Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Portal vein invasion (PVI) is a hallmark of metastatic potential of hepatocellular carcinoma (HCC) and is frequently found at a stage of moderately differentiated HCC. To identify genes involved in PVI of HCC associated with hepatitis C virus (HCV), we performed a comprehensive analysis of 12,600 genes in 35 moderately differentiated HCV-related HCCs by DNA microarray. Our supervised learning method identified 35 genes involved in PVI. Among the 35 identified genes, we focused on the inhibitor of DNA binding 2 (ID2), because it encodes a liver-rich dominant-negative helix-loop-helix protein. The microarray results for ID2 were reproduced by quantitative real-time reverse transcription (QRT)-PCR and Western blot analyses. In an independent set of HCV-related HCCs (n=28) and HCV-unrelated HCCs (n=14), our QRT-PCR showed that decrease in ID2 mRNA levels were associated with PVI in HCV-related HCC but not HCV-unrelated HCC. In conclusion, our results strongly suggest that ID2 plays an important role in PVI process of HCV-related HCC.
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PMID:Identification of ID2 associated with invasion of hepatitis C virus-related hepatocellular carcinoma by gene expression profile. 1708 83

The purpose of this study is to portray right portal vein embolization (PVE) as a valuable technique that helps in expanding the volume of the left liver lobe and discuss the relevant published work. We describe our experience with four patients who underwent PVE and analyse the value of CT and MRI in the preoperative evaluation of these patients. Four patients with hepatic malignancy (hepatocellular carcinoma) (n=2) and metastatic liver disease (n=2) underwent portal vein occlusion. PVE was carried out in three patients using polyvinyl alcohol and stainless steel coils. Portal vein ligation was carried out in the fourth patient. In patients who were candidates for right hepatectomy, CT volumetric analysis was carried out before the surgery to assess the total liver volume and the future remnant liver, which is the residual left hepatic volume (in cases of right hepatectomy) or left lateral segment volume (in cases of right tri-segmentectomy). Because the left lobe volumes were insufficient, patients were selected to undergo right PVE. Computed tomography volumetry was carried out 2-4 weeks after embolization to assess left hepatic lobe regeneration. Magnetic resonance volumetric analysis was carried out in two patients before and after embolization. All four patients had significant regeneration of the left lobe and tolerated the surgery with uneventful postoperative recovery.
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PMID:Assessment of future remnant liver regeneration after portal vein embolization using three-dimensional CT and MR volumetric analyses. 1710 25

Nonalcoholic steatohepatitis (NASH) may cause progressive hepatic fibrosis, cirrhosis, and hepatocellular carcinoma. Treatment, thus far, has been restricted to diet and weight loss, but without compelling results. In this study we aimed to evaluate the efficacy of orlistat therapy in obese patients with NASH. Fourteen obese patients with NASH underwent liver biopsy prior to and subsequent to 6 months treatment with orlistat (120 mg tid). Hepatic fat extension was graded as normal, mild, moderate, or severe. Hepatic fibrosis was scored on a scale from 0 to 4, with 0 denoting no fibrosis and 4, cirrhosis. Portal inflammation was scored as 0-3, with 0 = normal, 1 = mild, 2 = moderate, and 3 = severe inflammation. Fourteen patients had NASH associated with diabetes, hyperlipidemia, or obesity. Orlistat reduced fatty infiltration in 10 patients (70%; P<0.01), 3 of whom had normal liver fat content after treatment. Orlistat improved inflammatory activity by 2 grades in 28% and by 1 grade in 50% of patients and effected no change in 22% of patients. Five patients (35%) returned to normal inflammatory activity. Orlistat improved hepatic fibrosis by 2 grades in three patients (21%) and by 1 grade in seven patients (50%). There was no change in four patients (28%). Orlistat lowered aminotransferases levels, total cholesterol, triglycerides and low-density lipoprotein, respectively. Insulin resistance index and malonyl dialdehyde levels improved significantly after orlistat therapy, whereas HbAic remained unchanged. In conclusion, in obese patients with NASH, liver fibrosis and inflammation improved after therapy with orlistat.
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PMID:Orlistat reverse fatty infiltration and improves hepatic fibrosis in obese patients with nonalcoholic steatohepatitis (NASH). 1740 56

