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)

Hepatoblastoma, although rare, is the most common primary malignant neoplasm of the liver in children. In this paper we describe a case of hepatoblastoma with unusual cytologic features and present the histologic, immunocytochemical and ultrastructural features of this neoplasm. A 7-month-old girl presented with a large hepatic mass and metastatic nodules in both lungs. Intraoperative biopsy revealed a hepatoblastoma. Aspiration biopsy yielded a highly cellular aspirate with cords of pleomorphic cells embedded in a mucoid matrix. Histologic sections showed a diffusely infiltrative neoplasm composed of sheets and cords of highly pleomorphic cells. The neoplastic cells stained strongly positive for cytokeratin CAM 5.2 and AE1 and focally positive for alpha-fetoprotein, ferritin, carcinoembryonic antigen and vimentin. Ultrastructurally, the neoplastic cells had abundant intercellular junctions and intracytoplasmic aggregates of intermediate filaments. A mucoid matrix, to our knowledge, has not been reported as a finding on aspiration biopsy. This patient presented with pulmonary metastases, and thus we think the mucoid matrix may be a marker of a more aggressive variant of hepatoblastoma. This case illustrates additional cytologic features of hepatoblastoma and the usefulness of aspiration biopsy in the rapid diagnosis of this rare tumor.
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PMID:Hepatoblastoma. Report of a case with cytologic, histologic and ultrastructural findings. 751 34

Breast cancer markers (TM) are mainly useful for monitoring the course of disease after diagnosis and first line treatment with the control options of primary treatments early recognition of reactivation and efficiency control of palliative treatment. The best single and established marker is a polymorphic epithelial mucin of the MUC-1 family the prototype of which is CA 15-3 (successive markers: MCA, CA-549, TAG-12, CAM 26/29) followed by CEA with lower diagnostic sensitivity and specificity and TPA/TPS reflecting more the proliferative activity. Besides former TM combinations of CEA with one or more less specific markers (e.g. PAM, CRP, beta 2m, ferritin, GCDFP, HCG, total or boney AP, gamma GT), more recent studies recommend the use of fewer markers such as TPA/TPS + CEA or CA 15-3, CA 15-3 + CEA or MCA, CA M26 + CA M29, TAG12 + CA 15-3 + MCA and CEA + CA 15-3 + ESR.
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PMID:Serum marker combinations in human breast cancer (review). 819 81

Chloramphenicol is an antibiotic that consistently suppresses the bone marrow and induces sideroblastic anemia. It is also a rare cause of aplastic anemia. These toxicities are thought to be related to mitochondrial dysfunction, since chloramphenicol inhibits mitochondrial protein synthesis. We hypothesized that chloramphenicol-induced mitochondrial impairment alters the synthesis of ferritin and the transferrin receptor. After treating K562 erythroleukemia cells with a therapeutic dose of chloramphenicol (10 microg/ml) for 4 days, there was a marked decrease in cell surface transferrin receptor expression and de novo ferritin synthesis associated with significant decreases in cytochrome c oxidase activity, ATP levels, respiratory activity, and cell growth. Decreases in the transferrin receptor and ferritin were associated with reduced and unchanged message levels, respectively. The mechanism by which mitochondrial dysfunction alters these important proteins in iron homeostasis is not clear. A global decrease in synthetic processes seems unlikely, since the expression of the cellular adhesion proteins VLA4 and CD58 was not significantly decreased by chloramphenicol, nor were the message levels of beta-actin or ferritin. The alterations were not accompanied by changes in binding of the iron response protein (IRP) to the iron-responsive element (IRE), although cytosolic aconitase activity was reduced by 27% in chloramphenicol-treated cells. A disturbance in iron homeostasis due to alterations in the transferrin receptor and ferritin may explain the hypochromic-microcytic anemia and the accumulation of nonferritin iron in the mitochondria in some individuals after chloramphenicol therapy. Also, these studies provide evidence of a link between mitochondrial impairment and iron metabolism in K562 cells.
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PMID:Chloramphenicol-induced mitochondrial dysfunction is associated with decreased transferrin receptor expression and ferritin synthesis in K562 cells and is unrelated to IRE-IRP interactions. 1043 Jan 73

We have isolated and sequenced a genomic clone encoding the 24- and 26-kDa ferritin subunits in the mosquito Aedes aegypti (Rockefeller strain). The A. aegypti gene differs from other known ferritin genes in that it possesses an additional intron and an unusually large second intron. The additional intron is located within the 5' untranslated region, between the CAP site and the start codon. The second intron contains numerous putative transposable elements. In addition, unlike the human and rat ferritin genes, the A. aegypti ferritin gene is a single copy gene, located at 88.3% FLpter on the q-arm of chromosome 1. Primer extension analysis indicates that the A. aegypti ferritin gene has multiple transcriptional start sites. A differential usage of these sites is observed with varied cellular iron concentrations.
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PMID:Structure and location of a ferritin gene of the yellow fever mosquito Aedes aegypti. 1084 8

Cow's milk protein allergy (CMPA) is common in infants with variable clinical presentation including varied gastrointestinal manifestation. Cow's milk protein allergy chiefly, involving occurs in children below the age of 3 years, successful therapy depends on completely eliminating cow's milk proteins (CMP) from the child's diet. Ideally, with the replacement of hypo or an allergenic food. Symptoms suggestive of CMPA may be encountered in approximately 5 to 15% of infants emphasizing the importance of controlled elimination/milk challenge procedures. We report on an Egyptian male infant, who developed frequent attacks of hematemesis when begin to eat foods other than breast milk including cow's milk and its dairy products at the age of three months. Possible cow's milk protein allergy was suspected. Further diagnostic work-up was done including: Hb, hematocrit, MCV: iron, ferritin, CRP, occult blood in stools, antibodies to H-pylori and upper GIT endoscopy and biopsy from snip of duodenal mucosa. Measurement of serum cow milk protein specific IgE by radio allegro sorbent test (RAST) technique (immune CAP specific IgE method) and results revealed cow's milk protein allergy. It is concluded that cow's milk protein allergy should be considered in cases of hematemesis presented in early infancy in infants who fed cow's milk early and that hematemesis should be added to the list of clinical presentation of CMPA.
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PMID:Case report: hematemesis could be an unusual presentation of cow's milk protein allergy in children in Egypt. 2520 43