Role of tyrosine kinase inhibitors in the management of high-grade gliomas

References

• Ahluwalia MS, Gladson CL. Progress on antiangiogenic therapy for patients with malignant glioma. J. Oncol.2010, 689018 (2010).
   PubMedGoogle Scholar
• Folkman J. Role of angiogenesis in tumor growth and metastasis. Semin. Oncol.29(6), 15–18 (2002).
   PubMed Web of Science ®Google Scholar
• Jain RK, di Tomaso E, Duda DG, Loeffler JS, Sorensen AG, Batchelor TT. Angiogenesis in brain tumours. Nat. Rev. Neurosci.8(8), 610–622 (2007).
   PubMed Web of Science ®Google Scholar
• Batchelor TT, Duda DG, di Tomaso E et al. Phase II study of cediranib, an oral pan-vascular endothelial growth factor receptor tyrosine kinase inhibitor, in patients with recurrent glioblastoma. J. Clin. Oncol.28(17), 2817–2823 (2010).
   PubMed Web of Science ®Google Scholar
• Batchelor T, Mulholland P, Neyns. The efficacy of cediranib as monotherapy and in combination with lomustine compared to lomustine alone in patients with recurrent glioblastoma: a Phase III randomized study. Neuro. Oncol.12(Suppl. 4), iv69–iv78 (2010).
   Google Scholar
• Escudier B, Eisen T, Stadler WM et al. Sorafenib in advanced clear-cell renal-cell carcinoma. N. Engl. J. Med.356(2), 125–134 (2007).
   PubMed Web of Science ®Google Scholar
• Llovet JM, Ricci S, Mazzaferro V et al. Sorafenib in advanced hepatocellular carcinoma. 359(4), 378–390 (2008).
   Google Scholar
• Jane EP, Premkumar DR, Pollack IF. Coadministration of sorafenib with rottlerin potently inhibits cell proliferation and migration in human malignant glioma cells. N. Pharmacol. Exp. Ther.319(3), 1070–1080 (2006).
   PubMed Web of Science ®Google Scholar
• Yu CR, Friday BB, Lai JP et al. Cytotoxic synergy between the multikinase inhibitor sorafenib and the proteasome inhibitor bortezomib in vitro: induction of apoptosis through Akt and c-Jun NH2-terminal kinase pathways. Mol. Cancer Ther.5(9), 2378–2387 (2006).
   PubMed Web of Science ®Google Scholar
• Wen PY, Cloughesy T, Kuhn J et al. Phase I/II study of sorafenib and temsirolimus for patients with recurrent glioblastoma (GBM) (NABTC 05–02). ASCO Meeting Abstracts27(15 Suppl.), 2006 (2009).
   Google Scholar
• Prados M, Gilbert M, Kuhn J et al. Phase I/II study of sorefenib and erlotinib for patients with recurrent glioblastoma (GBM) (NABTC 05–02). ASCO Meeting Abstracts27(15S), 2005 (2009).
   Google Scholar
• Peereboom D, Ye X, Nabors B et al. NABTT 0502: Phase 2 trial of erlotinib and sorafenib for patients with progressive or recurrent glioblastoma multiforme. Presented at: Society for Neuro-Oncology Meeting. Dallas, TX, USA, 15–17 November 2007.
   Google Scholar
• Hainsworth JD, Ervin T, Friedman E et al. Concurrent radiotherapy and temozolomide followed by temozolomide and sorafenib in the first-line treatment of patients with glioblastoma multiforme. Cancer116(15), 3663–3669 (2010).
   PubMed Web of Science ®Google Scholar
• Reardon DA, Vredenburgh JJ, Desjardins A et al. Effect of CYP3A-inducing anti-epileptics on sorafenib exposure: results of a Phase II study of sorafenib plus daily temozolomide in adults with recurrent glioblastoma. J. Neurooncol.101(1), 57–66 (2011).
