Acute Myeloid Leukemia Research - AML, Symptoms, Treatment, Information

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In vitro selective suppression of feline myeloid colony formation is attributable to molecularly cloned strain of feline leukemia virus with unique long terminal repeat.

Nagashima N, Hisasue M, Nishigaki K, Miyazawa T, Kano R, Hasegawa A

Department of Pathobiology, Nihon University School of Veterinary Medicine, 1866, Kameino, Fujisawa, Kanagawa 252-8510, Japan.

Molecularly cloned feline leukemia virus (FeLV)-clone 33 (C-33), derived from a cat with acute myelocytic leukemia (AML), was examined to assess its relation to the pathogenesis of AML and myelodysplastic syndrome (MDS). To evaluate in vitro pathogenicity of FeLV C-33, bone marrow colony-forming assay was performed on marrow cells infected with FeLV C-33 or an FeLV subgroup A strain (61E, a molecularly cloned strain with minimal pathogenicity). The myeloid colony-forming activity of feline bone marrow mononuclear cells infected with FeLV C-33 was significantly lower than that of cells infected with 61E. This suggests that FeLV C-33 has myeloid lineage-specific pathogenicity for cats, and that FeLV C-33 infection is useful as an experimental model for investigating pathogenesis of MDS and AML.

Published 26 November 2004 in Res Vet Sci, 78(2): 151-4.
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Acute Myeloid Leukemia Research Today Archive:

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