p<0.01 were found for antibodies to p16 in breast, esophageal, and nasopharyngeal cancer as well as HCC [1].
• RESULTS: According to univariate analysis, the risk factors for early multinodular recurrence in HCC were microvascular tumor emboli, portal vein tumor thrombi, intrahepatic metastases, high Edmonson-Steiner classification, lack of tumor capsule formation, increased alpha-fetoprotein concentration, and tumor size [2].
• Extreme elevation of serum alpha fetoprotein in decompensated cirrhosis without HCC: an ominous sign [3].
• Multivariate analysis identified three predictors of early mortality (< 6 mo): bilirubin > 3.2 mg/dL (P < 0.01), HCC as first presentation of liver disease (P = 0.035), and creatinine > 1 mg/dL (P = 0.017) [4].

Psychiatry related information on HCC

• RESULTS: There were no significant differences in etiologic risk factors between HCC-CC and HCC patients: cirrhosis (50% vs 44%), chronic alcohol abuse (36% vs 43%), presence of hepatitis B surface antigen (HBsAg; 66% vs 78%) and presence of hepatitis C virus (HCV) antibody (13% vs 3%) [5].
• A recent case control study performed in Italy showed that the relative risk of HCC in patients with HCV infection and heavy alcohol consumption doubled [6].
• In two consensus development conferences held in Anchorage, Alaska and in Milan, Italy, chronic carriers of HBsAg, patients with cirrhosis, patients with rare metabolic liver diseases, and individuals with family histories of HCC were identified as patients at high risk for HCC and therefore as candidates for periodic screening [7].

High impact information on HCC

• IMPLICATIONS: Further studies are needed to clarify potential risk factors, including specific HCV genotypes, for progression to HCC among HCV carriers [8].
• In FNH, Ang-1 was significantly up-regulated, Ang-2 was down-regulated, and the Ang-1/Ang-2 ratio was highly and specifically increased in FNH compared with normal liver or other groups of lesions (FNH, 15.2-fold increase; HCC, 2.78; adenoma, 2.28; cirrhosis, 1.92; P < 0.01 for FNH vs. all groups, analysis of variance) [9].
• In looking for such a predisposition, we have compared the histocompatibility antigens (HLA) of 102 southern African blacks with histologically proved HCC with those of 208 healthy blacks [10].
• The results of studies of the spectra of HCO, trans-HOCO, HCC, C2-, CO2+, CO2-, C2H2+, C3H4+, HCOOH+, HOCO+, and HCO2- summarized in this Account illustrate the importance of supplementing familiar generalizations with experimental observations [11].
• Orthotopic liver transplantation (OLT) is the only curative therapy of HCC with underlying cirrhosis, but due to HCC metastasis and recurrence, its benefit is limited to a small population who meet the strict selection criteria [12].

Chemical compound and disease context of HCC

• No treatment, resection and ethanol injection in hepatocellular carcinoma: a retrospective analysis of survival in 391 patients with cirrhosis. Italian Cooperative HCC Study Group [13].
• CONCLUSION: This phase II study of nolatrexed in advanced HCC patients, demonstrated minimal activity and significant stomatitis [14].
• Data of the long-term benefit of subjects treated with IFN plus ribavirin are still not available; 5) pooling of published data suggests a slight preventive effect of IFN on HCC development in patients with HCV-related cirrhosis [15].
• This adenovirus, designated Ad.HS4.AFP.E1A/TRAIL, expresses E1A to mediate viral replication and TRAIL to enhance HCC-killing efficacy under the control of a modified AFP promoter [16].
• The specific rotations of 2-substituted butanes (X = F, Cl, CN, and HCC) were calculated at the B3LYP/aug-cc-pVDZ level as a function of the C-C-C-C torsion angle [17].

Biological context of HCC

• Forty frozen tumor tissues and 39 paired plasma samples from HCC patients were collected in Taiwan, to determine the relationship between albumin adducts in blood and DNA adducts in liver tissue as well as mutations in p53 and methylation of p16 [18].
• These data suggest that genetic, epigenetic and environmental exposure biomarkers in plasma may help in estimating the risk for the development of HCC [18].
• AIM: To study the epidemiology of HCC in Lebanon and prognostic factors predictive of early mortality [4].
• We investigated Th1/Th2 cytokine production as well as frequency and phenotype of circulating NKT cells in 14 healthy subjects and in patients during therapy with type C chronic hepatitis (CH; 14 cases) and hepatocellular carcinoma (HCC; 13 cases) [19].
• Although gene expression profiles in HCC derived in all three transgenic lines were highly similar, oncogene-specific gene expression signatures were identified at an early dysplastic stage of hepatocarcinogenesis [20].

