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)

Fanconi anaemia is an autosomal recessive disease, causing secondary aplastic anaemia and congenital abnormalities, associated with an increased risk of tumours. Liver cell adenoma and hepatocellular carcinoma have rarely been described. Clinical, radiological and histopathological features in three patients with Fanconi anaemia and liver tumours were analyzed. Only one patient had received androgens and none had chronic viral hepatitis. All had elevated serum ferritin with significant parenchymal iron overload. Alpha-fetoprotein levels were normal in all cases. Patient 1 had moderately differentiated hepatocellular carcinoma with venous invasion and satellite nodules. The patient underwent two consecutive resections. Patient 2 had hepatic nodules diagnosed at routine examination with radiological features of adenomas. The patient underwent resection, which showed liver cell adenoma with foci of carcinoma. Patient 3 had three nodules, with radiological and histological diagnosis of adenoma. In patients with Fanconi anaemia, androgen therapy and iron overload may contribute to the development of liver cell adenoma and hepatocellular carcinoma. Hepatocellular carcinoma may occur as a transformation of liver cell adenoma. With prolongation of survival, continued development of liver tumours can be expected. Routine detection should therefore be considered in these patients as curative resection can be performed.
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PMID:Liver tumours in patients with Fanconi anaemia: a report of three cases. 1878 75

Fast- and slow-proliferating human adenocarcinoma colorectal cells, HT-29 and HCA-7, respectively, overloaded with transferrin (Tf), Fe(III) citrate, Fe(III) chloride and Fe(II) sulfate were studied by synchrotron radiation total-reflection X-ray spectrometry (TXRF), TXRF-X-ray absorption near edge structure (TXRF-XANES), and micro-X-ray fluorescence imaging to obtain information on the intracellular storage of overloaded iron (Fe). The determined TfR1 mRNA expression for the investigated cells correlated with their proliferation rate. In all cases, the Fe XANES of cells overloaded with inorganic Fe was found to be similar to that of deliquescent Fe(III) sulfate characterized by a distorted octahedral geometry. A fitting model using a linear combination of the XANES of Tf and deliquescent Fe(III) sulfate allowed to explain the near edge structure recorded for HT-29 cells indicating that cellular overload with inorganic Fe results in a non-ferritin-like fast Fe storage. Hierarchical cluster analysis of XANES spectra recorded for Fe overloaded HT-29 and HCA-7 cells was able to distinguish between Fe treatments performed with different Fe species with a 95% hit rate, indicating clear differences in the Fe storage system. Micro-X-ray fluorescence imaging of Fe overloaded HT-29 cells revealed that Fe is primarily located in the cytosol of the cells. By characterizing the cellular Fe uptake, Fe/S content ratios were calculated based on the X-ray fluorescence signals of the analytes. These Fe/S ratios were dramatically lower for HCA-7 treated with organic Fe(III) treatments suggesting dissimilarities from the Tf-like Fe uptake.
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PMID:Iron overload of human colon adenocarcinoma cells studied by synchrotron-based X-ray techniques. 2675 51