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* '''[http://www.ccga.io/index.php/Acute_Myeloid_Leukemia_(AML)_and_Related_Precursor_Neoplasms Acute Myeloid Leukemia (AML) and Related Precursor Neoplasms]'''  

* '''[http://www.ccga.io/index.php/Acute_Myeloid_Leukemia_(AML)_and_Related_Precursor_Neoplasms Acute Myeloid Leukemia (AML) and Related Precursor Neoplasms]'''  

The frequency of mutations in ''RUNX1'' mutations has been found to be between 5-18% of all AML patients tested [3]. The most common chromosomal translocation is t(8;21)(q22;q22)(RUNX1-RUNX1T1) in ''de novo'' AML, at approximately 7% [2,6].  This translocation confers a favorable prognosis in AML and other neoplasms [2,5,6].  Another RUNX1 alteration is the (3;21)(q26;q22) (RUNX1-EVI1) translocation, in which the RUNT domain of RUNX1 is fused to the entire EVI1 gene.  This translocation is rarely found in patients diagnosed with de novo AML and is more common in those with therapy-related myelodysplastic syndrome (MDS)/AML[.  Other mutations in ''RUNX1'' include deletions, missense, splicing, frameshift, and nonsense mutations (mostly loss of function or decreased function), and occur at a frequency of approximately 10% in AML patients [6]. These mutations are mechanistically distinct from the chromosomal translocations and confer a worse prognosis [2,5,6].

The frequency of mutations in ''RUNX1'' mutations has been found to be between 5-18% of all AML patients tested [3]. The most common chromosomal translocation is t(8;21)(q22;q22)(RUNX1-RUNX1T1) in ''de novo'' AML, at approximately 7% [2,6].  This translocation confers a favorable prognosis in AML and other neoplasms [2,5,6].  Another RUNX1 alteration is the (3;21)(q26;q22) (RUNX1-EVI1) translocation, in which the RUNT domain of RUNX1 is fused to the entire EVI1 gene.  This translocation is rarely found in patients diagnosed with de novo AML and is more common in those with therapy-related myelodysplastic syndrome (MDS)/AML[9].  Other mutations in ''RUNX1'' include deletions, missense, splicing, frameshift, and nonsense mutations (mostly loss of function or decreased function), and occur at a frequency of approximately 10% in AML patients [6]. These mutations are mechanistically distinct from the chromosomal translocations and confer a worse prognosis [2,5,6].