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Expert Opinion on Drug Safety Volume 4, 2005 - Issue 2
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Review

The development and application of imatinib

Robin L Jones The Royal Marsden Hospital, Sarcoma Unit, Fulham Road, London, SW3 6JJ, UK. [email protected]
&
Ian R Judson The Royal Marsden Hospital, Sarcoma Unit, Fulham Road, London, SW3 6JJ, UK. [email protected]
Pages 183-191 | Published online: 22 Apr 2005

Bibliography

  • HANNAHAN D, WEINBERG RA: The hallmarks of cancer. Cell. (2000) 100:57–70.
  • SCHER HI, SARKIS A, REUTER V et al.: Changing pattern of expression of the epidermal growth factor receptor and transforming growth factor alpha in the progression of prostatic neoplasms. Clin. Cancer Res. (1995) 1:545–550.
  • MCLENDON RE, WIKSTRAND CJ, MATTHEWS MR et al: Glioma-associated antigen expression in oligodendroglial neoplasms: Tenascin and epidermal growth factor. ./. Histochem. Cytochem. (2000) 48:1103–1110.
  • FONTANINI G, DELAURENTIIS M, VIGNATI S et al.: Evaluation of epidermal growth factor-related growth factors and receptors and of neoangiogenesis in completely resected stage I-IIIA non-small-cell lung cancer: Amphiregulin and microvessel count are independent prognostic indicators of survival. Clin. Cancer Res. (1998) 4:241–249.
  • GRANDIS JR, MELHEM MF, GOODING WE et al.: Levels of TGF-alpha and EFGr protein in head and neck squamous cell carcinoma and patient survival. ./. Natl. Cancer Inst. (1998) 90:824–832.
  • SPRITZ RA, STRUNK KM, LEE ST et al: A YAC contig spanning a cluster of human Type III receptor protein tyrosine kinase genes (PDGFRA-KIT-KDR) in chromosome segment 4q12. Cenomics (1994) 22:431–436.
  • VAN ETTEN RA, JACKSON P, BALTIMORE D: The mouse Type IV c-abl gene product is a nuclear protein, and activation of transforming ability is associated with cytoplasmic localization. Cell (1989) 58(4):669–678.
  • DRUKER BJ, LYDON NB: Lessons learned from the development of an Abl tyrosine kinase inhibitor for chronic myelogenous leukaemia. .1 Clin. Invest. (2000) 105:3–7.
  • ANAFI M, GAZIT A, GILON C, BEN-NERIAH Y, LEVITZKI A: Selective interactions of transforming and normal abl proteins with ATP, tyrosine-copolymer substrates and tyrphostins. I Biol. Chem. (1992) 267(7):4518–4523.
  • ••An important study demonstrating thatselective inhibition was possible.
  • BUCHDUNGER E, ZIMMERMANN J, METT H et al.: Inhibition of the Abl protein-tyrosine kinase in vitro and in vivo by a 2-phenylaminopyrimidine derivative. Cancer Res. (1996) 56:100–104.
  • ••An essential study demonstrating activityboth in vitro and in vivo.
  • 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) 90:4947–4952.
  • FADERL S, TALPAZ M, ESTROV Z et al: The biology of chronic myeloid leukaemia. N. Engl. J. Med. (1999) 341:164–172.
  • SAWYERS CL: Chronic myeloid leukaemia. N Engl. j Med. (1999) 340:1330–1340.
  • NOWELL PC, HUNGERFORD DA: A minute chromosome in human chronic granulocytic leukaemia. Science (1960) 132:1497–1501.
  • ROWLEY JD: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature (1973) 243:290–293.
  • KALIDAS M, KANTARJIAN H, TALPAZ M: Chronic myelogenous leukaemia. JAMA (2001) 286:895–898.
  • DEININGER MW, GOLDMAN JM, LYNDON N, MELO JV: The tyrosine kinase inhibitor CGP57148B selectively inhibits the growth of BCR-ABL positive cells. Blood (1997) 90:3691–3698.
  • DRUKER BJ, TALPAZ M, RESTA DJ et al.: Efficacy and safety of a specific inhibitor of the BCR-Abl tyrosine kinase in chronic myeloid leukaemia. N Engl. I Med. (2001) 344:1031–1037.
  • ••An important trial demonstrating thatImatinib is a well-tolerated and effective therapy in chronic phase CML following IFN-a failure.
  • KANTARJIAN H, SAWYERS C, HOCHHAUS A et al.: Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukaemia. N Engl. Med. (2002) 346:645–652.