Portal venous thrombosis (PVT) is a condition associated with high morbidity. The etiologies of PVT include intra-abdominal inflammation or infection, surgical intervention, abdominal malignancies such as hepatocellular carcinoma (HCC) and pancreatic carcinoma, or abnormality in coagulation caused by various reasons such as liver cirrhosis. Management of PVT should be based on its etiology and the condition of the patient. We describe a cirrhotic patient with HCC who suffered from acute pancreatitis. PVT in the main trunk was detected at admission due to the episode of acute pancreatitis. The etiology of thrombosis was considered to be inflammation around the main portal trunk caused by pancreatitis rather than cirrhosis or HCC. We did not instigate any management for the thrombosis. Acute pancreatitis was relieved after conservative treatment. Follow-up imaging study performed 46 days after detection of thrombosis showed spontaneous complete resolution of the thrombus. Our experience may provide useful information for the management of such patients.
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PMID:Acute pancreatitis complicated with transient portal venous thrombosis in one patient with hepatocellular carcinoma and cirrhosis. 1752 8

Patients suffering from hepatocellular carcinoma (HCC) with tumor thrombus in the portal vein generally have a poor prognosis. Portal vein tumor thrombus must be distinguished from portal vein blood thrombus, and this identification plays a very important role in management of HCC. Conventional imaging modalities have limitations in discrimination of portal vein tumor thrombus. The application of positron emission tomography (PET) with (18)F-fluorodeoxyglucose ((18)F-FDG) for discrimination between tumor extension and blood thrombus has been reported in few cases of HCC, while portal tumor thrombosis and portal vein clot identified by (18)F-FDG PET/CT in HCC patients has not been reported so far. We present two HCC cases, one with portal vein tumor thrombus and one thrombosis who were identified with (18)F-FDG PET/CT. This report illustrates the complimentary value of combining the morphological and functional imaging in achieving a correct diagnosis in such clinical situations.
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PMID:Positron emission tomography/computed tomography with (18)F-fluorodeoxyglucose identifies tumor growth or thrombosis in the portal vein with hepatocellular carcinoma. 1772 16

Portal vein embolization (PVE) is a preparative procedure to facilitate major hepatectomy. Most patients with various hepatobiliary diseases were tolerable to right PVE. However, a few patients revealed marked deterioration of liver function after PVE, which made surgeons hesitate whether to carry out preplanned major hepatectomy. We report 2 cases of right liver resection after an episode of PVE-induced transient liver failure. The first patient was a 42-year-old male who had hepatocellular carcinoma in the cirrhotic liver background. After right PVE, serum aspartate and alanine aminotransferases raised to 1222 IU/L and 1908 IU/L, respectively. His liver function improved very slowly, and right lobectomy could be performed after waiting of 46 days. Postoperative restoration of liver function was also delayed, but he recovered after all. The second patient was a 53-year-old male with intrahepatic cholangiocarcinoma without jaundice. Serum total bilirubin rose to 10.7 mg/dL after right PVE, and decreased slowly. Right lobectomy was carried out after waiting of 45 days and postoperative course was uneventful. Meticulous liver transection without interruption of hepatic inflow, early infusion of gabexate mesilate, and intraportal infusion of glucose-insulin-potassium solution were adopted to protected the remnant liver. We think that transient liver failure after PVE is not contraindicated for major hepatectomy if there is no definite causal risk factor, but every effort should be paid to prevent posthepatectomy liver failure.
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PMID:Hepatectomy for patients with transient hepatic failure after preoperative portal vein embolization. 1801 25

Portal vein tumor thrombus (PVTT) is observed in a considerable number of hepatocellular carcinoma (HCC) cases. It is an exacerbating factor for patients afflicted with HCC. The sequelae of PVTT are considered to be a contraindication for the treatment of HCC in such patients. The survival of 10 HCC patients with PVTT treated with trans-hepatic arterial continuous injection chemotherapy was compared to 13 HCC patients with PVTT, who received best supportive care only, as a control to validate the efficacy of continuous trans-hepatic arterial injection chemotherapy using an implanted catheter for HCC with PVTT. There were no differences in the liver function and HCC stage between the two groups. The survival was significantly different between the two groups (P=0.01 by the log-rank test). The median survival time was 106 days in the treatment patients, whereas it was 65 days in the control patients. Multivariate analyses showed the therapy to be the only predictor for survival (risk ratio 0.144, P=0.016). The therapy was strongly associated with the PVTT prognosis. In conclusion, the importance of trans-arterial chemotherapy was demonstrated even in advanced dysfunctional cirrhotic HCC patients with PVTT. It is therefore necessary to develop a basic protocol to treat HCC with PVTT.
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PMID:Significance of trans-hepatic arterial chemotherapy for advanced hepatocellular carcinoma with portal vein tumor thrombus. 1863 97

