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 levels were measured by a sensitive double-antibody radioimmunoassay in 580 patients with a variety of malignant and nonmalignant gastrointestinal diseases to determine the incidence of levels elevated above 40 ng/ml. Over 200 normal control subjects have all had levels below 40 ng/ml. Fifteen % of 95 patients with gastric carcinoma, 3 percent of 191 patients with colorectal carcinoma, 24 percent of 45 patients with pancreatic carcinoma, 25 percent of 8 patients with biliary tract carcinoma, and 70 percent of 73 patients with hepatocellular carcinoma had elevated serum alpha-fetoprotein. None of 14 patients with esophageal or small bowel carcinoma had elevated levels. In contrast, 1 percent of 154 patients with nonmalignant, nonhepatic gastrointestinal disease had elevations of serum alpha-fetoprotein. Alpha-Fetoprotein appears to be a potential marker for tumor activity in some patients with certain gastrointestinal cancers.
Cancer Res 1975 Apr
PMID:Serum alpha-fetoprotein in patients with neoplasms of the gastrointestinal tract. 4 83

A staging scheme for hepatocellular carcinoma was presented at an International Symposium on Liver Cancer in Kampala, Uganda in 1971. Historical, clinical, and laboratory aspects of that staging scheme were examined for prognostic significance in 72 untreated patients with this disease studied at the Uganda Cancer Institute. The median survival for the entire group was 1 month. The presence of a serum bilirubin concentration of greater than 2 mg/100 ml or weight loss greater than 25 percent of body weight were the poorest prognostic features. Other factors with prognostic significance were visible abdominal collateral circulation, ascites, tumor differentiation, and serum levels of alkaline phosphatase, SGOT, alpha fetoprotein, and proline hydroxylase. A modified staging scheme is presented which defines three prognostically different groups of Ugandan patients. It is hoped this staging scheme will serve as a stimulus for analysis of similar prognostic features in other populations of patients with hepatocellular carcinoma.
Cancer 1975 May
PMID:A staging system for hepatocellular carcinoma: prognostic factors in Ugandan patients. 4 61

Hepatoma cells derived from The Jackson Laboratory mouse hepatoma BW7756 synthesized alpha fetoprotein (AFP) in vitro. The AFP was immunologically identical to that circulating in the sera of hepatoma-bearing mice. An in vitro cytotoxic effect of rabbit antiserum to AFP was studied in hepatoma cells obtained both from fresh cell suspensions and short-term cell culture. The use of intact and/or inactivated anti-AFP serum inhibited the growth of the AFP-producing cells. The cytotoxic effects of the antiserum depended on exposure time and serum concentration. The cytotoxicity was complement independent, as demonstrated by studies with heat-deactivated serum devoid of extrinsic complement. The control target cells included fresh cell suspensions of normal mouse liver and mouse muscle fibroblasts grown in short-term culture. Specificity of the antisera for the target cells was demonstrated by absorption with purified mouse AFP. The results could be explained by the presence of AFP on the hepatoma cell surface.
J Natl Cancer Inst 1975 Jun
PMID:Alpha fetoprotein: effect of heterologous antiserum on hepatoma cells in vitro. 4 52

The 14C activity of [14C]bleomycin bound to DNA in bleomycin-sensitive rat ascites hepatoma cells (AH-66) was 8.7 times higher than in resistant cells (AH-66F) when the cells were incubated with [14C]bleomycin. The difference in permeability to bleomycin was not significant; uptake of [14C]bleomycin by the sensitive cells was only 1.2 times larger than that by the resistant cells, and the radioactivity incorporated into the nuclei of sensitive cells was only 1.3-fold greater. The bleomycin-inactivating enzyme level in the resistant cells was 3.5 times higher than in the sensitive cells, indicating that the antibiotic incorporated into the resistent cells was reduced in DNA-binding activity to a large extent. The level of protein-free thiol compound in the sensitive cells was 1.8-fold higher than in the resistant cells, suggesting a possible enhancement of bleomycin action by intracellular thiol compound as is found in vitro. These factors probably affect the DNA strand scission and the sensitivity of cells to this antibiotic. Binding of [14C]bleomycin to DNA in vitro was studied in the presence and the absence of dithiothreitol. A large portion of the radioactivity bound in the presence of dithiothreitol was unstable to acid, but the acid-resistant binding was also enhanced by this thiol compound.
Cancer Res 1975 Aug
PMID:Binding of bleomycin to DNA in bleomycin-sensitive and -resistant rat ascites hepatoma cells. 5 Jan 29

Two chemically induced, antigenically distinct guinea pig hepatoma cell lines, line 1 and line 10, which are resistant to killing by rabbit anti-Forssman or specific antitumor antibody and complement, can be rendered susceptible when the cells are pretreated with metabolic inhibitors and drugs commonly used for the treatment of cancer patients. The effect appears within 7 hr after initial contact with the inhibitors and is dependent on temperature and on inhibitor concentration; the effect is reversible within 7 hr, and the process of reversion is also temperature dependent. Not all preparations of tumor cells were rendered susceptible following treatment with inhibitors. In some cases, susceptibility to killing by complement was observed with anti-Forssman antibody but not antitumor antibody. No clear correlation between known metabolic inhibitory activity of the inhibitors and conversion to the sensitive state could be made. The results suggest that properties of nucleated cells, which are under metabolic control, play an important role in the killing efficiency of antibody and complement.
Cancer Res 1975 Nov
PMID:Enhancing effect by metabolic inhibitors on the killing of tumor cells by antibody and complement. 5 4