  • O'BRIEN SG, GUILHOT F, LARSON RA et al: Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukaemia. N Engl. I Med. (2003) 348:994–1004.
  • ••A pivotal randomised trial demonstratingthe superiority of imatinib to IFN-a and cytarabine in chronic phase CML.
  • CORTES J, GILES F, O'BRIEN S et al: Result of high-dose imatinib mesylate in patients with Philadelphia chromosome-positive chronic myeloid leukaemia after failure of interferon-a. Blood (2003) 102:83–86.
  • •A trial demonstrating that higher dose of imatinib is well tolerated and induces a high cytogenetic complete response following IFN-a failure.
  • KANTARJIAN H, TALPAZ M, O'BRIEN S et al: High-dose imatinib mesylate therapy in newly diagnosed Philadelphia chromosome-positive chronic phase chronic myeloid leukaemia. Blood (2004) 103:2873–2878.
  • •Study revealing efficacy of high-dose imatinib in newly diagnosed chronic-phase CML.
  • TALPAZ M, SILVER RT, DRUKER BJ et al: Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukaemia: results of a Phase II study. Blood (2002) 99:1928–1937.
  • DRUKER BJ, SAWYERS CL, KANTARJIAN H et al.: Activity of a specific inhibitor of the BCR-Abl tyrosine kinase in the blast crisis of chronic myeloid leukaemia and acute lymphoblastic leukaemia with the Philadelphia chromosome. N Engl. I Med. (2001) 344:1038–1042.
  • •An important trial revealing substantial activity of imatinib in blast crisis of CML and Philadelphia chromosome-positive ALL.
  • SAWYERS CL, HOCHHAUS A, FELDMAN E et al.: Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukaemia in myeloid blast crisis: results of a Phase II study. Blood (2002) 99:3530–3539.
  • KANTARJIAN HM, CORTES J, O'BRIEN S et al: Imatinib mesylate (5TI571) therapy for Philadelphia chromosome-positive chronic myelogenous leukaemia in blast phase. Blood (2002) 99:3547–3553.
  • DEININGER MW, DRUKER BJ: Specific targeted therapy of chronic myelogenous leukaemia with imatinib. Pharmacol Rev (2003) 55:401–423.
  • BERGER U, ENGELICH G, REITER A, HOCHHAUS A, HEHLMANN RAND THE GERMAN CML STUDY GROUP: Imatinib and beyond - The new CML study IV. A randomized controlled comparison of imatinib vs imatinib/interferon-alpha vs imatinib/low-dose AraC vs imatinib after interferon-alpha failure in newly diagnosed chronic phase chronic myeloid leukemia. Ann. Haematol (2004) 83:258–264.
  • DEMATTEO RP, LEWIS JJ, LEUNG D, MUDAN SS, WOODRUFF JM, BRENNAN MF: Two hundred gastrointestinal stromal tumours: recurrence patterns and prognostic factors for survival. Ann. Surg. (2000) 231:51–58.
  • KINDBLOM L-G, REMOTTI HE, ALDENBORG F, MEIS-KINDBLOM JM: Gastrointestinal pacemaker cell tumour (GIPACT): gastrointestinal stromal tumours show phenotypic characteristics of the interstitial cells of Cajal. Am. I Pathol (1998) 152:1259–1269.
  • •A crucial publication on the pathology of GIST.
  • GRAADT VAN ROGGEN JF, VAN VELTHUYSEN ML, HOGENDOORN PC: The histopathological differential diagnosis of gastrointestinal stromal tumours. Clia Pathol (2001) 54:96–102.
  • RUMESSEN JJ, PETERS S, THUNEBERG L: Light- and electron microscopical studies of interstitial cells of Cajal and muscle cells at the submucosal border of human colon. Lab. Investig (1993) 68:481–495.
  • MIETTINEN M, LASOTA J: Gastrointestinal stromal tumours - definition, clinical, histological, immunohistochemical and molecular genetic features and differential diagnosis. Virchows Arch. (2001) 438:1–12.
  • MIETTINEN M, SOBIN LH, SARLOMO-RIKALA M: Immunohistochemical spectrum of GISTs at different sites and their differential diagnosis with a reference to CD117 (KIT). Mod. Pathol (2000) 13:1134–1142.
  • •Another important paper on the pathology of GIST.
  • MIETTINEN M, SARLOMO-RIKALA M, LASOTA J: Gastrointestinal stromal tumours: recent advances in understanding of their biology. Hum. Pathol (1999) 30:1213–1220.
  • FLETCHER CDM, BERMAN JJ, CORLESS C et al: Diagnosis of gastrointestinal stromal tumours: a consensus approach. Hum. Pathol (2002) 33:459–465.
