Deutsch
 
Hilfe Datenschutzhinweis Impressum
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

Explaining the in vitro and in vivo differences in leukemia therapy

MPG-Autoren
/persons/resource/persons56973

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

Externe Ressourcen
Es sind keine externen Ressourcen hinterlegt
Volltexte (beschränkter Zugriff)
Für Ihren IP-Bereich sind aktuell keine Volltexte freigegeben.
Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte in PuRe verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Lenaerts, T., Castagnetti, F., Traulsen, A., Pacheco, J. M., Rosti, G., & Dingli, D. (2011). Explaining the in vitro and in vivo differences in leukemia therapy. Cell Cycle, 10(10), 1540-1544. doi:10.4161/cc.10.10.15518.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-000F-D3C3-E
Zusammenfassung
The majority of patients with chronic myeloid leukemia in early chronic phase (CML-ECP) who are treated with imatinib achieve a complete cytogenetic response with a significant reduction in the risk of progression to advanced phases. Recent studies show that therapy of CML-ECP with nilotinib leads to a faster and deeper response compared to imatinib. However, in vitro data indicates that there is no detectable difference in inhibition of signaling downstream of Bcr-Abl between the two agents and that neither drug induces apoptosis of CML CD34(+) cells. We use a computational model of hematopoiesis and CML, combined with serial quantitative data of disease burden under imatinib and nilotinib therapy to explain this apparent disconnect between in vivo and in vitro responses. We show how a subtle difference in the differentiation rate of CML cells under therapy with either agent, with marginal impact onto the in vitro studies, translates into a significantly different reproductive fitness of treated cells in vivo, providing a sizeable difference, hence providing an explanation for the superior response observed with nilotinib.