Combinatorial targeting of FGF and ErbB receptors blocks growth and metastatic spread of breast cancer models

Introduction Targeting receptor tyrosine kinases (RTKs) with kinase inhibitors is a clinically validated anti-cancer approach. However, blocking one signaling pathway is often not sufficient to cause tumor regression and the effectiveness of individual inhibitors is often short-lived. As alterations...

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Veröffentlicht in:	Breast cancer research : BCR Jg. 15; H. 1; S. R8
Hauptverfasser:	Issa, Amine, Gill, Jason W, Heideman, Marinus R, Sahin, Ozgur, Wiemann, Stefan, Dey, Julien H, Hynes, Nancy E
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	London BioMed Central 23.01.2013
Schlagworte:	Animals Biomedical and Life Sciences Biomedicine Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - pathology Cancer Research Cell Proliferation - drug effects ErbB Receptors - antagonists & inhibitors ErbB Receptors - genetics Female Gene Expression Regulation, Neoplastic - drug effects Humans Imidazoles - administration & dosage Mice Molecular Targeted Therapy Oncology Phosphatidylinositol 3-Kinases - administration & dosage Phosphatidylinositol 3-Kinases - genetics Protein Kinase Inhibitors - administration & dosage Proto-Oncogene Proteins c-akt - genetics Purines - administration & dosage Quinolines - administration & dosage Receptors, Fibroblast Growth Factor - antagonists & inhibitors Receptors, Fibroblast Growth Factor - genetics Research Article Signal Transduction - drug effects Surgical Oncology TOR Serine-Threonine Kinases - genetics Xenograft Model Antitumor Assays ErbB Receptor Fibroblast Growth Factor Receptor Inhibitor Fibroblast Growth Factor Receptor 67NR Cell Circulate Tumor Cell
ISSN:	1465-542X, 1465-5411, 1465-542X
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Abstract	Introduction Targeting receptor tyrosine kinases (RTKs) with kinase inhibitors is a clinically validated anti-cancer approach. However, blocking one signaling pathway is often not sufficient to cause tumor regression and the effectiveness of individual inhibitors is often short-lived. As alterations in fibroblast growth factor receptor (FGFR) activity have been implicated in breast cancer, we examined in breast cancer models with autocrine FGFR activity the impact of targeting FGFRs in vivo with a selective kinase inhibitor in combination with an inhibitor of PI3K/mTOR or with a pan-ErbB inhibitor. Methods Using 4T1 or 67NR models of basal-like breast cancer, tumor growth was measured in mice treated with an FGFR inhibitor (dovitinib/TKI258), a PI3K/mTOR inhibitor (NVP-BEZ235) or a pan-ErbB inhibitor (AEE788) individually or in combination. To uncover mechanisms underlying inhibitor action, signaling pathway activity was examined in tumor lysates and transcriptome analysis carried out to identify pathways upregulated by FGFR inhibition. Anti-phosphotyrosine receptor antibody arrays (P-Tyr RTK) were also used to screen 4T1 tumors. Results The combination of dovitinib + NVP-BEZ235 causes tumor stasis and strong down-regulation of the FRS2/Erk and PI3K/Akt/mTOR signaling pathways. P-Tyr RTK arrays identified high levels of P-EGFR and P-ErbB2 in 4T1 tumors. Testing AEE788 in the tumor models revealed that the combination of dovitinib + AEE788 resulted in blockade of the PI3K/Akt/mTOR pathway, prolonged tumor stasis and in the 4T1 model, a significant decrease in lung metastasis. The results show that in vivo these breast cancer models become dependent upon co-activation of FGFR and ErbB receptors for PI3K pathway activity. Conclusions The work presented here shows that in the breast cancer models examined, the combination of dovitinib + NVP-BEZ235 or dovitinib + AEE788 results in strong inhibition of tumor growth and a block in metastatic spread. Only these combinations strongly down-regulate the FGFR/FRS2/Erk and PI3K/Akt/mTOR signaling pathways. The resultant decrease in mitosis and increase in apoptosis was consistently stronger in the dovitinib + AEE788 treatment-group, suggesting that targeting ErbB receptors has broader downstream effects compared to targeting only PI3K/mTOR. Considering that sub-classes of human breast tumors co-express ErbB receptors and FGFRs, these results have implications for targeted therapy.