The line-1 guinea pig hepatoma was used to study in vitro tumor cytotoxicity. Cytotoxicity was determined by measurement of the loss of tritiated thymidine-labeled target cells from culture vessels. With this technique, we demonstrated that significant tumor cytotoxicity was caused by lymphoid cells from tumor-immune guinea pigs, by cells from guinea pigs immunized against an antigen urelated to the tumor target, and by cell-free supernatants rich in lymphocyte mediators. Addition of normal peritoneal exudate cells enhanced the cytotoxic potential of a small number of highly purified immune lymphocytes, which suggested that recruitment of normal cells is an additional mechanism of tumor cell death in this system.
J Natl Cancer Inst 1975 Oct
PMID:Multiple in vitro mechanisms of tumor cytotoxicity demonstrated in the line-1 guinea pig hepatoma model. 5 20

The previously described glycoprotein that promotes tumour cell aggregation, derived from rat ascites hepatoma cells and capable of partial purification by chromatography, was found to be a mixture of 2 factors with different antigenic property. One was not absorbed by immunoadsorbent chromatography with anti-rat serum antibody and the other was. The action of the unabsorbed factor was clearly more potent than that of the absorbed factor. Both the factors were found in the serum of tumour bearing rats and the action of the unabsorbed factor was also more potent than that of the absorbed factor; its amount increased with time after i.p. inoculation of the cells. The serum of healthy rats contained the absorbed factor but not the unabsorbed factor. It was thus assumed that the unabsorbed factor was associated with the hepatoma cell surface itself and released into the serum, while the absorbed factor was associated with serum protein coating the cell.
Br J Cancer 1976 Jan
PMID:Characterization of tumour cell aggregation promoting factor from rat ascites hepatoma cells: Separation of two factors with different antigenic property. 5 93

Quantitative determinations of serum alpha-fetoprotein (AFP) by radioimmunoassay in 193 patients with hepatocellular carcinoma have demonstrated a wide variation in serum levels that appear to be relatively constant for each patient by the time that diagnosis is made. If there is no therapeutic intervention the serum AFP usually follows a gradual increase as the tumor progresses. A few patients have a fall in serum AFP as a preterminal event. Various forms of chemotherapy cause only minor and transient decrease in serum AFP. Surgical resection of tumor produces an immediate fall that parallels the catabolic decay rate for AFP. All AFP-positive patients treated with surgery had recurrence of their tumor with a rise in serum AFP preceeding clinical discovery. The correlation of serum AFP and effective treatment is demonstration of the usefulness of this oncofetal protein marker as an indicator of neoplastic activity for hepatocellular carcinoma and tumors with embryonal cell components and possibly for some other entodermally derived neoplasms.
Cancer 1976 Feb
PMID:Effect of surgical and chemotherapeutic treatment on alpha-fetoprotein levels in patients with hepatocellular carcinoma. 5 16

Alpha fetoprotein (AFP) synthesis by adult rats during gestation and hepatoma growth was determined in vitro with specific precipitations of radiolabeled AFP antisera after incubation of Spinner cultures of various rat tissues in arginine-free culture medium containing radiolabeled arginine. In general, AFP was synthesized by fetal liver, yolk sac, small intestine, and transplantable (tumor) tissue; none of the normal adult tissues, including testis or ovary, produced AFP. AFP synthesis (measured over 22 hours) was confined to the fetal liver (367 ng), yolk sac (1,368 ng), and to a small extent, the gastrointestinal tract during 19-day gestation. None of the maternal tissues produced AFP. When measured during growth of a transplantable hepatoma, AFP was synthesized only by the hepatoma tissue, though the nontumor tissue of the host contained AFP, due to release of AFP from the cultured tissue as it degenerated in vitro, but did not produce it (noninvolved tissues of hepatoma-bearing rats did not incorporate labeled arginine into AFP in vitro). Identifying fetal organs responsible for AFP synthesis explains observed AFP concentration changes in the postpartum period in rats, since elevated AFP in the mother is caused by AFP produced by the fetus which crosses the placenta or yolk sac to maternal circulation. Elevations above normal (.06 mcg/ml) adult rat concentrations occur in 3 circumstances in the nonpregnant rat: 1) development of AFP-producing tumors; 2) proliferation by normal liver cells; and 3) exposure to chemical carcinogens.
J Natl Cancer Inst 1976 Mar
PMID:Tissue sites of alpha fetoprotein synthesis by the rat during pregnancy and hepatoma growth. 5 49

Active or passive immunization of rats to alpha1-fetoprotein (AFP) does not consistently inhibit the growth of AFP-producing transplantable hepatomas in vivo, and anti-AFP does not kill these hepatomas in vitro. However, 3 of 14 rats in 1 experiment responded to passive immunization by reversal of tumor growth as evidenced by normalization of elevated AFP serum concentrations, and 1 of 9 rats actively immunized with rat AFP in complete Freund's adjuvant had suppressed growth of transplantable hepatoma 7777.
Cancer Res 1976 Feb
PMID:Effect of anti-alpha1-fetoprotein on alpha1-fetoprotein-producing rat tumors in vivo and in vitro. 5 92


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