Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroxin-binding globulin (TBG) is secreted by human hepatoma cell lines and was suggested as a tumor marker of primary hepatocellular carcinoma (HCC). However, the results of several clinical studies are contradictory. Therefore, we decided to investigate whether TBG is a valuable marker for early detection and/or followup of HCC. In 30 patients with HCC we determined TBG, thyroxine (T4), trijodothyronine (T3), alpha-feto-protein, ferritin and the sonographically determined tumor size. Twenty one of these patients had liver cirrhosis. In 19 patients hepatitis B-markers could be detected, 9 of whom with positive HBs antigen. Twenty two patients with liver cirrhosis served as controls. Serum TBG in HCC and liver cirrhosis was not significantly different (21.1 +/- 6.9 vs. 18.7 +/- 5.1 micrograms/ml). T4 (p less than 0.04) and the T4/TBG ratio (p less than 0.0002) were significantly lower in HCC. T3 and ferritin were comparable in both groups. TBG correlated with T4 (r = 0.6), but not with the sonographic tumor size, alpha-fetoprotein or ferritin. In 3 patients alpha-fetoprotein and TBG could be determined 3 to 36 months prior to the primary diagnosis of HCC. In none of these patients an increase of TBG was detected before diagnosis of HCC. In the 4 patients under chemotherapy, TBG decreased after the first course. Three of these patients showed further decreasing TBG values in spite of an increasing tumor size. We conclude that in our patients TBG is no valuable tumor marker for the early diagnosis or follow up of HCC.
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PMID:[Thyroxine-binding globulin--not a tumor marker of hepatocellular cancer]. 164 73

A murine monoclonal antibody (MAb 336) reactive with human hepatocellular carcinoma has been raised after immunizing BALB/c mice with whole HepG2 cells. MAb 336 (IgG1) was reactive with HepG2 (whole cells and membrane fractions), but not normal liver or peripheral blood cells. Immunohistological studies indicated that 12/16 hepatocellular carcinoma and 6/11 cirrhotic livers expressed MAb 336-associated antigen, and most normal human tissues and tissues derived from other cancers were unstained. Direct and competitive binding assays ruled out the possibility that this MAb reacts with alpha-fetoprotein, carcinoembryonic antigen, or ferritin. Western blot analysis indicated that MAb 336 reacts with an antigen of approximately 30,000 daltons. This MAb may be potentially useful for studying antigenic expression in hepatocellular carcinoma and as a targeting agent for radioimmunodetection and immunoconjugate therapy.
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PMID:A new murine monoclonal antibody against human hepatoma. 165 1

To clarify the pathogenesis of hepatic iron toxicity, we investigated the effect of chronic dietary iron overload on the expression of several genes in rat liver. After 10 wk of iron treatment, when only minor histological features of liver damage were appreciable, the level of pro-alpha 2(I)-collagen mRNA was already higher than in control liver and increased further at 30 wk of treatment. Also, the relative amount of L ferritin subunit mRNA was enhanced early by iron load and was even more elevated at the latest time point considered, whereas neither H ferritin subunit nor transferrin mRNA levels were affected by iron treatment. In contrast, after chronic iron treatment, no variations were found in the steady-state level of mRNAs transcribed from liver-specific and preferentially expressed genes (albumin, alpha-fetoprotein, apolipoprotein A-1), growth-related genes (c-myc, c-Ha-ras and c-fos) and stress-induced genes (heat shock protein 70). These results suggest that chronic dietary iron overload in rats can specifically activate target genes in the liver (i.e., L ferritin and procollagen) in the absence of either histological signs of severe liver damage or alterations in differentiated liver functions.
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PMID:Liver gene expression during chronic dietary iron overload in rats. 169 54

Genetic haemochromatosis is characterised by an inappropriately high rate of iron absorption by the small intestine. The disease is transmitted as an autosomal recessive condition. The gene frequency in the Caucasian population is approximately 1 in 20 and the disease frequency is 1 in 400. Excessive iron deposition occurs in the liver, pancreas, heart, pituitary and joints and hepatic iron concentrations above approximately 400 mumol/g dry weight are always associated with fibrosis and usually with cirrhosis and progressive liver failure. Accurate diagnosis depends upon the demonstration of elevated hepatic iron stores. An hepatic iron index [hepatic iron concentration (in mumol/g dry weight) divided by patient age] of greater than 2.0 distinguishes homozygous subjects from the other conditions in which slight increases in hepatic iron concentration may occur, e.g. in a subject heterozygous for haemochromatosis or alcoholic liver disease. If cirrhosis is present, patients are at a high risk of developing hepatocellular carcinoma. Therefore, they should undergo regular abdominal ultrasound and alpha-fetoprotein estimation. In the absence of cirrhosis, phlebotomy restores life expectancy to normal. Venesection should be continued until all excess iron stores are removed as judged by failure of a rise in haemoglobin concentration on cessation of phlebotomy. Screening of first degree relatives should commence from a young age (e.g. 10 years). If serum ferritin or transferrin saturation are abnormal, liver biopsy should be undertaken. HLA typing of the family allows for the identification of those siblings who are most likely to develop the disease. Secondary iron overload is often multifactorial in origin. Iron chelation therapy with subcutaneous deferoxamine (desferrioxamine) should only commence after careful consideration of the potential benefits in each individual patient.
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PMID:Current concepts in rational therapy for haemochromatosis. 171 64

