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. Author manuscript; available in PMC: 2010 Sep 1.
Published in final edited form as: Per Med. 2009 Nov 1;6(6):653. doi: 10.2217/pme.09.52

Figure 2. Model for evolution of genetic changes in acute myeloid leukemia.

Figure 2

A hypothetical model in which nonpathogenic somatic mutations (1–3) acquired over the lifespan of a stem cell are propagated in the malignant clone after it acquires a critical initiating mutation (4). Mutation 5 is a progression mutation that cooperates with the AML-initiating mutation 4 to contribute to AML development. Other mutations (represented by 6 and 7) do not cooperate with the AML-initiating mutation 4, and do not contribute to AML development. These subclones are lost, or fail to expand to the limit of detection by sequencing studies. AML: Acute myeloid leukemia; HSC: Hematopoietic stem cell.