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)

Hepatocellular carcinoma is a very malignant tumor that affects both Caucasian and Oriental populations. In the Caucasian patient, it frequently arises in a background of cirrhosis, most commonly the alcoholic type. In the present study, the alpha-feto-protein level was increased in less than half of the Caucasian patients. In comparison, hepatocellular carcinoma in Oriental patients most often occurs in livers with postinfectious cirrhosis. In the present study, both hepatitis B surface antigen and an increased alpha-fetoprotein level were present in three of four patients. If the tumor is present, however, it appears to behave similarly in both ethnic groups. Without resection, the prognosis is poor, regardless of the presence or absence of underlying cirrhosis or hepatitis B surface antigen status. A tissue diagnosis of hepatocellular carcinoma is most readily made by ultrasonographically guided fine-needle aspiration, which has an 81 percent sensitivity. The most important factor affecting survival is surgical resection. Clearly, the stage at diagnosis is also crucial, but even in more advanced disease, operation can improve survival. It also appears that an increased carcinoembryonic antigen level above normal or a markedly increased alpha-fetoprotein level or both are associated with poor survival. However, whether this is a reflection of tumor size alone, or in fact represents a more aggressive tumor is uncertain and will require further study.
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PMID:Hepatocellular carcinoma. A comparison of Oriental and Caucasian patients. 245 24

Hepatocellular carcinoma (HCC) is a rapidly fatal neoplasm of high worldwide prevalence. Fibromellar carcinoma (FLC), a variant of HCC, lacks the dismal prognosis of "ordinary" HCC (O-HCC) and is characterized by a diagnostic histologic appearance. The current study analyzes the clinical characteristics, immunohistochemistry, and treatment of nineteen cases of FLC. These data, together with a detailed review of the literature, further characterize this unique variant. FLC affects younger patients and lacks the male predominance of O-HCC. Also, FLC lacks specific association with cirrhosis, hepatitis B virus infection, use of oral contraceptives, and alcohol abuse, all of which are implicated in other hepatic tumors. This, along with differences in serum tumor marker prevalence (AFP, B12 binding protein) suggests that its pathogenesis differs from that of O-HCC. Despite these differences, FLC shares a common differentiation with O-HCC. The increased amounts in FLC of stainable alpha-1-antitrypsin, fibrinogen, and C-reactive protein, all of which are acute phase reactants and normal hepatocyte products, implies better differentiation of FLC cells. Finally, the better prognosis of FLC is supported by this study, since only two of the 19 patients died because of tumor. This contrasts with the reported survival of patients with O-HCC, usually measured in weeks. Hepatic transplantation may hold promise for future patients with "surgically unresectable" FLC as procedure-related complications are overcome.
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PMID:Fibrolamellar carcinoma of the liver: an immunohistochemical study of nineteen cases and a review of the literature. 245 77

Hepatocellular carcinoma (hepatoma) accounts for over 80% of primary liver tumors. Although relatively uncommon in North America and Europe, hepatocellular carcinoma is the dominant malignant carcinoma in Southeast Asia and South and West Africa. About 80% of the patients have cirrhosis. The tumor has a grim prognosis with an average survival time of 4.5-13 months after the onset of complaints. Beginning with the observation of the striking coincidence of the geographic distribution of hepatocellular carcinoma with the endemic distribution of virus hepatitis, many studies have demonstrated the close correlation of the carcinoma with chronic hepatitis B. In the endemic areas vertical perinatal transmission of the virus from mother to the newborn is an important route of transmission. While only about 10% of infected adults develop HBs antigen carrier status, the carrier rate of perinatal infections is about 95%. In chronic infection the virus DNA can be integrated into the host genome and may become carcinogenic with time. Many studies have substantiated an increased incidence of liver adenoma and resulting complications among women taking oral contraceptives; evidence for a relationship between oral contraceptives and hepatoma has not been established. No increase in hepatoma has been observed among young women following the introduction of oral contraceptives in the USA and in Denmark.
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PMID:[Hepatocellular carcinoma]. 246 47

