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Review

Future options for imatinib mesilate-resistant tumors

& , MD
Pages 1549-1560 | Published online: 09 Oct 2007

Bibliography

  • NILSSON B, BUMMING P, MEIS-KINDBLOM JM et al.: Gastrointestinal stromal tumors: the incidence, prevalence, clinical course, and prognostication in the preimatinib mesylate era – a population-based study in western Sweden. Cancer (2005) 103(4):821-829.
  • MIETTINEN M, SARLOMO-RIKALA M, LASOTA J: Gastrointestinal stromal tumors: recent advances in understanding of their biology. Hum. Pathol. (1999) 30(10):1213-1220.
  • KINDBLOM LG, REMOTTI HE, ALDENBORG F, MEIS-KINDBLOM JM: Gastrointestinal pacemaker cell tumor (GIPACT): gastrointestinal stromal tumors show phenotypic characteristics of the interstitial cells of Cajal. Am. J. Pathol. (1998) 152(5):1259-1269.
  • ROBINSON TL, SIRCAR K, HEWLETT BR et al.: Gastrointestinal stromal tumors may originate from a subset of CD34-positive interstitial cells of Cajal. Am. J. Pathol. (2000) 156(4):1157-1163.
  • SAKURAI S, FUKASAWA T, CHONG JM, TANAKA A, FUKAYAMA M: Embryonic form of smooth muscle myosin heavy chain (SMemb/MHC-B) in gastrointestinal stromal tumor and interstitial cells of Cajal. Am. J. Pathol. (1999) 154(1):23-28.
  • SIRCAR K, HEWLETT BR, HUIZINGA JD et al.: Interstitial cells of Cajal as precursors of gastrointestinal stromal tumors. Am. J. Surg. Pathol. (1999) 23(4):377-389.
  • HUIZINGA JD, THUNEBERG L, KLUPPEL M et al.: W/kit gene required for interstitial cells of Cajal and for intestinal pacemaker activity. Nature (1995) 373(6512):347-349.
  • KLUPPEL M, HUIZINGA JD, MALYSZ J, BERNSTEIN A: Developmental origin and kit-dependent development of the interstitial cells of Cajal in the mammalian small intestine. Dev. Dyn. (1998) 211(1):60-71.
  • RUBIN BP, SINGER S, TSAO C et al.: KIT activation is a ubiquitous feature of gastrointestinal stromal tumors. Cancer Res. (2001) 61(22):8118-8121.
  • SARLOMO-RIKALA M, KOVATICH AJ, BARUSEVICIUS A, MIETTINEN M: CD117: a sensitive marker for gastrointestinal stromal tumors that is more specific than CD34. Mod. Pathol. (1998) 11(8):728-734.
  • TORIHASHI S, NISHI K, TOKUTOMI Y et al.: Blockade of kit signaling induces transdifferentiation of interstitial cells of Cajal to a smooth muscle phenotype. Gastroenterology (1999) 117(1):140-148.
  • HIROTA S, ISOZAKI K, MORIYAMA Y et al.: Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors. Science (1998) 279(5350):577-580.
  • KITAMURA Y, HIROTA S, NISHIDA T: Molecular pathology of c-kit proto-oncogene and development of gastrointestinal stromal tumors. Ann. Chir. Gynaecol. (1998) 87(4):282-286.
  • PLAAT BE, HOLLEMA H, MOLENAAR WM et al.: Soft tissue leiomyosarcomas and malignant gastrointestinal stromal tumors: differences in clinical outcome and expression of multidrug resistance proteins. J. Clin. Oncol. (2000) 18(18):3211-3220.
  • CARROLL M, OHNO-JONES S, TAMURA S et al.: CGP 57148, a tyrosine kinase inhibitor, inhibits the growth of cells expressing BCR-ABL, TEL-ABL, and TEL-PDGFR fusion proteins. Blood (1997) 90(12):4947-4952.
  • BUCHDUNGER E, CIOFFI CL, LAW N et al.: Abl protein-tyrosine kinase inhibitor STI571 inhibits in vitro signal transduction mediated by c-kit and platelet-derived growth factor receptors. J. Pharmacol. Exp. Ther. (2000) 295(1):139-145.
  • HEINRICH MC, GRIFFITH DJ, DRUKER BJ et al.: Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor. Blood (2000) 96(3):925-932.
