Genomic analysis of germ line and somatic variants in familial myelodysplasia/acute myeloid leukemia.
Churpek, Jane E; Pyrtel, Khateriaa; Kanchi, Krishna-Latha; Shao, Jin; Koboldt, Daniel; Miller, Christopher A; Shen, Dong; Fulton, Robert; O'Laughlin, Michelle; Fronick, Catrina; Pusic, Iskra; Uy, Geoffrey L; Braunstein, Evan M; Levis, Mark; Ross, Julie; Elliott, Kevin; Heath, Sharon; Jiang, Allan; Westervelt, Peter; DiPersio, John F; Link, Daniel C; Walter, Matthew J; Welch, John; Wilson, Richard; Ley, Timothy J; Godley, Lucy A; Graubert, Timothy A.
; 126(22): 2484-90, 2015 Nov 26.
Artigo em Inglês | MEDLINE | ID: mdl-26492932
RUNX1 and CBFß Mutations and Activities of Their Wild-Type Alleles in AML.
Immune evasion by oncogenic proteins of acute myeloid leukemia.
Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation.
Heritable polymorphism predisposes to high BAALC expression in acute myeloid leukemia.
JMJD1C is required for the survival of acute myeloid leukemia by functioning as a coactivator for key transcription factors.
MiR144/451 Expression Is Repressed by RUNX1 During Megakaryopoiesis and Disturbed by RUNX1/ETO.
RUNX1 amplification in AML with myelodysplasia-related changes and ring 21 chromosomes.
[Correlations Between <i>AML1</i>-<i>ETO</i> Fusion Gene and Clinical Features of Acute Myeloid Leukemia in Sichuan.]
Runx1 deletion or dominant inhibition reduces Cebpa transcription via conserved promoter and distal enhancer sites to favor monopoiesis over granulopoiesis.
Gain of chromosome 21 or amplification of chromosome arm 21q is one mechanism for increased ERG expression in acute myeloid leukemia.