AbstractList	Targeting receptor tyrosine kinases (RTKs) with kinase inhibitors is a clinically validated anti-cancer approach. However, blocking one signaling pathway is often not sufficient to cause tumor regression and the effectiveness of individual inhibitors is often short-lived. As alterations in fibroblast growth factor receptor (FGFR) activity have been implicated in breast cancer, we examined in breast cancer models with autocrine FGFR activity the impact of targeting FGFRs in vivo with a selective kinase inhibitor in combination with an inhibitor of PI3K/mTOR or with a pan-ErbB inhibitor.INTRODUCTIONTargeting receptor tyrosine kinases (RTKs) with kinase inhibitors is a clinically validated anti-cancer approach. However, blocking one signaling pathway is often not sufficient to cause tumor regression and the effectiveness of individual inhibitors is often short-lived. As alterations in fibroblast growth factor receptor (FGFR) activity have been implicated in breast cancer, we examined in breast cancer models with autocrine FGFR activity the impact of targeting FGFRs in vivo with a selective kinase inhibitor in combination with an inhibitor of PI3K/mTOR or with a pan-ErbB inhibitor.Using 4T1 or 67NR models of basal-like breast cancer, tumor growth was measured in mice treated with an FGFR inhibitor (dovitinib/TKI258), a PI3K/mTOR inhibitor (NVP-BEZ235) or a pan-ErbB inhibitor (AEE788) individually or in combination. To uncover mechanisms underlying inhibitor action, signaling pathway activity was examined in tumor lysates and transcriptome analysis carried out to identify pathways upregulated by FGFR inhibition. Anti-phosphotyrosine receptor antibody arrays (P-Tyr RTK) were also used to screen 4T1 tumors.METHODSUsing 4T1 or 67NR models of basal-like breast cancer, tumor growth was measured in mice treated with an FGFR inhibitor (dovitinib/TKI258), a PI3K/mTOR inhibitor (NVP-BEZ235) or a pan-ErbB inhibitor (AEE788) individually or in combination. To uncover mechanisms underlying inhibitor action, signaling pathway activity was examined in tumor lysates and transcriptome analysis carried out to identify pathways upregulated by FGFR inhibition. Anti-phosphotyrosine receptor antibody arrays (P-Tyr RTK) were also used to screen 4T1 tumors.The combination of dovitinib + NVP-BEZ235 causes tumor stasis and strong down-regulation of the FRS2/Erk and PI3K/Akt/mTOR signaling pathways. P-Tyr RTK arrays identified high levels of P-EGFR and P-ErbB2 in 4T1 tumors. Testing AEE788 in the tumor models revealed that the combination of dovitinib + AEE788 resulted in blockade of the PI3K/Akt/mTOR pathway, prolonged tumor stasis and in the 4T1 model, a significant decrease in lung metastasis. The results show that in vivo these breast cancer models become dependent upon co-activation of FGFR and ErbB receptors for PI3K pathway activity.RESULTSThe combination of dovitinib + NVP-BEZ235 causes tumor stasis and strong down-regulation of the FRS2/Erk and PI3K/Akt/mTOR signaling pathways. P-Tyr RTK arrays identified high levels of P-EGFR and P-ErbB2 in 4T1 tumors. Testing AEE788 in the tumor models revealed that the combination of dovitinib + AEE788 resulted in blockade of the PI3K/Akt/mTOR pathway, prolonged tumor stasis and in the 4T1 model, a significant decrease in lung metastasis. The results show that in vivo these breast cancer models become dependent upon co-activation of FGFR and ErbB receptors for PI3K pathway activity.The work presented here shows that in the breast cancer models examined, the combination of dovitinib + NVP-BEZ235 or dovitinib + AEE788 results in strong inhibition of tumor growth and a block in metastatic spread. Only these combinations strongly down-regulate the FGFR/FRS2/Erk and PI3K/Akt/mTOR signaling pathways. The resultant decrease in mitosis and increase in apoptosis was consistently stronger in the dovitinib + AEE788 treatment-group, suggesting that targeting ErbB receptors has broader downstream effects compared to targeting only PI3K/mTOR. Considering that sub-classes of human breast tumors co-express ErbB receptors and FGFRs, these results have implications for targeted therapy.CONCLUSIONSThe work presented here shows that in the breast cancer models examined, the combination of dovitinib + NVP-BEZ235 or dovitinib + AEE788 results in strong inhibition of tumor growth and a block in metastatic spread. Only these combinations strongly down-regulate the FGFR/FRS2/Erk and PI3K/Akt/mTOR signaling pathways. The resultant decrease in mitosis and increase in apoptosis was consistently stronger in the dovitinib + AEE788 treatment-group, suggesting that targeting ErbB receptors has broader downstream effects compared to targeting only PI3K/mTOR. Considering that sub-classes of human breast tumors co-express ErbB receptors and FGFRs, these results have implications for targeted therapy. Targeting receptor tyrosine kinases (RTKs) with kinase inhibitors is a clinically validated anti-cancer approach. However, blocking one signaling pathway is often not sufficient to cause tumor regression and the effectiveness of individual inhibitors is often short-lived. As alterations in fibroblast growth factor receptor (FGFR) activity have been implicated in breast cancer, we examined in breast cancer models with autocrine FGFR activity the impact of targeting FGFRs in vivo with a selective kinase inhibitor in combination with an inhibitor of PI3K/mTOR or with a pan-ErbB inhibitor. Using 4T1 or 67NR models of basal-like breast cancer, tumor growth was measured in mice treated with an FGFR inhibitor (dovitinib/TKI258), a PI3K/mTOR inhibitor (NVP-BEZ235) or a pan-ErbB inhibitor (AEE788) individually or in combination. To uncover mechanisms underlying inhibitor action, signaling pathway activity was examined in tumor lysates and transcriptome analysis carried out to identify pathways upregulated by FGFR inhibition. Anti-phosphotyrosine receptor antibody arrays (P-Tyr RTK) were also used to screen 4T1 tumors. The combination of dovitinib + NVP-BEZ235 causes tumor stasis and strong down-regulation of the FRS2/Erk and PI3K/Akt/mTOR signaling pathways. P-Tyr RTK arrays identified high levels of P-EGFR and P-ErbB2 in 4T1 tumors. Testing AEE788 in the tumor models revealed that the combination of dovitinib + AEE788 resulted in blockade of the PI3K/Akt/mTOR pathway, prolonged tumor stasis and in the 4T1 model, a significant decrease in lung metastasis. The results show that in vivo these breast cancer models become dependent upon co-activation of FGFR and ErbB receptors for PI3K pathway activity. The work presented here shows that in the breast cancer models examined, the combination of dovitinib + NVP-BEZ235 or dovitinib + AEE788 results in strong inhibition of tumor growth and a block in metastatic spread. Only these combinations strongly down-regulate the FGFR/FRS2/Erk and PI3K/Akt/mTOR signaling pathways. The resultant decrease in mitosis and increase in apoptosis was consistently stronger in the dovitinib + AEE788 treatment-group, suggesting that targeting ErbB receptors has broader downstream effects compared to targeting