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portada fanconi anemia: clinical, cytogenetic and experimental aspects
Type
Physical Book
Illustrated by
Publisher
Author
Year
2011
Language
English
Pages
264
Format
Paperback
Dimensions
24.4 x 17.0 x 1.5 cm
Weight
0.46 kg.
ISBN
3642741819
ISBN13
9783642741814
Categories

fanconi anemia: clinical, cytogenetic and experimental aspects

Günter Obe (Illustrated by) · Traute M. Schroeder-Kurth (Illustrated by) · Arleen D. Auerbach (Illustrated by) · Springer · Paperback

fanconi anemia: clinical, cytogenetic and experimental aspects - Schroeder-Kurth, Traute M. ; Auerbach, Arleen D. ; Obe, Günter

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Synopsis "fanconi anemia: clinical, cytogenetic and experimental aspects"

Sixty years ago, G. Fanconi published a paper entitled: "Familiiire infantile pemiziosaartige Aniimie (pemizioses Blutbild und Konstitu- tion)", in which he reported that this type of severe aplastic anemia represents a hereditary disease distinct from other pancytopenias of childhood (Fanconi 1927). Later this syndrome was named Fan- coni anemia (FA; van Leeuwen 1933). A more recent study of the genetics of FA confirmed that the syndrome is inherited in an au- tosomal recessive manner (Schroeder et al. 1976). Prenatal diagno- sis in FA families showed that about 25% of fetuses are affected (Auerbach et al. 1985, 1986). In 1964, Schroeder et al. discovered high frequencies of chro- mosomal aberrations in cultured peripheral blood lymphocytes from patients with FA. Schuler et al. (1969) reported that cells from FA patients are particularly sensitive to the chromosome-breaking activity or clastogenic effect of a polyfunctional alkylating agent. Since that time, studies of baseline and induced frequencies of chromosomal aberrations have been used for the identification of patients with FA. There is now a large body of data concerning the possible mechanism(s) underlying the hypersensitivity of FA cells to DNA cross-linking agents, the biochemical basis for which is still unknown. Complementation analysis, using cells from different FA pa- tients, has demonstrated genetic heterogeneity in the syndrome.

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