Author/Authors :
Tirado، نويسنده , , Carlos A. and Meloni-Ehrig، نويسنده , , Aurelia M. and Wallenhorst، نويسنده , , Eian and Burks، نويسنده , , Kristine and Scheerle، نويسنده , , Jay and Morillon، نويسنده , , Maurice and Kelly، نويسنده , , JoAnn C. and Heritage، نويسنده , , Deborah and Spira، نويسنده , , Alexander L. Croft، نويسنده , , Calvin D. and Glasser، نويسنده , , Lewis and Butera، نويسنده , , James N. an، نويسنده ,
Abstract :
We report on two patients with myeloid disorders and complex karyotypes including a dicentric chromosome, dic(17;20)(p11.2;q11.2), resulting in the loss of most of 17p and 20q. The presence of the centromeres of chromosomes 17 and 20 in the dic(17;20), as well as the loss of TP53, were confirmed by fluorescence in situ hybridization. Deletions of 17p and 20q are recurrent abnormalities in hematologic disorders, particularly myelodysplastic syndrome and acute myeloid leukemia). However, a dic(17;20) is an uncommon finding. According to the few reports in the literature, dic(17;20) is associated with an unfavorable prognosis. The key mechanism might be the loss of TP53 as well as other tumor suppressor genes in 20q that may have a critical role in tumor genesis.