   PubMed Web of Science ®Google Scholar
• Demetri GD, van Oosterom AT, Garrett CR et al. Efficacy and safety of sunitinib in patients with advanced gastrointestinal stromal tumour after failure of imatinib: a randomised controlled trial. Lancet368(9544), 1329–1338 (2006).
   PubMed Web of Science ®Google Scholar
• Motzer RJ, Hutson TE, Tomczak P et al. Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. N. Engl. J. Med.356(2), 115–124 (2007).
   PubMed Web of Science ®Google Scholar
• Zhu AX, Raymond E. Early development of sunitinib in hepatocellular carcinoma. Expert Rev. Anticancer Ther.9(1), 143–150 (2009).
   PubMed Web of Science ®Google Scholar
• Neyns B, Sadones J, Chaskis C et al. Phase II study of sunitinib malate in patients with recurrent high-grade glioma. J. Neurooncol.103(3), 491–501 (2011).
   PubMed Web of Science ®Google Scholar
• Reardon DA, Vredenburgh JJ, Coan A et al. Phase I study of sunitinib and irinotecan for patients with recurrent malignant glioma. J. Neurooncol. DOI: 10.1007/s11060-011-0627-0 (2011) (Epub ahead of print).
   Google Scholar
• Sloan B, Scheinfeld NS. Pazopanib, a VEGF receptor tyrosine kinase inhibitor for cancer therapy. Curr. Opin. Investig. Drugs9(12), 1324–1335 (2008).
   PubMed Web of Science ®Google Scholar
• Iwamoto FM, Lamborn KR, Robins HI et al. Phase II trial of pazopanib (GW786034), an oral multi-targeted angiogenesis inhibitor, for adults with recurrent glioblastoma (North American Brain Tumor Consortium Study 06–02). Neuro Oncol.12(8), 855–861 (2010).
   PubMedGoogle Scholar
• Kurzrock R, Camacho L, Hong D et al. A Phase I dose-escalation study of the safety and pharmacokinetics of a XL184, a VEGFR and Met kinase inhibitor, administered orally to subjects with advanced malignancies. EJC Suppl.4(12), 405 (2006).
   Google Scholar
• Salgia R, Hong D, Sherman SI et al. A phase 1 dose-escalation study of the safety and pharmacokinetics (PK) of XL184, a VEGFR and MET kinase inhibitor, administered orally to patients (pts) with advanced malignancies. Mol. Cancer Ther.6(12), 3385S–3385S (2007).
   Google Scholar
• Christensen JG, Burrows J, Salgia R. c-Met as a target for human cancer and characterization of inhibitors for therapeutic intervention. Cancer Lett.225(1), 1–26 (2005).
   PubMed Web of Science ®Google Scholar
• Cancer Genome Atlas Research Network. Comprehensive genomic characterization defines human glioblastoma genes and core pathways. Nature455(7216), 1061–1068 (2008).
   PubMed Web of Science ®Google Scholar
• Abounader R, Laterra J. Scatter factor/hepatocyte growth factor in brain tumor growth and angiogenesis. Neuro Oncol.7(4), 436–451 (2005).
   PubMed Web of Science ®Google Scholar
• Wen PY, Prados M, Schiff D et al. Phase II study of XL184 (BMS 907351), an inhibitor of MET, VEGFR2, and RET, in patients (pts) with progressive glioblastoma (GB). ASCO Meeting Abstracts28(15 Suppl.), 2006 (2010).
   Google Scholar
• Sathornsumetee S, Rich JN. Vandetanib, a novel multitargeted kinase inhibitor, in cancer therapy. Drugs Today42(10), 657–670 (2006).
   PubMed Web of Science ®Google Scholar
• Rich JN, Sathornsumetee S, Keir ST et al. ZD6474, a novel tyrosine kinase inhibitor of vascular endothelial growth factor receptor and epidermal growth factor receptor, inhibits tumor growth of multiple nervous system tumors. Clin. Cancer Res.11(22), 8145–8157 (2005).
