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Somatic mutations and the hierarchy of hematopoiesis

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons56973

Traulsen,  Arne
Research Group Evolutionary Theory, Max Planck Institute for Evolutionary Biology, Max Planck Society;

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Zitation

Traulsen, A., Pacheco, J. M., Luzzatto, L., & Dingli, D. (2010). Somatic mutations and the hierarchy of hematopoiesis. BioEssays, 32(11), 1003-1008. doi:10.1002/bies.201000025.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-000F-D444-6
Zusammenfassung
Clonal disease is often regarded as almost synonymous with cancer. However, it is becoming increasingly clear that our bodies harbor numerous mutant clones that are not tumors, and mostly give rise to no disease at all. Here we discuss three somatic mutations arising within the hematopoietic system: BCR-ABL, characteristic of chronic myeloid leukemia; mutations of the PIG-A gene, characteristic of paroxysmal nocturnal hemoglobinuria; the V617F mutation in the JAK2 gene, characteristic of myeloproliferative diseases. The population frequencies of these three blood disorders fit well with a hierarchical model of hematopoiesis. The fate of any mutant clone will depend on the target cell and on the fitness advantage, if any, that the mutation confers on the cell. In general, we can expect that only a mutation in a hematopoietic stem cell will give long-term disease; the same mutation taking place in a cell located more downstream may produce just a ripple in the hematopoietic ocean.