Anatomical context of HCC

• We sought to clarify the prognostic value of preoperative peripheral blood leukocyte subset counts, especially the absolute monocyte count, in HCC patients who have undergone hepatic resection [21].
• However, biopsy specimens retain value for showing fibrosis/cirrhosis and dysplastic hepatocytes, both of which increase risks of HCC development [22].
• This cell line, designated Tong/HCC, has been grown in a hormone-supplemented medium for more than 18 months [23].
• METHODS: Thirty-six consecutive patients with PSC and HBC (32 with bile duct carcinoma, BDC, and four with hepatocellular carcinoma, HCC) were pair-matched to control patients referred for liver transplantation because of PSC but who did not have HBC [24].
• T cell infiltration and prognosis in HCC patients [25].

Associations of HCC with chemical compounds

• Independent predictors of early mortality are elevated bilirubin, creatinine and HCC as first manifestation of disease [4].
• Conclusion: The randomized controlled double-blind HECTOR trial showed no survival benefit for HCC patients treated with long-acting octreotide compared with placebo [26].
• Compared with the paired non-HCC liver tissues, genome-wide 5-methylcytosine content in HCC was reduced in all of the tested HCC samples (P < 0.001) [27].
• Dietary factors that appear to influence susceptibility to HCC include fat, protein and amino acids, vitamin A, selenium, and zinc [28].
• Our hypothesis dealt with the possible role of testosterone in the etiology of HCC, which shows a minimum of a 2- to 3-fold male excess in all populations world-wide [29].

Enzymatic interactions of HCC

• Furthermore, MARCKS was serine-phosphorylated in liver cirrhosis and HCC, and phosphorylated MARCKS was detected in a cytosolic fraction of these tissues [30].

Co-localisations of HCC

• RESULTS: Pro-collagen alpha1 (I) mRNA co-localized to alpha-SMA positive hepatic stellate cells within the region of increased collagen deposition in (i) the tumour capsule of encapsulated HCC, and (ii) the tumour junction of non-encapsulated HCC and colorectal metastasis [31].

Regulatory relationships of HCC

• CD80 transfected human hepatocellular carcinoma cells activate cytotoxic T lymphocytes to target HCC cells with shared tumor antigens [32].
• CONCLUSION: TFF-3 is commonly expressed in HCC and its expression correlates with tumor grade [33].
• HBxAg, Fas and FasL might express in the same area of carcinoma tissues and this co-expression could be found in most patients with HCC [34].
• The expression of MARCKS was down-regulated in HCC tissues, as compared with non-tumorous liver cirrhosis tissues from the same patients [30].
• CONCLUSION: COMP is highly expressed within the tumor cells of HCC, suggesting that COMP might play a role in the pathophysiology of this disease [35].

Other interactions of HCC

• Although the level of serum VEGF was significantly higher in all HCC patients than in healthy control, no significant difference, however was observed between HCV infected and HCV-free groups [36].
• To address this, we examined the CAD transcripts in six human HCC cell lines, one liver tissue from a non-HCC subject, and peripheral blood leukocytes (PBL) from three healthy individuals [37].
• MMP-9 activities of HFH-T2, HepG2-HBV and Hep3B were significantly higher than that of non-HBV-hepatocellular carcinoma SK-Hep1 and HepG2 (HCC origin, HBV not detected), as assayed by gelatin zymography [38].
• No positive 111In-OCT scans were obtained, indicating the absence of relevant amounts of functional SSTR2 in HCC [39].
• CONCLUSIONS: Our data suggest a negative effect of an ER(+) tumor on patient survival after curative resection of advanced HCC [40].

Analytical, diagnostic and therapeutic context of HCC

• METHODS: An observational follow-up cohort study of HCC cases diagnosed over a five-year period was carried out [4].
• PURPOSE: We conducted a case-control study to estimate the relative risk (RR) of HCC in relation to HCV infection among residents of the Fukuoka Prefecture, where HCC risk is among the highest in Japan, and to examine whether the risk differs according to HCV genotypes and/or HCV RNA titers [8].
• Surveillance plus chemoprevention in cirrhotic patients with HCV: a better outlook for HCC [41]?
• In six (50%), HCC developed, compared with 2 (8%) from a control group consisting of 24 patients without IFF matched according to age, sex, degree of fibrosis, liver iron amount and follow-up duration [42].
• DCP levels greater than 0.1 AU/ml (100 ng/ml) on ELISA are highly suggestive of HCC or tumor recurrence [43].

References