   PubMed Web of Science ®Google Scholar
• Yiin JJ, Hu B, Schornack PA et al. ZD6474, a multitargeted inhibitor for receptor tyrosine kinases, suppresses growth of gliomas expressing an epidermal growth factor receptor mutant, EGFRvIII, in the brain. Mol. Cancer Ther.9(4), 929–941 (2010).
   PubMed Web of Science ®Google Scholar
• Damiano V, Melisi D, Bianco C et al. Cooperative antitumor effect of multitargeted kinase inhibitor ZD6474 and ionizing radiation in glioblastoma. Clin. Cancer Res.11(15), 5639–5644 (2005).
   PubMed Web of Science ®Google Scholar
• Drappatz J, Norden AD, Wong ET et al. Phase I study of vandetanib with radiotherapy and temozolomide for newly diagnosed glioblastoma. Int. J. Radiat. Oncol. Biol. Phys.78(1), 85–90 (2010).
   PubMedGoogle Scholar
• Jost LM, Gschwind HP, Jalava T et al. Metabolism and disposition of vatalanib (PTK787/ZK-222584) in cancer patients. Drug Metab. Dispos.34(11), 1817–1828 (2006).
   PubMed Web of Science ®Google Scholar
• Saunders MP, Wilson R, Peeters M et al. Vandetanib with FOLFIRI in patients with advanced colorectal adenocarcinoma: results from an open-label, multicentre Phase I study. Cancer Chemother. Pharmacol.64(4), 665–672 (2009).
   PubMed Web of Science ®Google Scholar
• Scott EN, Meinhardt G, Jacques C, Laurent D, Thomas AL. Vatalanib: the clinical development of a tyrosine kinase inhibitor of angiogenesis in solid tumours. Expert Opin. Invest. Drugs16(3), 367–379 (2007).
   PubMed Web of Science ®Google Scholar
• Thomas AL, Morgan B, Horsfield MA et al. Phase I study of the safety, tolerability, pharmacokinetics, and pharmacodynamics of PTK787/ZK 222584 administered twice daily in patients with advanced cancer. J. Clin. Oncol.23(18), 4162–4171 (2005).
   PubMed Web of Science ®Google Scholar
• Goldbrunner RH, Bendszus M, Wood J, Kiderlen M, Sasaki M, Tonn JC. PTK787/ZK222584, an inhibitor of vascular endothelial growth factor receptor tyrosine kinases, decreases glioma growth and vascularization. Neurosurgery55(2), 426–432; discussion 432 (2004).
   PubMed Web of Science ®Google Scholar
• Conrad C, Friedman H, Reardon D et al. A Phase I/II trial of single-agent PTK 787/ZK 222584 (PTK/ZK), a novel, oral angiogenesis inhibitor, in patients with recurrent glioblastoma multiforme (GBM). ASCO Meeting Abstracts22(14 Suppl.), 1512 (2004).
   Google Scholar
• Reardon D, Friedman H, Yung WKA et al. A Phase I/II trial of PTK787/ZK 222584 (PTK/ZK), a novel, oral angiogenesis inhibitor, in combination with either temozolomide or lomustine for patients with recurrent glioblastoma multiforme (GBM). ASCO Meeting Abstracts22(14 Suppl.), 1513 (2004).
   Google Scholar
• Glen H, Mason S, Patel H, Macleod K, Brunton VG. E7080, a multi-targeted tyrosine kinase inhibitor suppresses tumour cell migration and invasion. BMC Cancer11(1), 309 (2011).
   PubMed Web of Science ®Google Scholar
• Hermanson M, Funa K, Hartman M et al. Platelet-derived growth factor and its receptors in human glioma tissue: expression of messenger RNA and protein suggests the presence of autocrine and paracrine loops. Cancer Res.52(11), 3213–3219 (1992).
   PubMed Web of Science ®Google Scholar
• Brennan C, Momota H, Hambardzumyan D et al. Glioblastoma subclasses can be defined by activity among signal transduction pathways and associated genomic alterations. PLoS One4(11), e7752 (2009).