  • JOENSUU H, ROBERTS PJ, SARLOMO-RIKALA M et al.: Effect of the tyrosine kinase inhibitor STI571 in a patient with a metastatic gastrointestinal stromal tumor. N. Engl. J. Med. (2001) 344(14):1052-1056.
  • DEMETRI GD, VON MEHREN M, BLANKE CD et al.: Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors. N. Engl. J. Med. (2002) 347(7):472-480.
  • VAN OOSTEROM AT, JUDSON I, VERWEIJ J et al.: Safety and efficacy of imatinib (STI571) in metastatic gastrointestinal stromal tumours: a Phase I study. Lancet (2001) 358(9291):1421-1423.
  • VERWEIJ J, CASALI PG, ZALCBERG J et al.: Progression-free survival in gastrointestinal stromal tumours with high-dose imatinib: randomised trial. Lancet (2004) 364(9440):1127-1134.
  • ZALCBERG JR, VERWEIJ J, CASALI PG et al.: Outcome of patients with advanced gastro-intestinal stromal tumors (GIST) crossing over to a daily imatinib dose of 800 mg (HD) after progression on 400 mg (LD)- an international, intergroup study of the EORTC, ISG and AGITG. J. Clin. Oncol. (Meeting Abstracts) (2004) 22(14S):9004.
  • MCARTHUR GA, DEMETRI GD, VAN OOSTEROM A et al.: Molecular and clinical analysis of locally advanced dermatofibrosarcoma protuberans treated with imatinib: Imatinib target exploration consortium study B2225. J. Clin. Oncol. (2005) 23(4):866-873.
  • TEFFERI A, PATNAIK MM, PARDANANI A: Eosinophilia: secondary, clonal and idiopathic. Br. J. Haematol. (2006) 133(5):468-492.
  • BENJAMIN RS, BLANKE CD, BLAY JY, BONVALOT S, EISENBERG B: Management of gastrointestinal stromal tumors in the imatinib era: selected case studies. Oncologist (2006) 11(1):9-20.
  • EISENBERG BL: Combining imatinib with surgery in gastrointestinal stromal tumors: rationale and ongoing trials. Clin. Colorect. Cancer (2006) 6(Suppl. 1):S24-S29.
  • CORLESS CL, SCHROEDER A, GRIFFITH D et al.: PDGFRA mutations in gastrointestinal stromal tumors: frequency, spectrum and in vitro sensitivity to imatinib. J. Clin. Oncol. (2005) 23(23):5357-5364.
  • HEINRICH MC, CORLESS CL, DEMETRI GD et al.: Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor. J. Clin. Oncol. (2003) 21(23):4342-4349.
  • DEBIEC-RYCHTER M, DUMEZ H, JUDSON I et al.: Use of c-KIT/PDGFRA mutational analysis to predict the clinical response to imatinib in patients with advanced gastrointestinal stromal tumours entered on Phase I and II studies of the EORTC soft tissue and bone sarcoma group. Eur. J. Cancer (2004) 40(5):689-695.
  • DEBIEC-RYCHTER M, SCIOT R, LE CESNE A et al.: KIT mutations and dose selection for imatinib in patients with advanced gastrointestinal stromal tumours. Eur. J. Cancer (2006) 42(8):1093-1103.
  • HEINRICH MC, CORLESS CL, BLANKE CD et al.: Molecular correlates of imatinib resistance in gastrointestinal stromal tumors. J. Clin. Oncol. (2006) 24(29):4764-4774.
  • ANTONESCU CR, BESMER P, GUO T et al.: Acquired resistance to imatinib in gastrointestinal stromal tumor occurs through secondary gene mutation. Clin. Cancer Res. (2005) 11(11):4182-4190.
  • WAKAI T, KANDA T, HIROTA S et al.: Late resistance to imatinib therapy in a metastatic gastrointestinal stromal tumour is associated with a second KIT mutation. Br. J. Cancer (2004) 90(11):2059-2061.
  • CHEN LL, TRENT JC, WU EF et al.: A missense mutation in KIT kinase domain 1 correlates with imatinib resistance in gastrointestinal stromal tumors. Cancer Res. (2004) 64(17):5913-5919.
  • TAMBORINI E, GABANTI E, LAGONIGRO MS et al.: KIT/Val654 Ala receptor detected in one imatinib-resistant GIST patient. Cancer Res. (2005) 65(3):1115; author reply 1115.
