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Anticancer Res. 2009 Jun;29(6):1867-71.

Combination of PI3K/mTOR inhibition demonstrates efficacy in human chordoma.

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  • 1Department of Orthopedic Surgery, Section of Orthopedic Oncology, Sarcoma Research Laboratory, Massachusetts General Hospital, Boston, MA 02114, U.S.A. jhschwab@partners.org

Abstract

BACKGROUND:

Chordomas are rare tumors of the axial skeleton for which surgical resection remains the most reliable means of cure. PI-103 is a inhibitor of PI3K/AKT and mTOR activation. This study aims to determine whether the PI3K/mTOR pathway was active in chordomas and whether their inhibition could lead to decreased proliferation and increased apoptosis.

MATERIALS AND METHODS:

Thirteen human chordoma were tested for activation of the PI3K/mTOR pathway. The human chordoma cell line UCH-1 was treated with increasing doses of PI-103. Inhibition of AKT and mTOR was examined and assays assessing proliferation and apoptosis were performed.

RESULTS:

The chordoma specimen demonstrated activation of the PI3K/mTOR pathway. PI-103 inhibited the AKT and mTOR activation in the UCH-1 cell line. PI-103 inhibited proliferation and induced apoptosis in UCH-1.

CONCLUSION:

The PI3K/AKT and mTOR signaling pathway is constitutively activated in chordoma. PI-103 decreases proliferation and induces apoptosis in the UCH-1 via inhibition of the PI3K/mTOR pathway.

PMID:
19528441
[PubMed - indexed for MEDLINE]
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