   PubMed Web of Science ®Google Scholar
• Kilic T, Alberta JA, Zdunek PR et al. Intracranial inhibition of platelet-derived growth factor-mediated glioblastoma cell growth by an orally active kinase inhibitor of the 2-phenylaminopyrimidine class. Cancer Res.60(18), 5143–5150 (2000).
   PubMed Web of Science ®Google Scholar
• Wen PY, Yung WK, Lamborn KR et al. Phase I/II study of imatinib mesylate for recurrent malignant gliomas: North American Brain Tumor Consortium Study 99–08. Clin. Cancer Res.12(16), 4899–4907 (2006).
   PubMed Web of Science ®Google Scholar
• Wen PY, Yung WK, Lamborn KR et al. Phase II study of imatinib mesylate for recurrent meningiomas (North American Brain Tumor Consortium study 01–08). Neuro Oncol.11(6), 853–860 (2009).
   PubMed Web of Science ®Google Scholar
• Desjardins A, Quinn JA, Vredenburgh JJ et al. Phase II study of imatinib mesylate and hydroxyurea for recurrent grade III malignant gliomas. J. Neuro-Oncol.83(1), 53–60 (2007).
   PubMed Web of Science ®Google Scholar
• Reardon DA, Egorin MJ, Quinn JA et al. Phase II study of imatinib mesylate plus hydroxyurea in adults with recurrent glioblastorna multiforme. J. Clin. Oncol.23(36), 9359–9368 (2005).
   PubMed Web of Science ®Google Scholar
• Reardon DA, Dresemann G, Taillibert S et al. Multicentre Phase II studies evaluating imatinib plus hydroxyurea in patients with progressive glioblastoma. Br. J. Cancer101(12), 1995–2004 (2009).
   PubMed Web of Science ®Google Scholar
• Dresemann G, Weller M, Rosenthal MA et al. Imatinib in combination with hydroxyurea versus hydroxyurea alone as oral therapy in patients with progressive pretreated glioblastoma resistant to standard dose temozolomide. J. Neurooncol.96(3), 393–402 (2010).
   PubMed Web of Science ®Google Scholar
• Dong Y, Jia L, Wang X et al. Selective inhibition of PDGFR by imatinib elicits the sustained activation of ERK and downstream receptor signaling in malignant glioma cells. Int J. Oncol.38(2), 555–569 (2011).
   PubMed Web of Science ®Google Scholar
• Stettner MR, Wang W, Nabors LB et al. Lyn kinase activity is the predominant cellular Src kinase activity in glioblastoma tumor cells. Cancer Res.65(13), 5535–5543 (2005).
   PubMed Web of Science ®Google Scholar
• Du J, Bernasconi P, Clauser KR et al. Bead-based profiling of tyrosine kinase phosphorylation identifies Src as a potential target for glioblastoma therapy. Nat. Biotechnol.27(1), 77–83 (2009).
   PubMed Web of Science ®Google Scholar
• Ahluwalia MS, Groot J, Liu WM, Gladson CL. Targeting Src in glioblastoma tumors and brain metastases: rationale and preclinical studies. Cancer Lett.298(2), 139–149 (2010).
   PubMed Web of Science ®Google Scholar
• Lu-Emerson C, Norden AD, Drappatz J et al. Retrospective study of dasatinib for recurrent glioblastoma after bevacizumab failure. J. Neurooncol.104(1), 287–291 (2010).
   Google Scholar
• Puttini M, Coluccia AM, Boschelli F et al.In vitro and in vivo activity of SKI-606, a novel Src-Abl inhibitor, against imatinib-resistant Bcr-Abl+ neoplastic cells. Cancer Res.66(23), 11314–11322 (2006).
   PubMed Web of Science ®Google Scholar
• Kimura S, Naito H, Segawa H et al. NS-187, a potent and selective dual Bcr-Abl/Lyn tyrosine kinase inhibitor, is a novel agent for imatinib-resistant leukemia. Blood106(12), 3948–3954 (2005).
