. 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?


    . Acute myeloid leukemia with complex karyotypes and abnormal chromosome 21: Amplification discloses overexpression of APP, ETS2, and ERG genes. Proc Natl Acad Sci U S A. 2004 Mar 16;101(11):3915-20. Epub 2004 Mar 8 PubMed.

    . The chromosome 21 transcription factor ETS2 transactivates the beta-APP promoter: implications for Down syndrome. Biochim Biophys Acta. 2003 Jul 28;1628(2):105-10. PubMed.

    . Expression of ETS proto-oncogenes in astrocytes in human cortex. Brain Res. 1988 Apr 26;447(1):149-53. PubMed.

    . Rearrangement of chromosome 21 in Alzheimer's disease. Ann Genet. 1986;29(4):226-8. PubMed.

    . Astrocyte apoptosis induced by HIV-1 transactivation of the c-kit protooncogene. Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3954-9. PubMed.

    . Myb and ets proteins are candidate regulators of c-kit expression in human hematopoietic cells. Blood. 1998 Mar 15;91(6):1934-46. PubMed.

    . Trans-activation of heparanase promoter by ETS transcription factors. Oncogene. 2003 Feb 13;22(6):919-23. PubMed.

    . Abeta(1-40) prevents heparanase-catalyzed degradation of heparan sulfate glycosaminoglycans and proteoglycans in vitro. A role for heparan sulfate proteoglycan turnover in Alzheimer's disease. J Biol Chem. 1997 Jul 4;272(27):17005-11. PubMed.

    . Heparanase expression in human leukemias is restricted to acute myeloid leukemias. Exp Hematol. 2002 Jan;30(1):34-41. PubMed.

    . Regulation of the human leukemia inhibitory factor gene by ETS transcription factors. Neuroimmunomodulation. 2004;11(1):10-9. PubMed.

    . Leukemia inhibitory factor and interleukin-11 promote maturation of murine and human megakaryocytes in vitro. J Cell Physiol. 1992 Nov;153(2):305-12. PubMed.

    . Deletion of the acetylcholinesterase locus at 7q22 associated with myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML). Leuk Res. 1996 Mar;20(3):235-41. PubMed.

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  1. Transdifferentiation—Alive Again?