. Bone marrow transdifferentiation in brain after transplantation: a retrospective study. Lancet. 2004 May 1;363(9419):1432-7. PubMed.


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  1. Would there be room for the suggestion that AML stem cells may also migrate to the brain to form astrocytes? It seems of interest that Baldus et al(1) find overexpression of APP, ETS2 and ERG genes in AML. Wolvetang and colleagues (2)show that ETS2 transactivates the beta-APP promoter. Amouyel et al (3) report the expression of ETS proto-oncogenes in astrocytes. Delabar et al (4) report the overexpression of ETS2 in AD. Interesting that HIV-1 infection induces expression of c-kit (5) and Ets-2 is suggested as playing a role in the expression of c-kit. (6) The study by Lu (7) that ETS2 transactivates the heparanase promoter and that Abeta(1-40) prevents heparanase-catalyzed degradation of heparan sulfate glycosaminoglycans and proteoglycans in vitro (8) is also of interest. Bitan et al (9) find that heparanase in human leukemias is restricted to acute myeloid leukemias. Finally, the fact that ETS-2 is able to bind to the LIF promoter to induce its transcription (10) and LIF is able to increase the activity of acetylcholinesterase (11) may be something to consider. Stephensen and colleagues (12) raise the possibility that acetylcholinesterase may be a myeloid tumour suppressor gene. What would be the implications for those with Down syndrome and and an already increased leukemic risk, using anticholinesterase agents? Furthermore, if acetylcholinesterase is actually a tumour promoter, would the anticholinesterases be useful the treatment of AML?

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