   PubMed Web of Science ®Google Scholar
• Santos FP, Kantarjian H, Cortes J, Quintas-Cardama A. Bafetinib, a dual Bcr-Abl/Lyn tyrosine kinase inhibitor for the potential treatment of leukemia. Curr. Opin. Investig. Drugs11(12), 1450–1465 (2011).
   Google Scholar
• Chakravarti A, Zhai G, Suzuki Y et al. The prognostic significance of phosphatidylinositol 3-kinase pathway activation in human gliomas. J. Clin. Oncol.22(10), 1926–1933 (2004).
   PubMed Web of Science ®Google Scholar
• Chang SM, Wen P, Cloughesy T et al. Phase II study of CCI-779 in patients with recurrent glioblastoma multiforme. Invest. New Drugs23(4), 357–361 (2005).
   PubMed Web of Science ®Google Scholar
• Galanis E, Buckner JC, Maurer MJ et al. Phase II trial of temsirolimus (CCI-779) in recurrent glioblastoma multiforme: a North Central Cancer Treatment Group Study. J. Clin. Oncol.23(23), 5294–5304 (2005).
   PubMed Web of Science ®Google Scholar
• Prasad G, Sottero T, Yang X et al. Inhibition of PI3K/mTOR pathways in glioblastoma and implications for combination therapy with temozolomide. Neuro Oncol.13(4), 384–392 (2011).
   PubMed Web of Science ®Google Scholar
• Papadopoulos KP, Tabernero J, Patnaik A et al. A Phase I dose-escalation study of the safety, pharmacokinetics, and pharmacodynamics of a novel PI3K inhibitor, XL765, administered orally to patients with advanced solid tumors. J. Clin. Oncol. (Meeting Abstracts)26, 3510 (2008).
   Google Scholar
• Bagci-Onder T, Wakimoto H, Anderegg M, Cameron C, Shah K. A dual PI3K/mTOR inhibitor, PI-103, cooperates with stem cell-delivered TRAIL in experimental glioma models. Cancer Res.71(1), 154–163 (2011).
   PubMed Web of Science ®Google Scholar
• Franceschi E, Cavallo G, Lonardi S et al. Gefitinib in patients with progressive high-grade gliomas: a multicentre Phase II study by Gruppo Italiano Cooperativo di Neuro-Oncologia (GICNO). Br. J. Cancer96(7), 1047–1051 (2007).
   PubMed Web of Science ®Google Scholar
• Rich JN, Reardon DA, Peery T et al. Phase II trial of gefitinib in recurrent glioblastoma. J. Clin. Oncol.22(1), 133–142 (2004).
   PubMed Web of Science ®Google Scholar
• Raizer JJ, Abrey LE, Lassman AB et al. A Phase I trial of erlotinib in patients with nonprogressive glioblastoma multiforme postradiation therapy, and recurrent malignant gliomas and meningiomas. Neuro Oncol.12(1), 87–94 (2010).
   PubMed Web of Science ®Google Scholar
• Raizer JJ, Abrey LE, Lassman AB et al. A Phase II trial of erlotinib in patients with recurrent malignant gliomas and nonprogressive glioblastoma multiforme postradiation therapy. Neuro Oncol.12(1), 95–103 (2010).
   PubMed Web of Science ®Google Scholar
• Vogelbaum MA, Peereboom D, Stevens G, Barnett GH, Brewer C. Response rate to single agent therapy with the EGFR tyrosine kinase inhibitor erlotinib in recurrent blioblastoma multiforme: results of a Phase II study. Proceedings of: Ninth Meeting of the Society for Neuro-Oncology. Toronto, Canada, 18–21 November 2004 (Abstract TA-359).
   Google Scholar
• Sathornsumetee S, Desjardins A, Vredenburgh JJ et al. Phase II trial of bevacizumab and erlotinib in patients with recurrent malignant glioma. Neuro Oncol.12(12), 1300–1310 (2010).