Hepatocellular carcinoma may share histologic features with a wide variety of epithelial tumors. To facilitate its pathologic diagnosis, clinical and pathologic material was reviewed from 62 patients with hepatocellular carcinoma and immunostaining was performed with polyclonal anti-carcinoembryonic antigen (pCEA), monoclonal anti-carcinoembryonic antigen (mCEA), anti-epithelial membrane antigen (EMA), and an antikeratin (KER AE1/AE3). Clinical information and follow-up were available for all patients from several sources. Cases with ambiguous clinical data or findings suggestive of metastatic carcinoma to the liver were excluded. In addition, the following tumors were immunostained and compared to hepatocellular carcinoma: 10 cholangiocarcinomas; 14 pancreatic adenocarcinomas; 4 gastric adenocarcinomas; 3 breast carcinomas; 5 renal carcinomas; 3 combined germ cell tumors of the testis; 3 adrenal cortical carcinomas; and 4 melanomas. The pCEA stained bile canaliculi in normal liver and in 39 of 62 (63%) hepatocellular carcinomas. This canalicular staining pattern of pCEA was unique to hepatocellular carcinoma. The mCEA (1 of 62, 1.6%) was almost always negative, and KER AE1/AE3 (9 of 59, 15.3%) was occasionally positive. The EMA stained 25 of 62 (40.3%). The adrenal cortical carcinomas and melanomas were negative for all antigens except rare pCEA and focal EMA staining in an adrenal tumor. Other carcinomas showed cytoplasmic pCEA (36 of 44, 81.8%), mCEA (40 of 46, 87.7%), EMA (41 of 43, 95.4%), and KER AE1/AE3 (42 of 44, 95.5%). Canalicular staining with pCEA is specific for hepatocellular carcinoma, while negativity with mCEA and KER AE1/AE3 is suggestive of hepatocellular differentiation.
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PMID:Immunoperoxidase staining as a diagnostic aid for hepatocellular carcinoma. 246 90

Hepatocellular carcinoma cells (Line-10), obtained from ascitic fluid after diethylnitrosamine treatment of Sewall Wright strain-2 guinea pigs, produce solid (primary) tumours, lymph-node and lung metastases and malignant ascites when reinjected into animals of the same strain. Monoclonal antibodies were raised against the tumour cells by immunizing BALB/c mice with viable ascitic hepatocellular Line-10 tumour cells. Three hybridomas producing anti-Line-10 monoclonal antibodies were selected for further studies (10TL1, 10TL40 and 10TL43) and compared with monoclonal antibodies against intermediate filament keratins. The anti-Line-10 monoclonal antibodies did not cross react with Line-1 hepatocellular carcinoma cells, nor with normal guinea pig hepatocytes. When ascitic Line-10 cells form high papillary projections on the peritoneal surface, they significantly reduced their antigen expression of 10TL40 and of 10TL43 defined antigens, while the expression of 10TL1 defined antigens remained unaltered. Invading Line-10 cells in the deep submesothelial stromal tissue, however, lost reactivity with MoAb 10TL43 but not with the MoAb's 10TL40 and 10TL1. The antigens on lung- and lymphnode metastases remained largely unaffected. The reactivity with MoAb's 10TL40 and with 10TL43 was also lost upon prolonged culturing of Line-10 cells. The reactivity of Line-10 and Line-1 cells with all monoclonal antibodies against keratin filaments remained unaltered. Line-1 cells could be distinguished from Line-10 cells by the absence of any reactivity with the MoAb's 10TL1, -40, -43, but also by the fact that 100% of the Line-1 cells were positive with antibodies against keratins 5/8, 18, and 7.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changing tumour antigen expression in metastatic hepatocellular carcinoma cells of the guinea pig. 246 49

Hepatocellular carcinoma and cirrhosis frequently coexist. In populations with a low incidence of hepatocellular carcinoma, the tumor often arises as a complication of long-standing symptomatic cirrhosis, which may be micronodular or macronodular and which is usually alcoholic in origin, and cirrhosis per se is the major etiologic association of the tumor. The relation between these two pathologic conditions in populations with a high incidence of hepatocellular carcinoma has not hitherto been analyzed. In this study the association was examined in 463 southern African black men with hepatocellular carcinoma. Cirrhosis, almost always macronodular and rarely showing features of alcholic toxicity, was present in 63.1% of the patients. No differences were found in the age structure, clinical features, hepatic function, serum alpha-fetoprotein concentrations, or hepatitis B virus status between patients with hepatocellular carcinoma with and without cirrhosis. Patients with cirrhosis survived slightly longer, but the difference was not biologically significant. It is concluded that the relation between hepatocellular carcinoma and cirrhosis in southern African blacks differs substantially from that in low incidence regions of the tumor.
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PMID:Hepatocellular carcinoma with and without cirrhosis. A comparison in southern African blacks. 247 Jun 34