  • HEINRICH MC, GRIFFITH DJ, DRUKER BJ, WAIT CL, OTT KA, ZIGLER AJ: Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor. Blood (2000) 96:925–932.
  • HEINRICH MC, RUBIN BP, LONGLEY BJ, FLETCHER JA: Biology and genetic aspects of gastrointestinal stromal tumours: KIT activation and cytogenetic alterations. Hum. Pathol (2002) 33:484–495.
  • BAUER S, CORLESS CL, HEINRICH MC: Response to imatinib mesylate of a gastrointestinal stromal tumour with very low expression of KIT. Cancer Chemother. Pharmacol (2003) 51:261–265.
  • SABAH M, LEADER M, KAY E: The problem with KIT: clinical implications and practical difficulties with CD117 immunostaining. Appl. Immunohistochem. Molec. Morphol (2003) 11:56–61.
  • ROBERTS PJ, EISENBERG B: Clinical presentation of gastrointestinal stromal tumours and treatment of operable disease. Eur. J. Cancer (2002) 38:S37–S38.
  • HEINRICH MC, BLAKE CD, DRUKER BJ, CORLESS CL: Inhibition of KIT tyrosine kinase activity: a novel molecular approach to the treatment of KIT-positive malignancies. J. Clin. Oncol. (2002) 20:1692–1703.
  • JUDSON I: Gastrointestinal stromal tumours (GIST): biology and treatment. Ann. Oncol (2002) 13:287–289.
  • RUBIN BP, SINGERS, TSAO C et al: KIT activation is a ubiquitous feature of gastrointestinal stromal tumours. Cancer Res. (2001) 61:8118–8121.
  • CORLESS CL, FLETCHER JA, HEINRICH MC: Biology of Gastrointestinal Stromal Tumours. Clin. Oncol. (2004) 22:3813–3825.
  • HIROTA S, ISOZAKI K, MORIYAMA Y et al.: Gain-of-function mutations of c-kit in human gastrointestinal stromal tumours. Science (1998) 279:577–580.
  • SINGERS, RUBIN BP, LUX ML et al: Prognostic value of KIT mutation type, mitotic activity and histologic subtype in gastrointestinal tumours. J. Clin. Oncol (2002) 20:3898–3905.
  • LASOTA J, JASINSKI M, SARLOMO-RIKALA M et al: Mutations in exon 11 of c-kit occur preferentially in malignant versus benign gastrointestinal stromal tumors and do not occur in leiomyomas or leimyosarcomas. Am. J. Pathol (1999) 154:53–60.
  • ERNST SI, HUBBS AE, PRZYGODZKI RM et al.: KIT mutations portends poor prognosis in gastrointestinal stromalismooth muscle tumors. Lab. Invest. (1998) 78:1633–1636.
  • LI SQ, O'LEARY TJ, SOBIN LH et al: Analysis of KIT mutation and protein expression in fine needle aspirates of gastrointestinal stromalismooth muscle tumors. Acta Cytol. (2000) 44:981–986.
  • MOSKALUK CA, TIAN Q, MARSHALL CR et al.: Mutations of c-kit JM domain are found in a minority of human gastrointestinal stromal tumors. Oncogene (1999) 18:1897–1902.
  • TANIGUCHI M, NISHIDA T, HIROTA S et al: Effect of c-kit mutation on prognosis of gastrointestinal stromal tumors. Cancer Res. (1999) 59:4297–4300.
  • LUX ML, RUBIN BP, BIASE TL et al.: KIT extracellular and kinase domain mutations in gastrointestinal stromal tumours. Am. J. Pathol (2000) 156:791–795.
  • VAN OOSTEROM A, JUDSON I, VERWEIJ J et al.: Safety and efficacy of imatinib (5TI571) in metastatic gastrointestinal stromal tumours: a Phase I study. Lancet (2001) 358:1421–1423.
  • ••An important Phase I trail revealing thesafety and efficacy of imatinib in GIST.
  • VERWEIJ J, VAN OOSTEROM A, BLAY J-Y et al: Imatinib mesylate (STI-571, Glivec, Gleevec) is an active agent for gastrointestinal stromal tumours, but does not yield responses in other soft-tissue sarcomas that are unselected for a molecular target: Results from an EORTC Soft Tissue bone Sarcoma Group Phase II study. Eur. J. Cancer (2003) 39:2006–2011.
  • ••A study demonstrating the tolerability andefficacy of imatinib in GIST.
  • DEMETRI GD, VON MEHREN M, BLANKE CD et al: Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumours. N Engl. J. Med. (2002) 347:472–480.
  • ••A pivotal randomized trial confirming theactivity of imatinib in GIST.
