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Prepublished online as a Blood First Edition Paper on May 15, 2003; DOI 10.1182/blood-2003-01-0114. This Article Full Text (PDF) All Versions of this Article: 2003-01-0114v1 102/6/2053    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Dufour, C. Articles by Pistoia, V. Search for Related Content PubMed PubMed Citation Articles by Dufour, C. Articles by Pistoia, V. Social Bookmarking                   What's this? Submitted January 15, 2003 Accepted April 22, 2003 TNF- and IFN- are over expressed in the bone marrow of Fanconi anemia patients and TNF- suppresses erythropoiesis in vitro Carlo Dufour*, Anna Corcione, Johanna Svahn, Riccardo Haupt, Vincenzo Poggi, Albert Nandor Bekassy, Rosanna Scime, Angela Pistorio, and Vito Pistoia Pediatric Hematology-Oncology, Giannina Gaslini Children's Hospital, Genova, Italy Laboratory of Oncology, Giannina Gaslini Children's Hospital, Genova, Italy Epidemiology and Biostatistics Section, Scientific Directorate, Giannina Gaslini Children's Hospital, Genova, Italy Pediatric Hematology Unit, Pausillipon Hospital, Napoli, Italy Pediatric Hematology-Oncology, University Children Hospital Lund, Lund, Sweden Department of Hematology and BMT Unit, V Cervello Hospital, Palermo, Italy * Corresponding author; email: carlodufour{at}ospedale-gaslini.ge.it. Rationale: In Fanconi Anemia (FA) C mice TNF- and IFN- have a key role in the pathogenesis of bone marrow failure. In FA subjects TNF- was found to be increased in the serum and overproduced by patient-derived B cell lines. In acquired aplastic anemia, a disease in which, similarly to FA, marrow failure occurs, TNF- and IFN- are known to act as late mediators of the stem cell damage and are over-expressed in patient marrow lymphocytes. Objectives: To evaluate, in marrow MNCs of FA patients, the expression of negative modulators of the hematopoiesis like TNF-, IFN-, MIP 1, surface Fas-Ligand and the role of TNF- on FA erythropoiesis in vitro. Findings: TNF- and IFN- were significantly over-expressed in stimulated marrow MNCs of FA patients as compared to normal controls. MIP1 and Fas-Ligand were undetectable in patients and controls. In bone marrow cultures, the addition of anti TNF- increased the size and significantly increased the number of CFU-e and BFU-e grown from FA patients but not from normal controls. 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