only PI3K/mTOR. Considering that sub-classes of human breast tumors co-express ErbB receptors and FGFRs, these results have implications for targeted therapy. Introduction Targeting receptor tyrosine kinases (RTKs) with kinase inhibitors is a clinically validated anti-cancer approach. However, blocking one signaling pathway is often not sufficient to cause tumor regression and the effectiveness of individual inhibitors is often short-lived. As alterations in fibroblast growth factor receptor (FGFR) activity have been implicated in breast cancer, we examined in breast cancer models with autocrine FGFR activity the impact of targeting FGFRs in vivo with a selective kinase inhibitor in combination with an inhibitor of PI3K/mTOR or with a pan-ErbB inhibitor. Methods Using 4T1 or 67NR models of basal-like breast cancer, tumor growth was measured in mice treated with an FGFR inhibitor (dovitinib/TKI258), a PI3K/mTOR inhibitor (NVP-BEZ235) or a pan-ErbB inhibitor (AEE788) individually or in combination. To uncover mechanisms underlying inhibitor action, signaling pathway activity was examined in tumor lysates and transcriptome analysis carried out to identify pathways upregulated by FGFR inhibition. Anti-phosphotyrosine receptor antibody arrays (P-Tyr RTK) were also used to screen 4T1 tumors. Results The combination of dovitinib + NVP-BEZ235 causes tumor stasis and strong down-regulation of the FRS2/Erk and PI3K/Akt/mTOR signaling pathways. P-Tyr RTK arrays identified high levels of P-EGFR and P-ErbB2 in 4T1 tumors. Testing AEE788 in the tumor models revealed that the combination of dovitinib + AEE788 resulted in blockade of the PI3K/Akt/mTOR pathway, prolonged tumor stasis and in the 4T1 model, a significant decrease in lung metastasis. The results show that in vivo these breast cancer models become dependent upon co-activation of FGFR and ErbB receptors for PI3K pathway activity. Conclusions The work presented here shows that in the breast cancer models examined, the combination of dovitinib + NVP-BEZ235 or dovitinib + AEE788 results in strong inhibition of tumor growth and a block in metastatic spread. Only these combinations strongly down-regulate the FGFR/FRS2/Erk and PI3K/Akt/mTOR signaling pathways. The resultant decrease in mitosis and increase in apoptosis was consistently stronger in the dovitinib + AEE788 treatment-group, suggesting that targeting ErbB receptors has broader downstream effects compared to targeting only PI3K/mTOR. Considering that sub-classes of human breast tumors co-express ErbB receptors and FGFRs, these results have implications for targeted therapy.
ArticleNumber	R8
Author	Issa, Amine Wiemann, Stefan Gill, Jason W Heideman, Marinus R Dey, Julien H Hynes, Nancy E Sahin, Ozgur
AuthorAffiliation	1 Mechanisms of Cancer, Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, Basel 4058, Switzerland 3 Current address: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston TX 77030, USA 4 University of Basel, Petersplatz 1, Basel 4003, Switzerland 5 Current address: Nestlé Research Center, Vers-chez-les-Blanc, 1000 Lausanne 26, Switzerland 2 Division of Molecular Genome analysis, German Cancer Research Center, Im Neuenheimer Feld 580, Heidelberg 69120, Germany
AuthorAffiliation_xml	– name: 4 University of Basel, Petersplatz 1, Basel 4003, Switzerland – name: 3 Current address: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston TX 77030, USA – name: 5 Current address: Nestlé Research Center, Vers-chez-les-Blanc, 1000 Lausanne 26, Switzerland – name: 2 Division of Molecular Genome analysis, German Cancer Research Center, Im Neuenheimer Feld 580, Heidelberg 69120, Germany – name: 1 Mechanisms of Cancer, Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, Basel 4058, Switzerland
