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)

Serum alpha-fetoprotein (AFP) levels were measured by radioimmunoassay in 89 healthy adult Chinese, 170 patients with histologically verified non-malignant liver diseases, and 14 hepatitis B surface antigen (HBsAg) carriers with normal liver histology. In 97% of the healthy adults, AFP levels were under 20 ng/ml, which is then regarded as the normal upper limit. Cases with supranormally elevated AFP levels ranged from 15-51% in chronic hepatic disorders and were 33% in acute hepatitis. None of the healthy HBsAg carriers had abnormal AFP level. HBs antigenemia was found to be related to AFP elevation in chronic active hepatitis, cirrhosis, and acute hepatitis but not in chronic persistent hepatitis and healthy HBsAg carriers. The correlation could be demonstrated only when the sensitive third generation test was employed to define seropositivity of HBsAg. Events after hepatic injury induced by hepatitis B virus, rather than the HBs antigenemia itself, are probably responsible for the association. Whether the association of HBsAg and elevated serum AFP in these nonmalignant hepatic disorders contributes to the higher risk of subsequent development of hepatocarcinoma in Taiwan is unknown and requires further long-term longitudinal study.
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PMID:Relationship of hepatitis B surface antigen to serum alpha-fetoprotein in nonmalignant diseases of the liver. 8 92

The bilirubin-binding ability of human alpha-fetoproteins, which were purified from fetal cord serum and from ascites fluid of a hepatoma-bearing patient, was examined by the difference spectrum and the Jacobsen peroxidase methods. The difference spectrum observed as a result of the specific binding of bilirubin to alpha-fetoprotein had a maximum at 482 nm, and this pattern was quite similar to that observed for serum albumin. The result obtained by the difference spectrum method showed that 1 mol of each alpha-fetoprotein bound 1 mol of bilirubin at pH 8.3 and that the dissociation constants of the complexes of bilirubin with fetal alpha-fetoprotein and hepatoma-derived alpha-fetoprotein were 2.6 x 10(-7) and 5.0 x 10(-7) M, respectively. The Jacobsen enzymatic method using horseradish peroxidase gave the same values for molar binding ratios and similar dissociation constants, 7.1 x 10(-7) M for fetal alpha-fetoprotein and 7.4 x 10(-7) M for hepatoma-derived alpha-fetoprotein. These results indicate that alpha-fetoprotein may function as a carrier protein for bilirubin as has been shown for serum albumin.
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PMID:alpha-Fetoprotein as a carrier protein in plasma and its bilirubin-binding ability. 8

Rat alpha-macrofetoprotein (AMF) and alpha-fetoprotein (AFP) are secreted by the fetal liver and become elevated in serum during hepatocarcinogenesis and in animals bearing hepatocellular carcinomas. It has been suggested that these fetal plasma proteins may be influenced by related control mechanisms. The experiments presented herein examined the early responses of these plasma proteins during hepatocarcinogenesis using the hepatocarcinogens acetylaminofluorene and diethylnitrosamine. Under these conditions, AFP serum concentrations were elevated within a few days of exposure to acetylaminofluorene, whereas AMF serum concentrations remained essentially normal. AFP became elevated after a number of weeks of exposure to diethylnitrosamine. In either regimen, AMF became elevated only later when large primary hepatocellular carcinomas were found. The time of appearance of AMF after transfer of an AFP-secreting Morris hepatoma indicated that AMF was elevated only in animals with extremely large, necrotic tumors. Thus, it appears that elevation of serum AFP resulted from either exposure to hepatocarcinogens or production by hepatocellular carcinomas, but that the elevations of serum AMF levels resulted from inflammatory injury or necrosis of tumor tissues.
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PMID:Rat alpha-macrofetoprotein (acute-phase alpha 2-macroglobulin) during hepatocarcinogenesis. 8 3

The expression of alpha-fetoprotein (AFP) was infestigated in a cloned cell culture derived from Morris hepatoma 7777, which shows a density-dependent variation in the AFP synthesis rate. The rate of secretion of AFP was found to be governed by the level of cytoplasmic mRNAAFP. Saturation hybridization of pulse-labeled RNA to excess cloned cDNAAFP was used to illustrate quantitatively how mRNAAFP is regulated in these tumor cells. It was found that the mRNAAFP level is primarily determined by its rate of transcription and mRNAAFP declines to 40% of its maximum level, and it accumulates at 20% of its maximum rate. The half-life of mRNAAFP was found to be 40 h, 5 to 6 times that of poly(A)-containing RNA. This difference in stability, in cells doubling every 20 h, results in a 2 1/2-fold increase in the fraction of mRNAAFP above that expected from the relative transcription rate of mRNAAFP. During maximal synthesis of AFP, mRNAAFP accumulates in the cytoplasm at a rate 25 times greater than an average middle abundance mRNA and 1000 times greater than the average low abundance mRNA. These results and the relatively high translational efficiency of mRNAAFP explain how cells can optimize production of an abundant protein.
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PMID:alpha-Fetoprotein gene expression. Control of alpha-fetoprotein mRNA levels in cultured rat hepatoma cells. 9 46

