Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients with primary hepatic tumours were treated by selective arterial embolisation with gelatin-foam fragments to induce necrosis. In the two with histologically proved hepatocellular carcinoma ultrasonography suggested that necrosis had been induced, as did the rapid initial falls in serum alpha-fetoprotein concentration by 95 and 81% of the original values respectively. Treatment was continued with a course of adriamycin, and both patients remained well and symptom free at 10 and 12 months. In the third patient, who had an expanding and highly vascular benign hepatic adenoma associated with use of a contraceptive pill, embolisation obliterated the tumour mass. Tumour embolisation should be regarded as only the first step in managing hepatocellular carcinoma and as a means of reducing appreciably the viable tumour mass before chemotherapy. It may be used as the primary and definitive treatment in patients with benign liver tumours.
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PMID:Non-operative arterial embolisation in primary liver tumours. 8 83

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

Geographic area, age and sex influence the epidemiology of hepatoma. Aetiological factors are aflatoxins, sex hormones, thorotrast, alpha 1-antitrypsin deficiency, immunosuppression, vinylchloride, parasites, cirrhosis of the liver, and the hepatitis-B virus. Early diagnosis of the tumour is possible using alpha 1-fetoprotein estimations and modern morphological methods, particularly scintiscanning. Tumour resection is therapeutically desirable, while selective chemotherapy remains palliative and liver transplantation failed to prolong survival.
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PMID:[Primary liver cell carcinoma, aetiology and clinical picture (author's transl)]. 9 Dec 71

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

Immunization of C3HA mice with homogenates of various normal definitive tissues, obtained from syngeneic, allogeneic and xenogeneic donors, resulted in an increase of antitumor resistance, as evidenced by a considerable retardation of growth of the transplantable strain-specific hepatoma 22a. The effect may be due to sensibilization of animals to the antigens of normal definitive cells, and, in particular to the tissue-specific antigens characteristic of cells of the tumor in question.
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PMID:[Antitumor resistance induced by immunization with normal definitive tissues]. 9 33

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

The inhibitory effect of vitamin A on tumor establishment and growth has been studied in two animal models. The C57L/J hepatoma, when placed in C57L/J mice receiving inoculations of vitamin A, showed slow growth and the hosts had significantly prolonged survival over untreated mice. The V-2 carcinoma, when implanted in the corneas of New Zealand white rabbits receiving injections of vitamin A, showed decreased vascular response in the limbic vessels. The absence of an induced vascular response prevents vascularization of the tumor and subsequent tumor growth. The evidence suggests that vitamin A may exert its inhibitory effect by modifying the normal vascular response to neoplastic tissue.
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PMID:Vitamin A effect on tumor angiogenesis. 9 97

Serum thyroxine-binding globulin (TBG), the major plasma transport protein for thyroid hormones in man, was shown to be altered under the influence of estrogen and in hypothyroidism. In order to study these alterations, we used an animal model. Synthesis of TBG was demonstrated in hepatocytes isolated from adult Rhesus monkeys, and in a monkey hepatocarcinoma continuous cell culture line (NCLP-6-E). When the hepatocytes were obtained from monkeys pretreated with beta-estradiol (E2), a specific 2.5-2.9 fold increase of TBG synthesis and secretion was shown; similar data were obtained with the tumor line. Furthermore, an increased TBG production was shown with these cells when T4 (from 10(-14) to 10(-11) M) was added to the culture medium. The in vitro results were correlated with in vivo data obtained by investigating the metabolism of TBG after iv injection of tracer doses of purified, radiolabelled TBG to normal, E2-treated and thyroidectomized monkeys. The main effect of estrogen administration was a marked increase of the production rate. During hypothyroidism, the catabolism and the production rate of TBG were decreased. In both conditions, there were significant changes in the distribution volume of TBG, the physiologic relevance of which remains to be investigated.
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PMID:[Hormonal control of thyroxine-binding globulin synthesis and metabolism (author's transl)]. 9 75

Lymphokine-containing supernatants derived from seven different human lymphoid cell lines and lymphokine-containing supernatants from concanavalin A-stimulated murine lymphocytes were found to be capable of reversibly inhibiting the migration of tumor cells in vitro. The tumor cell lines used in these studies were the P815 mastocytoma, Ehrlich ascites, Walker carcinosarcoma, Hepatoma 129, and Sarcoma 37. Preliminary physiochemical evidence suggests that the mediator, here termed TMIF, is distinct from MIF. In any case, these results suggest the possibility that lymphokines other than lymphotoxin or macrophage-activating factors may play a role in tumor immunity.
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PMID:Inhibition of migration of tumor cells in vitro by lymphokine-containing supernatants. 9 77


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