Histopathological, immunohistochemical and molecular analysis of 20 days Imatinib-treated mice revealed massive infiltration and increased size of liver and spleen. In contrast, spleens and livers from PD+ATO-treated mice demonstrated substantially normal tissue architecture. Moreover PD+ATO-treated mice showed significantly prolonged survival compared to Imatinib, confirming the PD+ATO-triggered inhibition of leukemic progression. Our preclinical in vitro and in vivo studies suggest that PD+ATO-treatment could represent an effective therapeutic strategy for the treatment of Imatinib-resistant Bcr-Abl+ leukemia, including those harbouring the T315I mutation.

L'inibizione di MEK potenzia l'effetto antitumorale del Triossido di Arsenico in cellule di Leucemia Mieloide Cronica Bcr-abl+ resistenti all'Imatinib: studio preclinico in vitro ed in vivo.

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2014

Abstract

Histopathological, immunohistochemical and molecular analysis of 20 days Imatinib-treated mice revealed massive infiltration and increased size of liver and spleen. In contrast, spleens and livers from PD+ATO-treated mice demonstrated substantially normal tissue architecture. Moreover PD+ATO-treated mice showed significantly prolonged survival compared to Imatinib, confirming the PD+ATO-triggered inhibition of leukemic progression. Our preclinical in vitro and in vivo studies suggest that PD+ATO-treatment could represent an effective therapeutic strategy for the treatment of Imatinib-resistant Bcr-Abl+ leukemia, including those harbouring the T315I mutation.
2014
Italiano
Arsenic trioxide
Chronic myeloid leukemia
Drug resistance
MEK inhibition
p73
Università degli Studi di Parma
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14242/273438
Il codice NBN di questa tesi è URN:NBN:IT:UNIPR-273438