  • TAMBORINI E, BONADIMAN L, GRECO A et al.: A new mutation in the KIT ATP pocket causes acquired resistance to imatinib in a gastrointestinal stromal tumor patient. Gastroenterology (2004) 127(1):294-299.
  • FLETCHER JA, CORLESS CL, DIMITRIJEVIC S et al.: Mechanisms of resistance to imatinib mesylate (IM) in advanced gastrointestinal stromal tumor (GIST). Proc. Am. Soc. Clin. Oncol. (2003) 22:(Abstract 3275).
  • BAUER S, HUBERT C, HEINRICH MC, BERTAGNOLLI M, DEMETRI GD, FLETCHER J: KIT hyperactivation in imatinib-resistant GIST: implications for salvage therapies. J. Clin. Oncol. (2005) 23(16 Suppl.):9034 (Meeting Abstracts).
  • MAHADEVAN D, COOKE L, RILEY C et al.: A novel tyrosine kinase switch is a mechanism of imatinib resistance in gastrointestinal stromal tumors. Oncogene (2007) 26(27):3909-3919.
  • COLE SP, SPARKS KE, FRASER K et al.: Pharmacological characterization of multidrug resistant MRP-transfected human tumor cells. Cancer Res. (1994) 54(22):5902-5910.
  • COLVIN OM: Drug resistance in the treatment of sarcomas. Semin. Oncol. (1997) 24(5):580-591.
  • KOMDEUR R, PLAAT BE, VAN DER GRAAF WT et al.: Expression of multidrug resistance proteins, P-gp, MRP1 and LRP, in soft tissue sarcomas analysed according to their histological type and grade. Eur. J. Cancer (2003) 39(7):909-916.
  • BURGER H, VAN TOL H, BOERSMA AW et al.: Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump. Blood (2004) 104(9):2940-2942.
  • HEGEDUS T, ORFI L, SEPRODI A et al.: Interaction of tyrosine kinase inhibitors with the human multidrug transporter proteins, MDR1 and MRP1. Biochim. Biophys. Acta (2002) 1587(2-3):318-325.
  • OZVEGY-LACZKA C, HEGEDUS T, VARADY G et al.: High-affinity interaction of tyrosine kinase inhibitors with the ABCG2 multidrug transporter. Mol. Pharmacol. (2004) 65(6):1485-1495.
  • THEOU N, GIL S, DEVOCELLE A et al.: Multidrug resistance proteins in gastrointestinal stromal tumors: site-dependent expression and initial response to imatinib. Clin. Cancer Res. (2005) 11(21):7593-7598.
  • TAKAHASHI R, TANAKA S, KITADAI Y et al.: Expression of vascular endothelial growth factor and angiogenesis in gastrointestinal stromal tumor of the stomach. Oncology (2003) 64(3):266.
  • BONO P, KRAUSE A, VON MEHREN M et al.: Serum KIT and KIT ligand levels in patients with gastrointestinal stromal tumors treated with imatinib. Blood (2004) 103(8):2929-2935.
  • TRENT JC, CHOI H, HUNT K et al.: Apoptotic and anti-vascular activity of imatinib in GIST patients. J. Clin. Oncol. (Meeting Abstracts) (2005) 23(16 Suppl.):9001.
  • ABRAMS TJ, LEE LB, MURRAY LJ, PRYER NK, CHERRINGTON JM: SU11248 inhibits KIT and platelet-derived growth factor receptor beta in preclinical models of human small cell lung cancer. Mol. Cancer Ther. (2003) 2(5):471-478.
  • MENDEL DB, LAIRD AD, XIN X et al.: In vivo antitumor activity of SU11248, a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor and platelet-derived growth factor receptors: determination of a pharmacokinetic/pharmacodynamic relationship. Clin. Cancer Res. (2003) 9(1):327-337.
  • O'FARRELL AM, ABRAMS TJ, YUEN HA et al.: SU11248 is a novel FLT3 tyrosine kinase inhibitor with potent activity in vitro and in vivo. Blood (2003) 101(9):3597-3605.
  • 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. Lancet (2006) 368(9544):1329-1338.
  • POLVERINO A, COXON A, STARNES C et al.: AMG 706, an oral, multikinase inhibitor that selectively targets vascular endothelial growth factor, platelet-derived growth factor, and Kit receptors, potently inhibits angiogenesis and induces regression in tumor xenografts. Cancer Res. (2006) 66(17):8715-8721.