The clinical value of serum ferritin level in patients with testicular cancer was studied. Seven cases of seminoma and nine cases of non-seminoma from 1983 to 1989 were evaluated. The serum levels of ferritin, human chorionic gonadotropin (beta-HCG), alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA) and lactate dehydrogenase (LDH) were estimated before and after treatment. Abnormally high values of serum ferritin before treatment were noted in 4/7 (57%) in seminoma, 3/9 (33%) in non-seminoma and 7/16 (44%) in total. The total rate showing abnormally high values of serum ferritin was lower than that of beta-HCG and LDH. Meanwhile it was the same as that of AFP and higher than that of CEA. Changes in the serum ferritin level did not always correspond with the clinical course. In 3 out of 6 tumor free patients, higher levels of serum ferritin before treatment became normal after treatment. In one patient with a high level of serum ferritin before treatment, the level of serum ferritin remained higher and retroperitoneal lymph node metastasis developed after treatment. In 9 cases with normal serum ferritin level, 7 showed the normal range of ferritin level throughout the treatment course. These findings suggests that in some patients with testicular cancer, the serum ferritin level might serve as a tumor marker indicating the efficacy of the treatment and the tumor recurrence.
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PMID:[Significance of serum ferritin level in testicular tumors]. 171 5

Localization of ferritin in testicular tumors was studied by the immunohistochemical method and the usefulness of ferritin was evaluated compared with the clinical course. Seven cases of seminoma and 9 cases of non-seminoma were used for the study. Formalin-fixed, paraffin-embedded tissue sections were stained by the avidin-biotin complex method. Commercial rabbit anti-human ferritin polyclonal antibody in 1/100 dilution was allowed to react at room temperature for one hour. In normal testicular tissues, the epithelium in germinal cells was not stained for ferritin. In seminomas, some tumor nests were stained for ferritin. Interstitial cells, especially histiocytes, were also stained for ferritin. In stained tumor cells, cytoplasm was stained uniformly. Necrotic cells were not stained. The same findings were obtained in non-seminomas. In metastatic lesions and tumor thrombi in the vessels, some tumor cells were stained as intensely as in the origin. A case was calculated positive if more than 5% of the tumor cells in the specimen were stained. The positive rate in ferritin immunostaining was significantly higher than that of human chorionic gonadotropin (beta-HCG), alpha-fetoprotein (AFP) and carcinoembryonic antigen (CEA) immunostaining with the same materials. The specimens from cases with abnormally high serum ferritin level, were stained more intensely than those from cases with normal serum ferritin level. The result suggests that ferritin might be a useful tumor marker in some of testicular tumors.
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PMID:[Analysis of ferritin immunostaining in testicular tumors]. 171 6

The levels of tumor markers were determined in 173 patients with rectal cancer recurrences by radioimmunoassay. An increase in a CEA level was observed most frequently (92.5%). An increase in the levels of alpha-fetoprotein, ferritin and beta 2-microglobulin was observed in 61.7, 56.6 and 46.3%, respectively. CA-19-9, a carbohydrate antigen, was of no importance for the detection of cancer of this site, and an increase in its titer was observed in 15.5% only. Thus the most specific and effective diagnostic test for the diagnosis of rectal cancer recurrences is the determination of a CEA level.
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PMID:[Radioimmunological determination of tumor markers in the diagnosis of recurrences of rectal cancer]. 171 31

Blood levels of carcinoembryonic antigen (CEA), alpha-fetoprotein, ferritin, ACTH. triiodothyronine and thyroxin were measured by radioimmunoassay in 217 cases of lung, hepatopancreatoduodenal and colonic cancer, 61 patients with nontumor pathology of those sites and in 37 healthy controls. CEA proved the most reliable marker of lung and colonic cancer and tumor-related mechanical jaundice, its lowest concentration in 65-100% of cancer patients exceeding the highest levels observed in controls. In the colorectal group, CEA level returned to normal after radical surgery and rose again at recurrence or distant metastases. Ferritin, cortisol and ACTH appeared less efficient.
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PMID:[Tumor markers--a diagnostic and prognostic test]. 185 87

A cell line, HuH-33 was cultured in vitro from a patient with hepatocellular carcinoma. This cell line has been in continuous culture over 12 month period with slow growth potential. HuH-33 was composed spindle-or polygonal-shaped cells as a major population. Chromosome number of the cells were widely distributed even in the primary culture. HuH-33 was transplantable into nude mice and secreted alpha-fetoprotein, albumin, beta 2 microglobulin, ferritin and tissue polypeptide antigen.
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PMID:[Tissue culture course of a human hepatoma cell line]. 196 86

Carcinogenic metal levels in serum and tissue samples were measured in patients with bronchopulmonary or colorectal cancer. The cadmium and nickel tissue levels in the patients with lung cancer were significantly higher than in the controls. A statistical correlation was found between chromium and cadmium, as well as between cadmium and nickel in patients with colorectal cancer. In addition, prior to the operation, the tumor markers alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), carbohydrate antigen (Ca 19-9), polypeptide histidio antigen (TPA) and ferritin were analyzed. Their average concentrations were correlated with the existing concentrations of the metals. This was done for both types of cancer. Tumor marker detection showed an increase of CEA and TPA in patients with colorectal cancer. A statistical correlation was observed between AFP and zinc tumor tissue.
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PMID:Comparative analysis of certain metals and tumor markers in bronchopulmonary cancer and colorectal cancers. Metals and tumor markers in the neoplastic process. 210


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