In 1977 and 1978 the serum concentration of alpha-1-fetoprotein (AFP) in 3200 patients was measured for diagnostic purposes. Values above 320 ng/ml were observed in 75 patients; they underwent closer study. The final diagnoses were hepatoma (50), germ cell tumors (15), other malignant tumors (6) and acute hepatitis (4). Also, chronic hepatitis and liver coma may be associated with AFP values above 320 ng/ml. Repeated measurements usually provide further diagnostic information.
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PMID:[Severely increased alpha fetoprotein and associated diseases]. 9 51

Epidermal growth factor stimulated both [3H]thymidine uptake and proliferation of rat AH66 hepatoma cells. However, the increase in cell number was not accompanied by a proportional increase in the levels of alpha-fetoprotein of the culture media. The effects of EGF on the cell proliferation were antagonized by N6,O2'-dibutyryl cAMP.
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PMID:Epidermal growth factor stimulates proliferation of rat hepatoma cells producing alpha-fetoprotein. 9 54

The immunocellular response to fetal antigens was studied in ten patients with hepatocarcinomas. Homogenized extracts of human fetal liver and purified human alpha-fetoprotein were used as antigen substances. The control group included 15 patients with cirrhosis of the liver. The level of circulating T lymphocytes (E-rosettes) was also registered. Patients with hepatocarcinoma showed a definite response to both antigens, determined by the degree of inhibition of leukocyte migration. The migration indices were as follows: x = 0.65 +/- 0.16 for homogenized fetal liver antigen, and x = 0.79 +/- 0.13 for alpha-fetoprotein antigen. These values were 0.93 +/- 0.13 and 0.95 +/- 0.15 respectively in the cirrhotic patients. The differences in the migration indices for the two groups were statistically significant with both antigens (p less than 0.0005 and p less than 0.005). The decrease of the number of T lymphocytes in patients with hepatomas was also significant (p less than 0.005). The determination with homogenized fetal antigen was more sensitive than with alpha-fetoprotein (p less than 0.01). A significant relationship between the severity of the tumor and the immunocellular response could also be seen (r = 0.84; p less than 0.001). Response tended to diminish as the tumor progressed. The disappearance of immunocellular response seemed to depend at least in part on the decreasing number of T lymphocytes, since there was a significant inverse correlation between the two parameters (r = -0.75; p less than 0.01).
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PMID:[Immunocellular response to fetal antigens in patients with hepatoma (author's transl)]. 9 78

Mice bearing the BW7756 hepatoma were passively immunized using rabbit antiserum to murine alpha-fetoprotein (AFP) administered in constant or increasing doses. Control tumor-bearing mice were inoculated with saline or nonimmune rabbit serum (NRS) (constant or increasing doses), or were left untreated. The tumor growth curves from mice receiving constant or increasing doses of anti-AFP or constant doses of NRS showed suppression of hepatoma growth; but in both groups of anti-AFP-treated mice this was accompanied by gross anatomical changes, including necrosis, more extensive than in the NRS-treated or other control mice. AFP blood levels roughly paralleled the tumor growth responses. Since an immunological response against the rabbit serum was elicited in the host, it is possible that circulating immune complexes play some role in tumor suppression. Changes observed in liver- and spleen-to-body weight ratios may also reflect a response to circulating immune complexes.
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PMID:Immunobiologic studies in hepatoma-bearing mice passively immunized to alpha-fetoprotein. 9 91

Herpesvirus saimiri (HVS) is an oncogenic virus for a variety of nonhuman primates. HVS does not produce overt disease upon inoculation in the natural host (squirrel monkey) but consistently induces neoplasms including lymphomas and lymphocytic leukemias in 4 other species of monkeys. Various drugs inhibit replication of HVS in vitro including cytosine arabinoside and adenine arabinoside. In addition, the lymphoma and leukemia induced in owl monkeys responds to vincristine and prednisolone, cyclophosphamide, cytosine arabinoside, and human interferon. Of the various chemical carcinogens studied, the antitumor agent procarbazine induces neoplasms in a variety of species including monkeys. Thus far this compound has induced acute myelogenous leukemia (AML), lymphoma, and hemangiosarcomas in macaques. We have induced primary liver tumors in macaques with several nitrosamines and aflatoxin B1 and these tumors produce alpha-fetoprotein (AFP) which can be assayed for both diagnosis and therapy. Thus far, therapy of hepatocellular carcinoma has been most successful with surgical resection; and the tumor mass and serum AFP have been less responsive to single agent chemotherapy. These nonhuman primate models are useful for an understanding of the cause, diagnosis, prevention, and treatment of the human disease.
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PMID:Nonhuman primate models for lymphoma, leukemia, and other neoplasms. 16 36

The clinical course and pathological patterns of a group of 13 patients with both primary liver cell carcinoma and Hepatitis B surface antigen (HBsAg) are described and contrasted with those of 43 patients with primary liver cell carcinoma but without HBsAg. HBsAg-positive carcinoma patients demonstrated a higher incidence of splenomegaly, transudative ascites, and the presence of alpha-fetoprotein, although none of these reached statistical significance. Serum bilirubin was significantly higher in patients with HBsAg. HBsAg-positive carcinoma patients most frequently originated from countries where the presence of HBsAg is high in the general population. Survival time from the diagnosis of primary liver cell carcinoma was shorter in patients with HBsAg.
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PMID:Primary liver cell carcinoma in the presence or absence of hepatitis B antigen. 18 15


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