  • ROSEN L, KURZROCK R, JACKSON E et al.: Safety and pharmacokinetics of AMG 706 in patients with advanced solid tumors. J. Clin. Oncol. (Meeting Abstracts) (2005) 23(16S):3013.
  • BENJAMIN R, SCHÖFFSKI P, HARTMANN JT et al.: Initial results of a multicenter, single-arm Phase II study of AMG 706, an oral multikinase inhibitor, for the treatment of advanced imatinib-resistant gastrointestinal stromal tumors (GIST). CTOS Meeting, Venice, Italy (2 – 4 November 2006).
  • CHOI H, CHARNSANGAVEJ C, FARIA SC et al.: Correlation of computed tomography and positron emission tomography in patients with metastatic gastrointestinal stromal tumor treated at a single institution with imatinib mesylate: proposal of new computed tomography response criteria. J. Clin. Oncol. (2007) 25(13):1753-1759.
  • WOOD JM, BOLD G, BUCHDUNGER E et al.: PTK787/ZK 222584, a novel and potent inhibitor of vascular endothelial growth factor receptor tyrosine kinases, impairs vascular endothelial growth factor-induced responses and tumor growth after oral administration. Cancer Res. (2000) 60(8):2178-2189.
  • DREVS J, MULLER-DRIVER R, WITTIG C et al.: PTK787/ZK 222584, a specific vascular endothelial growth factor-receptor tyrosine kinase inhibitor, affects the anatomy of the tumor vascular bed and the functional vascular properties as detected by dynamic enhanced magnetic resonance imaging. Cancer Res. (2002) 62(14):4015-4022.
  • 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. (2005) 23(18):4162-4171.
  • JOENSUU H, DE BRAUD F, COCO P et al.: A Phase II, open-label study of PTK787/ZK222584 in the treatment of metastatic gastrointestinal stromal tumors (GISTs) resistant to imatinib mesylate. J. Clin. Oncol. (Meeting Abstracts) (2006) 24(18S):9531.
  • CARLOMAGNO F, ANAGANTI S, GUIDA T et al.: BAY 43-9006 inhibition of oncogenic RET mutants. J. Natl. Cancer Inst. (2006) 98(5):326-334.
  • WILHELM SM, CARTER C, TANG L et al.: BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis. Cancer Res. (2004) 64(19):7099-7109.
  • ESCUDIER B, SZCZYLIK C, EISEN T et al.: Randomized Phase III trial of the Raf kinase and VEGFR inhibitor sorafenib (BAY 43-9006) in patients with advanced renal cell carcinoma (RCC). J. Clin. Oncol. (Meeting Abstracts) (2005) 23(16 Suppl.):LBA4510.
  • RATAIN MJ, EISEN T, STADLER WM et al.: Phase II placebo-controlled randomized discontinuation trial of sorafenib in patients with metastatic renal cell carcinoma. J. Clin. Oncol. (2006) 24(16):2505-2512.
  • GEDRICH R, SULLIVAN E, SHI H et al.: Sorafenib (BAY 43-9006) inhibits imatinib-resistant mutant KIT signaling. Eur. J. Cancer (2006) 4(12):S173 (Abstract 572).
  • GUIDA T, ANAGANTI S, PROVITERA L et al.: Sorafenib inhibits imatinib-resistant KIT and platelet-derived growth factor receptor β gatekeeper mutants. Clin. Cancer Res. (2007) 13(11):3363-3369.
  • PRENEN H, DEWAELE B, COOLS J et al.: In vitro activity of the multi-targeted kinase inhibitor sorafenib (BAY43-9006) against gastrointestinal stromal tumor (GIST) mutants refractory to imatinib mesylate. Eur. J. Cancer (2006) 4(12):S171 (Abstract 563).
  • WEDGE SR, KENDREW J, HENNEQUIN LF et al.: AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer. Cancer Res. (2005) 65(10):4389-4400.
  • DREVS J, MEDINGER M, MROSS K et al.: Phase I clinical evaluation of AZD2171, a highly potent VEGF receptor tyrosine kinase inhibitor, in patients with advanced tumors. J. Clin. Oncol. (Meeting Abstracts) (2005) 23(16S):3002.
  • FABBRO D, RUETZ S, BODIS S et al.: PKC412-α protein kinase inhibitor with a broad therapeutic potential. Anticancer Drug Des. (2000) 15(1):17-28.
