Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1864663 (HCC)
 2,985 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HCC is the most frequent primary malignancy of the liver and one of the most common cancers in the world. HCC is substantially a complication of liver cirrhosis, and because HBV and HCV are the predominant causes of chronic liver disease and cirrhosis worldwide, they have a propensity to lead to HCC. Common sites of HCC metastases include the lung, lymph nodes, and portal vein. Bony metastases are rare, and when they do occur the disease is usually far advanced and is associated with clinical manifestations of abdominal pain, weight loss, jaundice, hepato-splenomegaly, ascities, deranged LFTs, and elevated AFP. We report here a patient with asymptomatic advanced HCC, normal LFTs, and normal AFP values presenting with spinal cord compression.
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PMID:Asymptomatic advanced hepatocellular carcinoma presenting with spinal cord compression. 1574 89

We constructed a novel hepatocellular carcinoma-specific conditionally replicative adenovirus (CRAd). 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. An insulator HS-4 was placed in front of the AFP promoter to enhance the fidelity of the heterologous promoter. This virus was shown to have specific cytolytic activity in AFP-expressing HCC cells in vitro. Furthermore, the replication efficiency of Ad.HS4.AFP.E1A/TRAIL correlated well with AFP expression of the host cells, showing a 100-fold and 1 000 000-fold decrease in the low-and non-AFP-expressing HCC cells, respectively, compared to the high AFP-expressing HCC cells. An increase in mRNA of TRAIL and the elevated Caspase-3 activity were also observed in Ad.HS4.AFP.E1A/TRAIL-infected HCC cells. These results indicated that TRAIL expression from the viral vector activated the Caspase-3 enzymatic capacity and the HCC cells were sensitive to TRAIL. In vivo, Ad.HS4.AFP.E1A/TRAIL effectively prevented the growth of low AFP-expressing BEL-7404 xenografts. These results indicate that Ad.HS4.AFP.E1A/TRAIL could provide a new strategy of gene therapy for HCC.
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PMID:A tumor-specific conditionally replicative adenovirus vector expressing TRAIL for gene therapy of hepatocellular carcinoma. 1608 83

Retrospective study in Clinicopathology of 66 surgical liver tissue from adult Thai patients admitted at Rajavithi Hospital, in Bangkok, during December 2002-September 2003 (10 month periods). The main purposes are: 1) To find the correlation of HBV, HCV with CH, LC, HCC. 2) To compare the correlation of Hepatocyte, AFP, CEA (IHC) in malignant cells, which one is the best usage to confirm the diagnosis of HCC in both primary and metastasis. 3) To review the clinicopathology of all these 66 liver samples. The results were significant correlation of HBsAg (serology) with HCC (p = 0.010), and also significant correlation of HBsAg (IHC in liver tissue) with CH, LC (p = 0.038, 0.021 respectively). Although no significant correlation (p > 0.05) of HCV (positive anti HCV) with CH, LC, HCC; the causes due to the small sample sizes and short period study are possibly bias factors. The authors concluded that Hepatocyte or Hep-Par I is the best immunocellular marker for malignant liver cells both in primary and metastasis (p < 0.001). The AFP, CEA show no correlation (p = 0.999, 0.670). The authors found other interesting non-viral related liver disease, common, uncommon, tumor and tumor-like (pseudotumor) lesions in the liver from the present study. The results of significant correlation of HBV (HBsAg) with CH, LC, HCC is one good evidence to further support The National HBV Vaccine Program for the uninfected population, which has been sponsored by the Thai Government, The Ministry of Public Health since 1992 and be one of the best and successful Thai Public-Health Policy.
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PMID:Correlation of HBV and HCV with CH, LC, HCC in liver biopsied tissue at Rajavithi Hospital. 1608 20

