Fig. 1: The two-hit model for B cell precursor ALL. | Leukemia

Fig. 1: The two-hit model for B cell precursor ALL.

From: Can we prevent childhood Leukaemia?

Fig. 1

Initiating genetic lesions are primarily ETV6-RUNX1 or hyperdiploidy, probably occurring as developmental accidents. They arise in utero possibly in foetal liver early B lineage lymphopoiesis [78]. Secondary mutations are primarily RAG-mediated copy number alterations. ~1% figure: ALL is initiated in utero at a rate that exceeds by 100-fold, the incidence of disease indicating a low penetrance and a critical role for factors promoting chronic inflammation and the secondary mutations. Adapted from [7]. See text for references.

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