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Dual inhibition of PI3K and mTOR inhibits autocrine and paracrine proliferative loops in PI3K/Akt/mTOR-addicted lymphomas.

Identifieur interne : 001438 ( Main/Exploration ); précédent : 001437; suivant : 001439

Dual inhibition of PI3K and mTOR inhibits autocrine and paracrine proliferative loops in PI3K/Akt/mTOR-addicted lymphomas.

Auteurs : Aadra P. Bhatt [États-Unis] ; Prasanna M. Bhende ; Sang-Hoon Sin ; Debasmita Roy ; Dirk P. Dittmer ; Blossom Damania

Source :

RBID : pubmed:20299510

Descripteurs français

English descriptors

Abstract

Primary effusion lymphoma (PEL) constitutes a subset of non-Hodgkin lymphoma whose incidence is highly increased in the context of HIV infection. Kaposi sarcoma-associated herpesvirus is the causative agent of PEL. The phosphatidylinositol 3-kinase (PI3K) signaling pathway plays a critical role in cell proliferation and survival, and this pathway is dysregulated in many different cancers, including PEL, which display activated PI3K, Akt, and mammalian target of rapamycin (mTOR) kinases. PELs rely heavily on PI3K/Akt/mTOR signaling, are dependent on autocrine and paracrine growth factors, and also have a poor prognosis with reported median survival times of less than 6 months. We compared different compounds that inhibit the PI3K/Akt/mTOR pathway in PEL. Although compounds that modulated activity of only a single pathway member inhibited PEL proliferation, the use of a novel compound, NVP-BEZ235, that dually inhibits both PI3K and mTOR kinases was significantly more efficacious in culture and in a PEL xenograft tumor model. NVP-BEZ235 was effective at low nanomolar concentrations and has oral bioavailability. We also report a novel mechanism for NVP-BEZ235 involving the suppression of multiple autocrine and paracrine growth factors required for lymphoma survival. Our data have broad applicability for the treatment of cytokine-dependent tumors with PI3K/mTOR dual inhibitors.

DOI: 10.1182/blood-2009-10-251082
PubMed: 20299510
PubMed Central: PMC2881502


Affiliations:


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Le document en format XML

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<div type="abstract" xml:lang="en">Primary effusion lymphoma (PEL) constitutes a subset of non-Hodgkin lymphoma whose incidence is highly increased in the context of HIV infection. Kaposi sarcoma-associated herpesvirus is the causative agent of PEL. The phosphatidylinositol 3-kinase (PI3K) signaling pathway plays a critical role in cell proliferation and survival, and this pathway is dysregulated in many different cancers, including PEL, which display activated PI3K, Akt, and mammalian target of rapamycin (mTOR) kinases. PELs rely heavily on PI3K/Akt/mTOR signaling, are dependent on autocrine and paracrine growth factors, and also have a poor prognosis with reported median survival times of less than 6 months. We compared different compounds that inhibit the PI3K/Akt/mTOR pathway in PEL. Although compounds that modulated activity of only a single pathway member inhibited PEL proliferation, the use of a novel compound, NVP-BEZ235, that dually inhibits both PI3K and mTOR kinases was significantly more efficacious in culture and in a PEL xenograft tumor model. NVP-BEZ235 was effective at low nanomolar concentrations and has oral bioavailability. We also report a novel mechanism for NVP-BEZ235 involving the suppression of multiple autocrine and paracrine growth factors required for lymphoma survival. Our data have broad applicability for the treatment of cytokine-dependent tumors with PI3K/mTOR dual inhibitors.</div>
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<Reference>
<Citation>Blood. 2000 Jan 15;95(2):627-32</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10627472</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Blood. 2007 Nov 1;110(9):3102-11</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">17656647</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Blood. 2000 Aug 15;96(4):1599-601</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10942415</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cancer Res. 2000 Sep 1;60(17):4873-80</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10987301</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cancer Res. 2001 Mar 15;61(6):2641-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11289142</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Clin Invest. 2001 Oct;108(7):1001-13</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11581301</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Biol Chem. 2002 Jul 12;277(28):25226-32</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11994296</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Clin Invest. 2002 Oct;110(7):923-32</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12370270</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Nat Med. 2002 Nov;8(11):1281-7</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12379847</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Anticancer Drugs. 2003 Feb;14(2):167-73</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12569304</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cancer Cell. 2003 Feb;3(2):131-43</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12620408</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cell. 2003 Nov 26;115(5):577-90</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">14651849</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Biol Chem. 2004 Jan 23;279(4):2737-46</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">14576155</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Virol. 2004 Feb;78(4):1918-27</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">14747556</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4821-6</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15047889</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cancer Res. 2004 Apr 15;64(8):2774-81</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15087393</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cancer Cell. 2004 Jul;6(1):91-9</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15261145</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Nature. 1995 Dec 21-28;378(6559):785-9</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">8524413</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Blood. 1997 Apr 15;89(8):2635-43</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">9108380</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cell. 1997 Oct 17;91(2):231-41</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">9346240</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Science. 1997 Oct 24;278(5338):687-9</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">9381178</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Science. 1998 Nov 13;282(5392):1318-21</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">9812896</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Leukemia. 1999 Apr;13(4):634-40</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10214873</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Nat Cell Biol. 2004 Nov;6(11):1122-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15467718</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Science. 2005 Feb 18;307(5712):1098-101</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15718470</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Pathol. 2005 May;206(1):68-75</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15751051</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Mol Cell. 2005 Apr 15;18(2):143-5</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15837416</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Clin Oncol. 2005 Jul 1;23(19):4372-80</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15994147</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Blood. 2006 Jan 15;107(2):760-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16189274</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Biol Chem. 2008 Feb 15;283(7):3979-87</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">18056705</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Drug Resist Updat. 2008 Feb-Apr;11(1-2):32-50</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">18166498</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Virol. 2008 Jul;82(13):6514-23</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">18434405</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cancer Res. 2008 Jun 15;68(12):4640-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">18559509</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Oncogene. 2008 Jun 26;27(28):3999-4007</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">18278068</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Mol Cancer Ther. 2008 Jul;7(7):1851-63</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">18606717</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cancer Res. 2008 Oct 1;68(19):8022-30</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">18829560</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Haematologica. 2009 Aug;94(8):1170-4</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">19608668</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Curr Opin Cell Biol. 2009 Apr;21(2):154-65</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">19230644</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Mol Cancer Ther. 2006 Feb;5(2):430-7</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16505118</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cancer Res. 2006 Apr 1;66(7):3658-66</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16585191</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Blood. 2006 May 15;107(10):4053-62</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16418332</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cancer Cell. 2006 Aug;10(2):133-43</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16904612</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cell. 2006 Sep 8;126(5):955-68</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16959574</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Virol. 2007 Feb;81(4):1912-22</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">17121789</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Blood. 2007 Mar 1;109(5):2165-73</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">17082322</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cancer Cell. 2007 May;11(5):395-406</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">17482130</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cell. 2007 Jun 29;129(7):1261-74</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">17604717</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Leukemia. 2000 Feb;14(2):285-91</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10673746</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
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