To clarify the characteristics of hepatocellular carcinoma (HCC) with bile duct invasion, we retrospectively analyzed clinical features and surgical outcome of HCC with bile duct invasion (b(+) group, n = 15) compared to those without bile duct invasion (b(-) group, n = 256). In the b(+) group, four patients (27%) showed obstructive jaundice, and a diagnosis of bile duct invasion was obtained preoperatively in seven patients (47%). The levels of serum bilirubin and carbohydrate antigen 19-9 were significantly higher in the b(+) group. Macroscopically, confluent multinodular type and infiltrative type were predominant in the b(+) group (P = 0.002). Microscopically, capsule infiltration (P = 0.040) and intrahepatic metastasis (P = 0.013) were predominant in the b(+) group. Portal vein invasion was associated significantly with the b(+) group (P = 0.004); however, the frequency of hepatic vein invasion was similar (P = 0.096). The median survival after resection was significantly shorter in the b(+) group than in the b(-) group (11.4 vs. 56.1 months, P = 0.002), and eight of 11 intrahepatic recurrences in the b(+) group occurred within 3 months after surgery. HCC with bile duct invasion has an infiltrative nature and a high risk of intrahepatic recurrence, resulting in poor prognosis.
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PMID:Clinicopathologic characteristics of hepatocellular carcinoma with bile duct invasion. 1901 45

Bile duct invasion is rare in patients with hepatocellular carcinoma (HCC). We show the usefulness of selective transcatheter hepatic arterial embolization (TAE) followed by microwave coagulation therapy (MCT) in a case of HCC with portal and biliary tumor thrombi that ruptured into the biliary system. A 70-year-old man with HCC was admitted because of melena and postprandial abdominal pain. Four years earlier, he had undergone posterior segmentectomy of the liver for HCC. Portal venous thrombus was detected on computed tomography (CT) 3 months earlier. On admission laboratory tests revealed the following values: serum alkaline phosphatase, 760 IU/L; total serum bilirubin, 11.9 mg/dL; direct bilirubin, 9.8 mg/dL; serum hemoglobin, 7.7 g/dL; alpha-fetoprotein 103.9 ng/mL; and PIVKA-2, 52,655 mAU/mL. Serum examinations were positive for anti-hepatitis C virus antibody but negative for hepatitis B surface antigens. Ultrasonography revealed a hypoechoic mass in the right branch of the bile duct at the hepatic hilum. Doppler ultrasonography showed blood flow in the mass. CT showed diffuse tumor involvement throughout the liver parenchyma and the presence of a high-density substance in the right intrahepatic bile duct. The diagnosis was hemobilia secondary to HCC in the right hepatic lobe. The symptoms recurred, and emergency TAE was performed 5 days after the onset of hemobilia. The symptoms subsided, and liver function improved. Endoscopic retrograde cholangiography revealed obstruction of the right intrahepatic bile duct. Surgery was performed 15 days after TAE, and MCT of the right hepatic hilum was performed. After MCT, CT revealed necrosis of the right hepatic hilum. Seven months after TAE, the patient died of liver failure with no recurrence of hemobilia.
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PMID:Transcatheter hepatic arterial embolization followed by microwave ablation for hemobilia from hepatocellular carcinoma. 1902 68

Portal vein tumor thrombus (PVTT) in hepatocellular carcinoma (HCC) is a common entity. In colorectal liver metastasis, microscopic tumor invasion into the intrahepatic portal vein is also usually observed, but the incidence of macroscopic tumor thrombus in the first branch and trunk of the portal vein is rare. Most reported cases of PVTT from colorectal cancer had concomitant metastatic nodules in liver parenchyma, and the PVTT was continuous with the liver nodule, like PVTT in HCC. We present a case of PVTT from colorectal cancer with no definite metastatic nodules in liver parenchyma. A 58-year old man underwent laparoscopic high anterior resection for rectosigmoid carcinoma accompanied by bulky tumor thrombus in the branch of the inferior mesenteric vein. Six months later, he received left lobectomy and left caudate resection for liver metastasis. The resected specimen demonstrated there was no metastatic nodule in liver parenchyma and that the left portal system was filled with the tumor thrombus. The patient is alive with no sign of recurrence 66 months after hepatectomy. Even if there is a macroscopic PVTT from colorectal cancer, a better prognosis may be expected when the tumor can be completely resected en-bloc by anatomic hepatectomy including PVTT.
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PMID:Portal vein tumor thrombus from colorectal cancer with no definite metastatic nodules in liver parenchyma. 1929 Apr 61


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