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   FASEB  J. 2005 Mar 22; [Epub ahead of print] _Related Articles,_
(http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Display&dopt=pubmed_pubmed
&from_uid=15784722&tool=ExternalSearch)  _Links_
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(http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3051&uid=15784722&db=PubMed&url=http://www.fasebj.org/cgi/pmidlookup?view=reprint&pmid=15784722)

Identification of mTOR as a  novel bifunctional target in chronic myeloid
leukemia: dissection of  growth-inhibitory and VEGF-suppressive effects of
rapamycin in leukemic  cells.

Mayerhofer M, Aichberger KJ, Florian S, Krauth MT,  Hauswirth AW, Derdak S,
Sperr WR, Esterbauer H, Wagner O, Marosi C, Pickl WF,  Deininger M, Weisberg E,
Druker BJ, Griffin JD, Sillaber C, Valent  P.

The mammalian target of rapamycin (mTOR) has recently been  described to be
constitutively activated in Bcr-Abl-transformed cells and to  mediate
rapamycin-induced inhibition of growth in respective cell lines. We
have  recently
shown that rapamycin down-regulates expression of vascular endothelial  growth
factor (VEGF), a mediator of leukemia-associated angiogenesis, in primary  CML
cells. In the present study, we analyzed growth-inhibitory in vitro and in  vivo
effects of rapamycin on primary CML cells and asked whether
rapamycin-induced suppression of VEGF in leukemic cells is related to
growth  inhibition.
Rapamycin dose dependently inhibited growth of primary CML cells  obtained from
patients with imatinib-responsive or imatinib-resistant disease as  well as
growth of Bcr-Abl-transformed imatinib-resistant cell lines. Moreover,  we
observed potent cytoreductive effects of rapamycin in a patient with
imatinib-resistant Bcr-Abl+ leukemia. The growth-inhibitory effects of
rapamycin  on CML
cells were found to be associated with G1 cell cycle arrest and with 
induction of
apoptosis. In all cell types tested, rapamycin was found to  down-regulate
expression of VEGF. However, exogenously added VEGF did not  counteract the
rapamycin-induced decrease in proliferation. In conclusion,  rapamycin inhibits
growth of CML cells in vitro and in vivo and, in addition,  down-regulates
expression of VEGF. Both effects may contribute to the  antileukemic activity of
the drug in CML.

PMID: 15784722 [PubMed - as  supplied by publisher]


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