  • GROWNEY JD, CLARK JJ, ADELSPERGER J et al.: Activation mutations of human c-KIT resistant to imatinib mesylate are sensitive to the tyrosine kinase inhibitor PKC412. Blood (2005) 106(2):721-724.
  • DEBIEC-RYCHTER M, COOLS J, DUMEZ H et al.: Mechanisms of resistance to imatinib mesylate in gastrointestinal stromal tumors and activity of the PKC412 inhibitor against imatinib-resistant mutants. Gastroenterology (2005) 128(2):270-279.
  • PRICL S, TAMBORINI E, NEGRI T et al.: A clinical/modeling investigation of the activity of PKC412 against an imatinib-resistant gastrointestinal stromal tumor (GIST) carrying a D842V mutation in PDGFRA. AACR Annual Meeting (2007):(Abstract 3266).
  • REICHARDT P, PINK D, LINDNER T et al.: A Phase I/II trial of the oral PKC-inhibitor PKC412 (PKC) in combination with imatinib mesylate (IM) in patients (pts) with gastrointestinal stromal tumor (GIST) refractory to IM. J. Clin. Oncol. (2005) 23(16S):3016.
  • PAPADOPOULOS KP, RODON JA, MITA AC et al.: A Phase I dose-escalation study of the safety and pharmacokinetics of a novel spectrum selective kinase inhibitor, XL820, administered orally to patients with solid tumors. Eur. J. Cancer (2006) 4:S33 (Abstract 97).
  • GARTON AJ, CREW APA, FRANKLIN M et al.: OSI-930: a novel selective inhibitor of Kit and kinase insert domain receptor tyrosine kinases with antitumor activity in mouse xenograft models. Cancer Res. (2006) 66(2):1015-1024.
  • PETTI F, THELEMANN A, KAHLER J et al.: Temporal quantitation of mutant Kit tyrosine kinase signaling attenuated by a novel thiophene kinase inhibitor OSI-930. Mol. Cancer Ther. (2005) 4(8):1186-1197.
  • GOLEMOVIC M, VERSTOVSEK S, GILES F et al.: AMN107, a novel aminopyrimidine inhibitor of Bcr-Abl, has in vitro activity against imatinib-resistant chronic myeloid leukemia. Clin. Cancer Res. (2005) 11(13):4941-4947.
  • PRENEN H, GUETENS G, DE BOECK G et al.: Cellular uptake of the tyrosine kinase inhibitors imatinib and AMN107 in gastrointestinal stromal tumor cell lines. Pharmacology (2006) 77(1):11-16.
  • REICHARDT P, CASALI PG, BLAY J et al.: A Phase I study of AMN107 alone and in combination with imatinib in patients (pts) with imatinib-resistant gastrointestinal stromal tumors (GIST). J. Clin. Oncol. (2006) 24(18S):9545.
  • SHAH NP, NICOLL JM, NAGAR B et al.: Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. Cancer Cell (2002) 2(2):117-125.
  • CORLESS CL, FLETCHER JA, HEINRICH MC: Biology of gastrointestinal stromal tumors. J. Clin. Oncol. (2004) 22(18):3813-3825.
  • SCHITTENHELM MM, SHIRAGA S, SCHROEDER A et al.: Dasatinib (BMS-354825), a dual SRC/ABL kinase inhibitor, inhibits the kinase activity of wild-type, juxtamembrane, and activation loop mutant KIT isoforms associated with human malignancies. Cancer Res. (2006) 66(1):473-481.
  • PANDEY A, VOLKOTS DL, SEROOGY JM et al.: Identification of orally active, potent, and selective 4-piperazinylquinazolines as antagonists of the platelet-derived growth factor receptor tyrosine kinase family. J. Med. Chem. (2002) 45(17):3772-3793.
  • YU JC, LOKKER NA, HOLLENBACH S et al.: Efficacy of the novel selective platelet-derived growth factor receptor antagonist CT52923 on cellular proliferation, migration, and suppression of neointima following vascular injury. J. Pharmacol. Exp. Ther. (2001) 298(3):1172-1178.
  • DEANGELO DJ, STONE RM, HEANEY ML et al.: Phase I clinical results with tandutinib (MLN518), a novel FLT3 antagonist, in patients with acute myelogenous leukemia or high-risk myelodysplastic syndrome: safety, pharmacokinetics, and pharmacodynamics. Blood (2006) 108(12):3674-3681.