A 69-year-old man had radiofrequency ablation therapy (following RFA) for type C cirrhosis with hepatoma (following HCC) of S7 in November 2001. Afterward the patient was followed as an outpatient, but he had been admitted to our hospital due to jaundice confirmed in March 2004. His abdominal wall appeared to be soft and flat, and we could not detect a tumor mass by palpating either. Even though he exhibited no actual symptom of anemia, jaundice was found in the bulbar conjunctiva at the time of admission. Laboratory findings showed a mild inflammation and anemia on his admission, and biochemical data showed a rise of hepatobiliary enzyme with jaundice. A rise of tumor marker (AFP, PIVKA-II) was recognized, too. We performed percutaneous transhepatic bile duct drainage (following PTBD) to decrease jaundice because abdominal echography and CT showed an extension of tumor thrombosis in bile duct and right hepatic duct by HCC of S8. However, a check of T-Bil. was 7.29 mg/dl and showed some slight decrease. Therefore, we administered prostaglandin E1 (following PGE1) at first with an intra-arterial injection catheter aiming to protect the hepatocyte. One week later, we performed hepatic artery injection chemotherapy (CDDP+5-FU) for four weeks. We confirmed a manifested improvement in T-Bil to be 1.92 mg/dl at the end of hepatic artery injections as well as a manifested decrease in hepatobiliary enzyme. We confirmed a decrease of HCC of S8 by abdominal CT, and the response rate was PR. Afterward the patient was conservatively treated even though pancytopenia was present, and was discharged from the hospital in June 2004. The hepatic artery injection chemotherapy used together with PGE1 was effective for the HCC patient with jaundice.
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PMID:[The hepatic artery injection chemotherapy and prostaglandin E1 administration for hepatocellular carcinoma invading the biliary tract with jaundice]. 1631 59

Hepatitis C is a major public health problem. General screening is not advisable and should be limited to risk groups. The gold standard for the assessment of disease severity is liver biopsy. AST and ALT do not correlate with histology. Serum HCV RNA by qualitative assay and HCV genotype should be determined prior to therapy. Response to antiviral therapy should be assessed by testing AST, ALT and qualitative HCV RNA. Repeat liver biopsy is not necessary. The incidence of HCC related to HCV infection is rising. Early detection by a cost effective screening program is essential. In patients with liver cirrhosis caused by hepatitis C, alpha fetoprotein and liver sonography should be done every 6 months. Upper GI endoscopy is recommended every 1-4 years in cirrhotic patients. Over 350 000 000 people are infected with HBV worldwide, and chronic HBV infection is the leading cause of liver cancer and tenth leading cause of death. HBs Ag, HBeAg and HBV DNA positive patients should be monitored for 6 months before treatment. Patients treated with antiviral therapy should be tested for HBAg, HBeAg and HBV DNA at the end of treatment and every 6 months thereafter to assess virologic response. Monitoring of serum HBV DNA is done by PCR. Patients treated with lamivudine should be tested for YMDD mutation. Ultrasound and AFP monitoring are recommended for detection of HCC, but results are not always reliable. Approximately 40% -70% of HIV infected patients have coinfection with HCV, HBV and HDV. HIV/HCV coinfected patients have an increased risk of progressive liver disease and should be treated accordingly.
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PMID:[Monitoring patients with chronic hepatitis during and after therapy]. 1638 Dec 36

The purpose was to determine the response and survival and to analyse the feasibility of single-session, whole-liver SIRT in patients with non-resectable, otherwise non-responding liver cancer. Thirty-nine patients qualified for SIRT. Eighteen patients suffered from colorectal-cancer metastases (CRC), breast-cancer metastases (MBC, 7), HCC (5) and other tumours (9). Response was assessed by tumour-markers and CT-imaging. At 2-4, 5-7 and 8-9 months follow-up in 3/17, 5/15 and 5/10 of CRC-patients CEA-levels were higher than before. In the MBC group 1-3 and 4-6 months after SIRT tumour-marker-levels were higher in 2/6 and 3/3 patients, respectively. In all HCC-patients AFP-levels dropped 1-3 months after SIRT. Using RECIST, in the CRC-group progressive liver disease (PD) was found in 4/17, 2/12, 2/10 and 2/5 patients at 2-4, 5-8, 9-10 and 12-14 months follow-up. Concerning MBC, after 3 months 7/7 patients presented with stable-disease (SD) or partial-response (PR). At 5-6 months, 1/5 patients showed PD. All HCC-patients showed SD/PR at 2-3 months with no PD at 5-8 months. In the mixed-group 5/6 patients presented with SD/PR at 3-4 months and with SD in 2/3 patients at 5-6 months. The median time-to-PD was 6.5, 8.5 and 8 months for the CRC-, MBC- and mixed-group, respectively. SIRT is a promising, liver-targeted approach for patients with otherwise treatment-refractory liver tumours.
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PMID:Mid-term results in otherwise treatment refractory primary or secondary liver confined tumours treated with selective internal radiation therapy (SIRT) using (90)Yttrium resin-microspheres. 1714 21

A case of liver transplantation for HCC complicating BA in an eight-month old infant is reported. HCC in BA is extremely rare. Screening of AFP and ultrasonographic examination should be performed regularly in patients with secondary biliary cirrhosis for early detection of HCC.
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PMID:Early occurrence of hepatocellular carcinoma in biliary atresia treated by liver transplantation. 1723 35