   PubMed Web of Science ®Google Scholar
• Brown PD, Krishnan S, Sarkaria JN et al. Phase I/II trial of erlotinib and temozolomide with radiation therapy in the treatment of newly diagnosed glioblastoma multiforme: North Central Cancer Treatment Group Study N0177. J. Clin. Oncol.26(34), 5603–5609 (2008).
   PubMed Web of Science ®Google Scholar
• Peereboom DM, Shepard DR, Ahluwalia MS et al. Phase II trial of erlotinib with temozolomide and radiation in patients with newly diagnosed glioblastoma multiforme. J. Neurooncol.98(1), 93–99 (2009).
   PubMed Web of Science ®Google Scholar
• Prados MD, Chang SM, Butowski N et al. Phase II study of erlotinib plus temozolomide during and after radiation therapy in patients with newly diagnosed glioblastoma multiforme or gliosarcoma. J. Clin. Oncol.27(4), 579–584 (2009).
   PubMed Web of Science ®Google Scholar
• Mellinghoff IK, Wang MY, Vivanco I et al. Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors. N. Engl. J. Med.353(19), 2012–2024 (2005).
   PubMed Web of Science ®Google Scholar
• Stommel JM, Kimmelman AC, Ying H et al. Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapies. Science318(5848), 287–290 (2007).
   PubMed Web of Science ®Google Scholar
• Robins HI, Wen PY, Chang SM et al. Phase I study of erlotinib and CCI-779 (temsirolimus) for patients with recurrent malignant gliomas (MG) (NABTC 04–02). ASCO Meeting Abstracts25(18 Suppl.), 2057 (2007).
   Google Scholar
• Haas-Kogan DA, Prados MD, Tihan T et al. Epidermal growth factor receptor, protein kinase B/Akt, and glioma response to erlotinib. J. Natl Cancer Inst.97(12), 880–887 (2005).
   PubMed Web of Science ®Google Scholar
• Thiessen B, Stewart C, Tsao M et al. A Phase I/II trial of GW572016 (lapatinib) in recurrent glioblastoma multiforme: clinical outcomes, pharmacokinetics and molecular correlation. Cancer Chemother. Pharmacol.65(2), 353–361 (2010).
   PubMed Web of Science ®Google Scholar
• Mir O, Blanchet B, Goldwasser F. Drug-induced effects on erlotinib metabolism. N. Engl. J. Med.365(4), 379–380 (2011).
   PubMed Web of Science ®Google Scholar
• Muldoon LL, Soussain C, Jahnke K et al. Chemotherapy delivery issues in central nervous system malignancy: a reality check. J. Clin. Oncol.25(16), 2295–2305 (2007).
   PubMed Web of Science ®Google Scholar
• Agarwal S, Sane R, Ohlfest JR, Elmquist WF. The role of the breast cancer resistance protein (ABCG2) in the distribution of sorafenib to the brain. J. Pharmacol. Exp. Ther.336(1), 223–233 (2011).
   PubMed Web of Science ®Google Scholar
• Agarwal S, Sane R, Gallardo JL, Ohlfest JR, Elmquist WF. Distribution of gefitinib to the brain is limited by P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2)-mediated active efflux. J. Pharmacol. Exp. Ther.334(1), 147–155 (2010).
   PubMed Web of Science ®Google Scholar
• Tang SC, Lagas JS, Lankheet NA et al. Brain accumulation of sunitinib is restricted by P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) and can be enhanced by oral elacridar and sunitinib coadministration. Int. J. Cancer DOI: 10.1002/ijc.26000 (2011) (Epub ahead of print).
   Google Scholar
• Lagas JS, van Waterschoot RA, van Tilburg VA et al. Brain accumulation of dasatinib is restricted by P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) and can be enhanced by elacridar treatment. Clin. Cancer Res.15(7), 2344–2351 (2009).
   PubMed Web of Science ®Google Scholar