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Träfflista för sökning "WFRF:(Druid Henrik) srt2:(2010-2014);lar1:(lu)"

Sökning: WFRF:(Druid Henrik) > (2010-2014) > Lunds universitet

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1.
  • Bergmann, Olaf, et al. (författare)
  • Cardiomyocyte Renewal in Humans
  • 2012
  • Ingår i: Circulation Research. - 0009-7330 .- 1524-4571. ; 110:1, s. 17-18
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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2.
  • Nordigården, Amanda, et al. (författare)
  • Irreversible pan-ERBB inhibitor canertinib elicits anti-leukaemic effects and induces the regression of FLT3-ITD transformed cells in mice
  • 2011
  • Ingår i: British Journal of Haematology. - : Blackwell Publishing. - 0007-1048 .- 1365-2141. ; 155:2, s. 198-208
  • Tidskriftsartikel (refereegranskat)abstract
    • Recent findings have indicated that tyrosine kinase inhibitors (TKIs) targeting the ERBB receptor family display anti-leukaemic effects, despite the lack of receptor expression on human leukaemic cells. The occurrence of activating mutations in the gene encoding FMS-like tyrosine kinase 3 (FLT3) in patients with acute myeloid leukaemia (AML) has rendered inhibition of this receptor a promising therapeutic target. Due to possibility of cross-reactivity, we investigated the effect of the irreversible pan-ERBB inhibitor canertinib (CI-1033) on leukaemic cells expressing FLT3. The drug had anti-proliferative and apoptotic effects on primary AML cells and human leukaemic cell lines expressing mutated FLT3. In several AML patient samples, a blast cell population expressing FLT3-internal tandem duplication (ITD) was eradicated by canertinib. Canertinib inhibited receptor autophosphorylation and kinase activity of both mutated and FLT3 ligand stimulated wildtype FLT3, leading to inhibition of the PI3-kinase and MAP kinase pathways. Apoptotic induction was dependent on pro-apoptotic BH3-only protein BCL2L11/BIM because siRNA silencing attenuated apoptosis. Moreover, the drug induced regression of cells expressing FLT3-ITD in a murine in vivo-transplantation model at previously described tolerated doses. These results indicate that canertinib, as an irreversible TKI, could constitute a novel treatment regimen in patients with mutated or overexpressed FLT3.
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