Case 1 was operated for HCC in September, 2002. After then TAE was performed two times for remnant liver recurrence. A year later, huge recurrence of left liver and tumor thrombus in IVC and PV were detected. After starting oral UFT administration, AFP lever went down within normal limit and tumor thrombus and early enhancement disappeared by CT scan. But after about a year, AFP level went up and TAE was performed two times, the patient died in July, 2007. Case 2 was operated for HCC in August, 2004. Re-operation was performed for recurrence of remnant liver in January, 2006. But recurrence was detected and TAE was performed in November. Ascites and leg edema appeared in June, 2007. Many recurrences of right liver, tumor thrombus in right hepatic vein and hilar hepatic lymph node were detected, UFT administration was started. After then, AFP level went down and tumor size reduced markedly by CT scan. We presents two cases effectively treated by oral UFT administration.
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PMID:[Two cases of advanced hepatocellular carcinoma (HCC) effectively treated by oral UFT administration]. 1901 43

Golgi protein-73 (GP73) is a newly identified candidate serum marker for HCC, but GP73 study now is lesser in Asian population. The aims of this study were to determine how GP73 is detected in the serum of healthy, hepatitis B, cirrhosis and HCC by western blotting and RT-PCR, and to establish the sensitivity and specificity of serum GP73 protein and RNA for diagnosing HCC. Serum GP73 was detected by western blotting and RT-PCR, and quantified by densitometric analysis. GP73 was measured in serum from 124 patients with various forms of liver. AFP was tested using commercially available electrochemiluminescence immunoassay. The median sGP73 in patients with HBV-related HCC was significantly higher (P < 0.001) than in healthy individuals and in patients with other diseases. When sGP73 protein was used to detect HBV-related HCC, it had a sensitivity of 77.4% and a specificity of 83.9%, at the optimal cut-off value of 7.4 relative units. The area under the receiver-operating characteristic curve was 0.89. GP73 RNA in patients with HBV-related HCC had a sensitivity of 87.1% and a specificity of 83.9% and AUROC of 0.92. AFP in patients with HCC had a sensitivity of 48.4% and a specificity of 96.8% and AUROC of 0.77. GP73 protein and RNA can be found in the serum of patients with HBV-related HCC obviously higher than of other liver diseases in Asian. GP73 was better than AFP for the diagnosis of HBV-related HCC. RT-PCR is a more sensitive and superior method of quantification than Western blot. Furthermore, our data need to be confirmed in larger cohorts of patients.
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PMID:GP73, a resident Golgi glycoprotein, is sensibility and specificity for hepatocellular carcinoma of diagnosis in a hepatitis B-endemic Asian population. 1939 52

The identification and characterization of tumor-associated antigens (TAAs) and their use in antigen mini-arrays for cancer immunodiagnosis has been of interest recently as an approach to cancer detection. In this study, autoantibodies in sera from a patient with HCC were used as probes to immunoscreen a HepG2 cDNA expression library for the identification of TAAs involved in malignant liver transformation. Recombinant proteins from two genes identified in this manner, Sui1 and RalA were expressed, purified and used as antigens in immunoassays to detect the presence of antibodies in sera from 77 patients with HCC, 30 with chronic hepatitis (CH), 30 with liver cirrhosis (LC) and 82 normal human sera (NHS). The prevalence of antibody to Sui1 and RalA in HCC were 11.7% (9/77) and 19.5% (15/77), respectively, which were significantly higher than prevalence in liver cirrhosis (3.3% and 3.3%), chronic hepatitis (0% and 0%) and normal human sera (0% and 0%). When Sui1 and RalA were added to a panel of eight other TAAs used in a previous study, the final cumulative prevalence of anti-TAA antibodies in HCC to the 10 TAA array was raised to 66.2% (51/77). The specificity for HCC compared with LC, CH and NHS, was 66.7%, 80.0%, and 87.8%, respectively. When anti-TAA was added to abnormal serum AFP as combined diagnostic markers, it raised the diagnostic sensitivity from 66.2% to 88.7%. AFP and anti-TAA were independent markers and the simultaneous use of these two markers significantly resulted in the increased sensitivity of HCC detection.
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PMID:Autoantibodies to tumor-associated antigens combined with abnormal alpha-fetoprotein enhance immunodiagnosis of hepatocellular carcinoma. 1968 63


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