Acute promyelocytic leukemia (APL) is a subtype of acute myeloid leukemia (AML). It is characterized by the t(15;17)(q22;q11.2) chromosomal translocation that.

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Most mutations in cancer genomes are thought to be acquired after the initiating event,which may cause genomic instability and drive clonal evolution. However, for acutemyeloid leukemia (AML), normal karyotypes are common, and genomic instability is unusual.To better understand clonal evolution in AML, we sequenced the genomes of M3-AML sampleswith a known initiating event (PML-RARA) versus the genomes of normal karyotype M1-AML samples and the exomes of hematopoieticstem/progenitor cells (HSPCs) from healthy people. Collectively, the data suggestthat most of the mutations found in AML genomes are actually random events that occurredin HSPCs before they acquired the initiating mutation; the mutational history of thatcell is “captured” as the clone expands. In many cases, only one or two additional,cooperating mutations are needed to generate the malignant founding clone. Cells fromthe founding clone can acquire additional cooperating mutations, yielding subclonesthat can contribute to disease progression and/or relapse.Graphical Abstract. Please enable JavaScript to view the Cell Press Commenting GuidelinesTo submit a comment for a journal article, please use the space above and note the following:. We will review submitted comments within 2 business days.

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Ley 1455 De 2011 Pdf Online

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