  • CORBIN AS, GRISWOLD IJ, LA ROSEE P et al.: Sensitivity of oncogenic KIT mutants to the kinase inhibitors MLN518 and PD180970. Blood (2004) 104(12):3754-3757.
  • CHAO SH, PRICE DH: Flavopiridol inactivates P-TEFb and blocks most RNA polymerase II transcription in vivo. J. Biol. Chem. (2001) 276(34):31793-31799.
  • LU X, BURGAN WE, CERRA MA et al.: Transcriptional signature of flavopiridol-induced tumor cell death. Mol. Cancer Ther. (2004) 3(7):861-872.
  • SAMBOL EB, AMBROSINI G, GEHA RC et al.: Flavopiridol targets c-KIT transcription and induces apoptosis in gastrointestinal stromal tumor cells. Cancer Res. (2006) 66(11):5858-5866.
  • ISAACS JS, XU W, NECKERS L: Heat shock protein 90 as a molecular target for cancer therapeutics. Cancer Cell (2003) 3(3):213-217.
  • PRATT WB, TOFT DO: Regulation of signaling protein function and trafficking by the hsp90/hsp70-based chaperone machinery. Exp. Biol. Med. (Maywood) (2003) 228(2):111-133.
  • CSERMELY P, SCHNAIDER T, SOTI C, PROHASZKA Z, NARDAI G: The 90-kDa molecular chaperone family: structure, function, and clinical applications. A comprehensive review. Pharmacol. Ther. (1998) 79(2):129-168.
  • FUMO G, AKIN C, METCALFE DD, NECKERS L: 17-Allylamino-17-demethoxygeldanamycin (17-AAG) is effective in down-regulating mutated, constitutively activated KIT protein in human mast cells. Blood (2004) 103(3):1078-1084.
  • SYDOR JR, NORMANT E, PIEN CS et al.: Development of 17-allylamino-17-demethoxygeldanamycin hydroquinone hydrochloride (IPI-504), an anti-cancer agent directed against Hsp90. Proc. Natl. Acad. Sci. USA (2006) 103(46):17408-17413.
  • SCHULTE TW, NECKERS LM: The benzoquinone ansamycin 17-allylamino-17-demethoxygeldanamycin binds to HSP90 and shares important biologic activities with geldanamycin. Cancer Chemother. Pharmacol. (1998) 42(4):273-279.
  • KAMAL A, BOEHM MF, BURROWS FJ: Therapeutic and diagnostic implications of Hsp90 activation. Trends Mol. Med. (2004) 10(6):283-290.
  • BAUER S, YU LK, DEMETRI GD, FLETCHER JA: Heat shock protein 90 inhibition in imatinib-resistant gastrointestinal stromal tumor. Cancer Res. (2006) 66(18):9153-9161.
  • DEMETRI GD, GEORGE SA, VAN DEN ABBEELE AW et al.: Inhibition of heat shock protein 90 (Hsp90) with the novel agent IPI-504 to overcome resistance to tyrosine kinase inhibitors (TKIs) in metastatic GIST: results of a Phase I trial. 2007 Gastrointestinal Cancer Symposium, Barcelona, Spain (27 – 30 June 2007).
  • VAN OOSTEROM AT, DUMEZ H, DESAI J et al.: Combination signal transduction inhibition: a Phase I/II trial of the oral mTOR-inhibitor everolimus (E, RAD001) and imatinib mesylate (IM) in patients (pts) with gastrointestinal stromal tumor (GIST) refractory to IM. J. Clin. Oncol. (Meeting Abstracts) (2004) 22(14S):3002.
  • VAN OOSTEROM A, REICHARDT P, BLAY JY et al.: A Phase I/II trial of the oral mTOR-inhibitor everolimus (E) and imatinib mesylate (IM) in patients (pts) with gastrointestinal stromal tumor (GIST) refractory to IM: study update. J. Clin. Oncol. (Meeting Abstracts) (2005) 23(16S):9033.
  • SKAGGS BJ, GORRE ME, RYVKIN A et al.: Phosphorylation of the ATP-binding loop directs oncogenicity of drug-resistant BCR-ABL mutants. Proc. Natl. Acad. Sci. USA (2006) 103(51):19466-19471.

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