Author_xml	– sequence: 1 givenname: Amine surname: Issa fullname: Issa, Amine organization: Mechanisms of Cancer, Friedrich Miescher Institute for Biomedical Research – sequence: 2 givenname: Jason W surname: Gill fullname: Gill, Jason W organization: Mechanisms of Cancer, Friedrich Miescher Institute for Biomedical Research – sequence: 3 givenname: Marinus R surname: Heideman fullname: Heideman, Marinus R organization: Mechanisms of Cancer, Friedrich Miescher Institute for Biomedical Research – sequence: 4 givenname: Ozgur surname: Sahin fullname: Sahin, Ozgur organization: Division of Molecular Genome analysis, German Cancer Research Center, Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 5 givenname: Stefan surname: Wiemann fullname: Wiemann, Stefan organization: Division of Molecular Genome analysis, German Cancer Research Center – sequence: 6 givenname: Julien H surname: Dey fullname: Dey, Julien H organization: Mechanisms of Cancer, Friedrich Miescher Institute for Biomedical Research, University of Basel, Nestlé Research Center – sequence: 7 givenname: Nancy E surname: Hynes fullname: Hynes, Nancy E email: nancy.hynes@fmi.ch organization: Mechanisms of Cancer, Friedrich Miescher Institute for Biomedical Research, University of Basel
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Cites_doi	10.1158/0008-5472.CAN-09-4479 10.1074/jbc.M404252200 10.1038/sj.onc.1202392 10.1158/1078-0432.CCR-04-2129 10.1038/nrclinonc.2011.177 10.1371/journal.pone.0014117 10.1021/jm2006222 10.1038/nrc2780 10.1128/MCB.18.9.5042 10.1038/onc.2010.626 10.1158/0008-5472.CAN-03-3681 10.1158/0008-5472.CAN-08-1044 10.1073/pnas.1537685100 10.1016/j.bbrc.2011.03.002 10.1038/nature11017 10.1093/nar/gkn923 10.1038/nrc1477 10.1038/sj.onc.1207816 10.1158/0008-5472.CAN-06-4685 10.1038/nrc1609 10.1126/scitranslmed.3001539 10.1158/0008-5472.CAN-10-0918 10.1016/j.cell.2010.06.011 10.1126/scitranslmed.3000389 10.1016/j.ccr.2010.10.031 10.1038/nature11412 10.1038/nature11249 10.1016/S1535-6108(02)00097-1 10.1128/MCB.20.9.3210-3223.2000 10.1093/nar/gkq973 10.1186/bcr1665 10.1126/science.1142946 10.1158/2159-8290.CD-11-0106 10.1158/1535-7163.MCT-08-0017 10.1158/1078-0432.CCR-04-1665
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Keywords	ErbB Receptor Fibroblast Growth Factor Receptor Inhibitor Fibroblast Growth Factor Receptor 67NR Cell Circulate Tumor Cell
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References	HA Lane (3187_CR27) 2000; 20 SK Marsh (3187_CR38) 1999; 18 SM Maira (3187_CR10) 2008; 7 MA Olayioye (3187_CR17) 1998; 18 JM Wood (3187_CR32) 2000; 60 V Theodorou (3187_CR37) 2004; 23 NE Hynes (3187_CR2) 2005; 5 P Traxler (3187_CR11) 2004; 64 PJ Stephens (3187_CR13) 2012; 486 CR Schnell (3187_CR31) 2008; 68 DB Agus (3187_CR26) 2002; 2 D Szklarczyk (3187_CR15) 2011; 39 HM Stern (3187_CR3) 2012; 4 S Chandarlapaty (3187_CR24) 2011; 19 DN Amin (3187_CR22) 2010; 2 MA Lemmon (3187_CR1) 2010; 141 SH Lee (3187_CR8) 2005; 11 CL Arteaga (3187_CR20) 2012; 9 YW Park (3187_CR21) 2005; 11 KE Ware (3187_CR34) 2010; 5 AC Faber (3187_CR29) 2011; 1 N Turner (3187_CR6) 2010; 10 TR Wilson (3187_CR23) 2012; 487 MM Mueller (3187_CR18) 2004; 4 P Sini (3187_CR30) 2008; 68 V Serra (3187_CR25) 2011; 30 JM Stommel (3187_CR33) 2007; 318 S Elbauomy Elsheikh (3187_CR4) 2007; 9 NE Hynes (3187_CR5) 2010; 70 W Huang da (3187_CR16) 2009; 37 CJ Aslakson (3187_CR7) 1992; 52 JH Dey (3187_CR9) 2010; 70 Cancer Genome Atlas Network (3187_CR12) 2012; 490 BA Pulaski (3187_CR14) 2001 AB Motoyama (3187_CR28) 2002; 62 K Azuma (3187_CR36) 2011; 407 M Koziczak (3187_CR35) 2004; 279 V Guagnano (3187_CR39) 2011; 54 T Holbro (3187_CR19) 2003; 100 12853564 - Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8933-8 9710588 - Mol Cell Biol. 1998 Sep;18(9):5042-51 20570901 - Cancer Res. 2010 Jul 1;70(13):5199-202 10757805 - Mol Cell Biol. 2000 May;20(9):3210-23 18606717 - Mol Cancer Ther. 2008 Jul;7(7):1851-63 10023681 - Oncogene. 1999 Jan 28;18(4):1053-60 20602996 - Cell. 2010 Jun 25;141(7):1117-34 15756022 - Clin Cancer Res. 2005 Mar 1;11(5):1963-73 22763448 - Nature. 2012 Jul 26;487(7408):505-9 18701483 - Cancer Res. 2008 Aug 15;68(16):6598-607 21215704 - Cancer Cell. 2011 Jan 18;19(1):58-71 22145099 - Cancer Discov. 2011 Sep;1(4):352-65 19033363 - Nucleic Acids Res. 2009 Jan;37(1):1-13 15864276 - Nat Rev Cancer. 2005 May;5(5):341-54 21936542 - J Med Chem. 2011 Oct 27;54(20):7066-83 22124364 - Nat Rev Clin Oncol. 2012 Jan;9(1):16-32 21278786 - Oncogene. 2011 Jun 2;30(22):2547-57 17872411 - Science. 2007 Oct 12;318(5848):287-90 10786682 - Cancer Res. 2000 Apr 15;60(8):2178-89 1540948 - Cancer Res. 1992 Mar 15;52(6):1399-405 15377668 - J Biol Chem. 2004 Nov 26;279(48):50004-11 12036928 - Cancer Res. 2002 Jun 1;62(11):3151-8 15208658 - Oncogene. 2004 Aug 12;23(36):6047-55 15897558 - Clin Cancer Res. 2005 May 15;11(10):3633-41 15516957 - Nat Rev Cancer. 2004 Nov;4(11):839-49 20371474 - Sci Transl Med. 2010 Jan 27;2(16):16ra7 18316624 - Cancer Res. 2008 Mar 1;68(5):1581-92 15256466 - Cancer Res. 2004 Jul 15;64(14):4931-41 22722201 - Nature. 2012 Jun 21;486(7403):400-4 17397528 - Breast Cancer Res. 2007;9(2):R23 21152424 - PLoS One. 2010;5(11):e14117 12204533 - Cancer Cell. 2002 Aug;2(2):127-37 20460524 - Cancer Res. 2010 May 15;70(10):4151-62 23000897 - Nature. 2012 Oct 4;490(7418):61-70 21377448 - Biochem Biophys Res Commun. 2011 Apr 1;407(1):219-24 21045058 - Nucleic Acids Res. 2011 Jan;39(Database issue):D561-8 20094046 - Nat Rev Cancer. 2010 Feb;10(2):116-29 18432775 - Curr Protoc Immunol. 2001 May;Chapter 20:Unit 20.2 22461643 - Sci Transl Med. 2012 Mar 28;4(127):127rv2
References_xml	– volume: 70 start-page: 4151 year: 2010 ident: 3187_CR9 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-09-4479 – volume: 52 start-page: 1399 year: 1992 ident: 3187_CR7 publication-title: Cancer Res – volume: 279 start-page: 50004 year: 2004 ident: 3187_CR35 publication-title: J Biol Chem doi: 10.1074/jbc.M404252200 – volume: 62 start-page: 3151 year: 2002 ident: 3187_CR28 publication-title: Cancer Res – volume: 18 start-page: 1053 year: 1999 ident: 3187_CR38 publication-title: Oncogene doi: 10.1038/sj.onc.1202392 – volume: 11 start-page: 3633 year: 2005 ident: 3187_CR8 publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-04-2129 – volume: 9 start-page: 16 year: 2012 ident: 3187_CR20 publication-title: Nat Rev Clin Oncol doi: 10.1038/nrclinonc.2011.177 – volume: 5 start-page: e14117 year: 2010 ident: 3187_CR34 publication-title: PLoS One doi: 10.1371/journal.pone.0014117 – volume: 54 start-page: 7066 year: 2011 ident: 3187_CR39 publication-title: J Med Chem doi: 10.1021/jm2006222 – volume: 10 start-page: 116 year: 2010 ident: 3187_CR6 publication-title: Nat Rev Cancer doi: 10.1038/nrc2780 – volume: 18 start-page: 5042 year: 1998 ident: 3187_CR17 publication-title: Mol Cell Biol doi: 10.1128/MCB.18.9.5042 – volume: 30 start-page: 2547 year: 2011 ident: 3187_CR25 publication-title: Oncogene doi: 10.1038/onc.2010.626 – volume: 64 start-page: 4931 year: 2004 ident: 3187_CR11 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-03-3681 – volume: 68 start-page: 6598 year: 2008 ident: 3187_CR31 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-08-1044 – volume: 100 start-page: 8933 year: 2003 ident: 3187_CR19 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.1537685100 – volume: 407 start-page: 219 year: 2011 ident: 3187_CR36 publication-title: Biochem Biophys Res Commun doi: 10.1016/j.bbrc.2011.03.002 – volume: 486 start-page: 400 year: 2012 ident: 3187_CR13 publication-title: Nature doi: 10.1038/nature11017 – volume-title: Curr Protoc Immunol year: 2001 ident: 3187_CR14 – volume: 37 start-page: 1 year: 2009 ident: 3187_CR16 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkn923 – volume: 4 start-page: 839 year: 2004 ident: 3187_CR18 publication-title: Nat Rev Cancer doi: 10.1038/nrc1477 – volume: 23 start-page: 6047 year: 2004 ident: 3187_CR37 publication-title: Oncogene doi: 10.1038/sj.onc.1207816 – volume: 68 start-page: 1581 year: 2008 ident: 3187_CR30 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-06-4685 – volume: 60 start-page: 2178 year: 2000 ident: 3187_CR32 publication-title: Cancer Res – volume: 5 start-page: 341 year: 2005 ident: 3187_CR2 publication-title: Nat Rev Cancer doi: 10.1038/nrc1609 – volume: 4 start-page: 127rv122 year: 2012 ident: 3187_CR3 publication-title: Sci Transl Med doi: 10.1126/scitranslmed.3001539 – volume: 70 start-page: 5199 year: 2010 ident: 3187_CR5 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-10-0918 – volume: 141 start-page: 1117 year: 2010 ident: 3187_CR1 publication-title: Cell doi: 10.1016/j.cell.2010.06.011 – volume: 2 start-page: 16ra17 year: 2010 ident: 3187_CR22 publication-title: Sci Transl Med doi: 10.1126/scitranslmed.3000389 – volume: 19 start-page: 58 year: 2011 ident: 3187_CR24 publication-title: Cancer Cell doi: 10.1016/j.ccr.2010.10.031 – volume: 490 start-page: 61 year: 2012 ident: 3187_CR12 publication-title: Nature doi: 10.1038/nature11412 – volume: 487 start-page: 505 year: 2012 ident: 3187_CR23 publication-title: Nature doi: 10.1038/nature11249 – volume: 2 start-page: 127 year: 2002 ident: 3187_CR26 publication-title: Cancer Cell doi: 10.1016/S1535-6108(02)00097-1 – volume: 20 start-page: 3210 year: 2000 ident: 3187_CR27 publication-title: Mol Cell Biol doi: 10.1128/MCB.20.9.3210-3223.2000 – volume: 39 start-page: D561 year: 2011 ident: 3187_CR15 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkq973 – volume: 9 start-page: R23 year: 2007 ident: 3187_CR4 publication-title: Breast Cancer Res doi: 10.1186/bcr1665 – volume: 318 start-page: 287 year: 2007 ident: 3187_CR33 publication-title: Science doi: 10.1126/science.1142946 – volume: 1 start-page: 352 year: 2011 ident: 3187_CR29 publication-title: Cancer Discov doi: 10.1158/2159-8290.CD-11-0106 – volume: 7 start-page: 1851 year: 2008 ident: 3187_CR10 publication-title: Mol Cancer Ther doi: 10.1158/1535-7163.MCT-08-0017 – volume: 11 start-page: 1963 year: 2005 ident: 3187_CR21 publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-04-1665 – reference: 15516957 - Nat Rev Cancer. 2004 Nov;4(11):839-49 – reference: 18432775 - Curr Protoc Immunol. 2001 May;Chapter 20:Unit 20.2 – reference: 1540948 - Cancer Res. 1992 Mar 15;52(6):1399-405 – reference: 21215704 - Cancer Cell. 2011 Jan 18;19(1):58-71 – reference: 12036928 - Cancer Res. 2002 Jun 1;62(11):3151-8 – reference: 12853564 - Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8933-8 – reference: 22124364 - Nat Rev Clin Oncol. 