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2014 ; 38
(4
): 503-8
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Crizotinib (PF-2341066) induces apoptosis due to downregulation of pSTAT3 and
BCL-2 family proteins in NPM-ALK(+) anaplastic large cell lymphoma
#MMPMID24486291
Hamedani FS
; Cinar M
; Mo Z
; Cervania MA
; Amin HM
; Alkan S
Leuk Res
2014[Apr]; 38
(4
): 503-8
PMID24486291
show ga
Nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) is an aberrant fusion gene
product with tyrosine kinase activity and is expressed in substantial subset of
anaplastic large cell lymphomas (ALCL). It has been shown that NPM-ALK binds to
and activates signal transducer and activator of transcription 3 (STAT3).
Although NPM-ALK(+) ALCL overall shows a better prognosis, there is a sub-group
of patients who relapses and is resistant to conventional chemotherapeutic
regimens. NPM-ALK is a potential target for small molecule kinase inhibitors.
Crizotinib (PF-2341066) is a small, orally bioavailable molecule that inhibits
growth of tumors with ALK activity as shown in a subgroup of non-small lung
cancer patients with EML4-ALK expression. In this study, we have investigated the
in vitro effects of Crizotinib in ALCL cell line with NPM-ALK fusion. Crizotinib
induced marked downregulation of STAT3 phosphorylation, which was associated with
significant apoptotic cell death. Apoptosis induction was attributed to caspase-3
cleavage and marked downregulation of the Bcl-2 family of proteins including
MCL-1. These findings implicate that Crizotinib has excellent potential to treat
patients with NPM-ALK(+) ALCL through induction of apoptotic cell death and
downregulation of major oncogenic proteins in this aggressive lymphoma.