Hepatocellular carcinoma occurs primarily in individuals with chronic hepatitis B infection and cirrhosis. This tumor is curable only when diagnosed at an early stage and then surgically resected. Therefore, screening tests have been used to identify small tumors in high-risk patients. Currently, the most sensitive and specific tests available involve measurement of serum alpha-fetoprotein levels and high-resolution ultrasonography. The results of these tests are often complementary in making a diagnosis. To be most cost-effective, the frequency of screening can be adjusted to the degree of risk of hepatocellular carcinoma.
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PMID:Screening for hepatocellular carcinoma in high-risk individuals. A clinical review. 247 78

Lectin affinity electrophoresis of serum alpha-fetoprotein (AFP) was carried out on samples obtained from patients with benign and malignant diseases and on cord blood, and separated AFP bands were detected by antibody-affinity blotting. The following major bands were identified by determination of kinetic constants: AFP-C1 and -C2 with concanavalin A, AFP-L1, -L2 and -L3 with Lens culinaris agglutinin A, AFP-P1, -P2, -P3, -P4 and -P5 with erythroagglutinating phytohemagglutinin, and AFP-A1, -A2 and -A3 with Allomyrina dichotoma lectin. AFP bands with the lowest number had either low or no affinity and those with higher numbers had higher affinities for respective lectins. AFP from cord blood and chronic liver disease was characterized by the predominance of AFP-C2, AFP-L1, AFP-P2 and AFP-A3. Hepatocellular carcinoma was differentiated from the benign liver disease by increased proportions of AFP-L3 and AFP-P4. Extrahepatic tumors had additional increases of AFP-C1, AFP-L2, AFP-P5 and AFP-A1 (or slow-migrating AFP-Als, particularly in yolk sac tumor).
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PMID:Lectin affinity electrophoresis of alpha-fetoprotein in cancer diagnosis. 247 60

Hepatocellular carcinoma (HCC) may be detected at a relatively early stage in patients with liver cirrhosis regularly followed by screening programs using ultrasonography (US) and alpha-fetoprotein (AFP) measurement. Using both tests in 214 consecutive cirrhotic patients with no clinical signs of liver cancer, we detected HCC in 20 cases (9.4%). The sensitivity of US was greater (85%) than that of AFP (75%), and the combination of the two methods had a sensitivity of 100%. Only 50% of patients with focal liver lesions at US had a final diagnosis of HCC that was obtained in the majority of cases by US-guided fine needle biopsy.
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PMID:Early detection of hepatocellular carcinoma in patients with cirrhosis by alphafetoprotein, ultrasound and fine-needle biopsy. 248 42

Lymphokine-activated killer activity and natural killer activity in hepatocellular carcinoma patients were assessed. Maximum lymphokine-activated killer activity was induced at 3 to 5 days of incubation, and lymphokine-activated killer activity tended to increase in a manner dose dependent of recombinant interleukin-2. However, the maximum increase of lymphokine-activated killer activity in hepatocellular carcinoma was not as high as that of normal subjects or liver cirrhosis patients. Lymphokine-activated killer activity was impaired in hepatocellular carcinoma as compared to that in normal subjects. Hepatocellular carcinoma seemed to consist of two groups: i.e. a high-lymphokine-activated killer activity group and a low-lymphokine-activated killer activity group. Reduction of natural killer activity was also observed in hepatocellular carcinoma as compared with that in normal subjects and patients with liver cirrhosis. No correlation could be demonstrated between natural killer activity and lymphokine-activated killer activity in normal subjects, liver cirrhosis patients and hepatocellular carcinoma patients. With regard to the presence of HBsAg or alpha-fetoprotein concentration in the sera, there was no significant difference in natural killer and lymphokine-activated killer activity in hepatocellular carcinoma patients. Patients with a small mass lesion showed a low lymphokine-activated killer activity, and depressed lymphokine-activated killer activity was not necessarily related to tumor size. In comparison with the high-lymphokine-activated killer group, the low-lymphokine-activated killer group showed a significant decrease in gamma-interferon production and a preserved function of indocyanine green clearance.
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PMID:Defective function of lymphokine-activated killer cells and natural killer cells in patients with hepatocellular carcinoma. 253 90


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