2012 Jan;9(1):16-32 – reference: 21278786 - Oncogene. 2011 Jun 2;30(22):2547-57 – reference: 10786682 - Cancer Res. 2000 Apr 15;60(8):2178-89 – reference: 17872411 - Science. 2007 Oct 12;318(5848):287-90 – reference: 10757805 - Mol Cell Biol. 2000 May;20(9):3210-23 – reference: 17397528 - Breast Cancer Res. 2007;9(2):R23 – reference: 22145099 - Cancer Discov. 2011 Sep;1(4):352-65 – reference: 15756022 - Clin Cancer Res. 2005 Mar 1;11(5):1963-73 – reference: 23000897 - Nature. 2012 Oct 4;490(7418):61-70 – reference: 22722201 - Nature. 2012 Jun 21;486(7403):400-4 – reference: 20371474 - Sci Transl Med. 2010 Jan 27;2(16):16ra7 – reference: 15256466 - Cancer Res. 2004 Jul 15;64(14):4931-41 – reference: 18701483 - Cancer Res. 2008 Aug 15;68(16):6598-607 – reference: 20602996 - Cell. 2010 Jun 25;141(7):1117-34 – reference: 12204533 - Cancer Cell. 2002 Aug;2(2):127-37 – reference: 18606717 - Mol Cancer Ther. 2008 Jul;7(7):1851-63 – reference: 15864276 - Nat Rev Cancer. 2005 May;5(5):341-54 – reference: 21045058 - Nucleic Acids Res. 2011 Jan;39(Database issue):D561-8 – reference: 19033363 - Nucleic Acids Res. 2009 Jan;37(1):1-13 – reference: 20094046 - Nat Rev Cancer. 2010 Feb;10(2):116-29 – reference: 21936542 - J Med Chem. 2011 Oct 27;54(20):7066-83 – reference: 20460524 - Cancer Res. 2010 May 15;70(10):4151-62 – reference: 10023681 - Oncogene. 1999 Jan 28;18(4):1053-60 – reference: 9710588 - Mol Cell Biol. 1998 Sep;18(9):5042-51 – reference: 20570901 - Cancer Res. 2010 Jul 1;70(13):5199-202 – reference: 22461643 - Sci Transl Med. 2012 Mar 28;4(127):127rv2 – reference: 18316624 - Cancer Res. 2008 Mar 1;68(5):1581-92 – reference: 15208658 - Oncogene. 2004 Aug 12;23(36):6047-55 – reference: 15377668 - J Biol Chem. 2004 Nov 26;279(48):50004-11 – reference: 15897558 - Clin Cancer Res. 2005 May 15;11(10):3633-41 – reference: 21377448 - Biochem Biophys Res Commun. 2011 Apr 1;407(1):219-24 – reference: 21152424 - PLoS One. 2010;5(11):e14117 – reference: 22763448 - Nature. 2012 Jul 26;487(7408):505-9
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Snippet	Introduction Targeting receptor tyrosine kinases (RTKs) with kinase inhibitors is a clinically validated anti-cancer approach. However, blocking one signaling... Targeting receptor tyrosine kinases (RTKs) with kinase inhibitors is a clinically validated anti-cancer approach. However, blocking one signaling pathway is...
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SubjectTerms	Animals Biomedical and Life Sciences Biomedicine Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - pathology Cancer Research Cell Proliferation - drug effects ErbB Receptors - antagonists & inhibitors ErbB Receptors - genetics Female Gene Expression Regulation, Neoplastic - drug effects Humans Imidazoles - administration & dosage Mice Molecular Targeted Therapy Oncology Phosphatidylinositol 3-Kinases - administration & dosage Phosphatidylinositol 3-Kinases - genetics Protein Kinase Inhibitors - administration & dosage Proto-Oncogene Proteins c-akt - genetics Purines - administration & dosage Quinolines - administration & dosage Receptors, Fibroblast Growth Factor - antagonists & inhibitors Receptors, Fibroblast Growth Factor - genetics Research Article Signal Transduction - drug effects Surgical Oncology TOR Serine-Threonine Kinases - genetics Xenograft Model Antitumor Assays
Title	Combinatorial targeting of FGF and ErbB receptors blocks growth and metastatic spread of breast cancer models
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