  • VERWEIJ J, CASALI PG, ZALCBERG J et al: Early efficacy comparison of two doses of imatinib for the treatment of advanced gastrointestinal stromal tumours (GIST): Interim results of a randomised Phase III trial from the EORTC-STBSG, ISG and AGITG. Proc. Am. Soc. Clin. Oncol (2003) 814:abstract 3272.
  • BENJAMIN RS, RANKIN C, FLETCHER C et al: Phase III dose-randomized study of imatinib mesylate (STI571) for GIST: Intergroup S0033 early results. Proc. Am. Soc. Clin. Oncol (2003) 814:abstract 3271.
  • VERWEIJ J, CASALI P, ZALCBERG J et al: Progression-free survival in gastrointestinal stromal tumours with high-dose imatinib: randomised trial. Lancet (2004) 364:1127–1134.
  • •Initial results of the EORTC study comparing two doses of imatinib, with Improved disease-free survival in the higher dose arm.
  • HEINRICH MC, CORLESS CL, DUENSING A et al: PDGFRA activating mutations in gastrointestinal stromal tumors. Science (2003) 299:708–710.
  • •An important publication on PDGFRA mutation in GIST.
  • HEINRICH MC, CORLESS CL, DEMETRI GD et al.: Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumour. Oncol (2003) 23:4342–4349.
  • ••A study confirming that mutational statusis predictive of response to imatinib.
  • 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 into Phase I and II studies of the EORTC Soft Tissue and Bone Sarcoma Group. Eur. J. Cancer (2004) 40:689–695.
  • ••A further study demonstrating thatmutational status is predictive of response to imatinib.
  • MAKI RG, AWAN RA, DIXON RH, JHANWAR S, ANTONESCU CR: Differential sensitivity to imatinib of 2 patients with metastatic sarcoma arising from dermatofibrosarcoma protuberans. Int J. Cancer (2002) 100(6):623–626.
  • APPERLEY JF, GARDEMBAS M, MELO JV et al.: Response to imatinib in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor beta. N Engl. J. Med. (2002) 347(7):481–487.
  • GLEICH GJ, LEIFERMAN KM, PARDANANI A, TEFFERI A, BUTTERFIELD JH: Treatment of hypereosinophilic syndrome with imatinib mesilate. Lancet (2002) 359:1577–1578.
  • GORRE ME, MOHAMMED M, ELLWOOD K et al: Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science (2001) 293:876–880.
  • HOCHHAUS A, KRIEL S, CORBIN A et al.: Molecular and chromosomal mechanisms of resistance to imatinib (5TI571) therapy. Leukaemia (2002) 16:2190–2196.
  • HOCHHAUS A, KRIEL S, CORBIN A et al: Roots of clinical resistance to STI-571 cancer therapy. Science (2001) 293:2163a.
  • BARTHE C, CONY-MAKHOUL P, MELO JV, REIFFERS J, MAHON FX: Roots of clinical resistance to STI-571 cancer therapy. Science (2001) 293:2163a.
  • BRANFORD S, RUDZKI Z, WALSH S et al.: High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukaemia or Ph-positive acute lymphoblastic leukaemia who develop imatinib (STI571) resistance. Blood (2002) 99:3472–3475.
  • VON BUBNOFF N, SCHNELLER F, PESCHEL C, DUYSTER J: BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome-positive leukaemia to STI-571: a prospective study. Lancet (2002) 359:487–491.
  • SHAH NP, NICOLL JM, GORRE ME, PAQUETTE RL, FORD J, SAWYERS CL: Resistance to Gleevec: Sequence analysis reveals a spectrum of BCR/ABL kinase domain mutations in both acquired- and de novo- resistant cases of chronic myelogenous leukaemia (CML) in myeloid blast crisis. Blood (2001) 98\(suppl. 1):770a.
  • DOREY K, ENGEN JR, KRETZSCHMAR J et al: Phosphorylation and structure-based functional studies reveal a positive and a negative role for the activation loop of the c-Abl tyrosine kinase. Oncogene (2001) 20:8075–8084.
  • DAUB H, SPECHT K, ULLRICH A: Strategies to overcome resistance to targeted protein kinase inhibitors. Nat. Rev Drug Discov. (2004) 3:1001–1010.
  • BRANFORD S, RUDZKI Z, WALSH S et al.: Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis. Blood (2003) 102:276–283.
  • LA ROSEE P, O'DWYER ME, DRUKER BJ: Insights from pre-clinical studies for new combination treatment

Websites

  • www.spirit-cml.org STI571 Prospective International Randomized Trial (2004).

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