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Scapula as an uncommon site of Langerhans cell histiocytosis in an infant

least 13 complementation groups have been distinguished: A, B, C, D1, D2, E, F, G, I, J, L, M and N. Complementation groups in 13 reported FA patients with VACTERL phenotype were also analyzed and all patients were assigned to complementation groups A, C, D1, E, F, and G. The small number of VACTERL patients makes determination of the specific complementation groups of FA difficult. Although the etiology and pathogenesis of VACTERL association are not known, an adriamycin rat model has been used as a reliable model for the VACTERL association. Adriamycin intercalates with DNA, resulting in inhibition of DNA and RNA syntheses, DNA fragmentation, and altered DNA repair. Recent evidence suggests that FA proteins function as signal transducers and DNA-processing molecules in a DNA damage response network. The mechanism by which an FA gene mutation leads to a multitude of congenital anomalies observed in FA is, however, unknown. We speculated that defects in DNA damage responses play a part in both embryogenesis and hematopoiesis. In conclusion, the curative treatment for FA is allogeneic stem cell transplantation, which is more successful in younger patients with a smaller cumulative volume of transfused blood prior to transplantation. In patients with congenital malformations a timely diagnosis of FA can lead to appropriate genetic counseling and therapy. References