Format

Send to

Choose Destination
See comment in PubMed Commons below
Anticancer Res. 2012 Mar;32(3):893-9.

CSF-1R up-regulation is associated with response to pharmacotherapy targeting tyrosine kinase activity in AML cell lines.

Author information

1
Temple University School of Medicine, Department of Neuroscience, 3500 N. Broad St., Medical Education and Research Bld, Rm 746, Philadelphia, PA 19140-5104, USA.

Abstract

BACKGROUND:

The oncogenic potential of colony stimulating factor 1 receptor (CSF-1R) has been well described, while its relevance for human acute myelogenous leukemia (AML) is still undetermined. In a recent clinical trial for AML, sunitinib was found to hold potential therapeutic benefit, however, the mechanism for this remains unknown.

MATERIALS AND METHODS:

In this study, we treated three myeloid cell lines, Mono-Mac 1, THP-1, and U937, with sunitinib, and a small-molecule CSF-1R inhibitor (cFMS-I) to test the anticancer effect of such treatment.

RESULTS:

Mono-Mac 1 cells had inhibited proliferation and extracellular-signal regulated kinase activity as a result of CSF-1R inhibition and a dose-dependent increase in CSF-1R expression with both sunitinib and cFMS-I.

CONCLUSION:

Our results suggest potential for CSF-1R as an important target of sunitinib or other similar drugs. Future study of CSF-1R may produce more targeted therapeutic approaches and aid in the development of personalized medicine for AML.

PMID:
22399609
PMCID:
PMC3601026
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center