Clinical relevance of a pharmacogenetic approach using multiple candidate genes to predict response and resistance to imatinib therapy in chronic myeloid leukemia

Clinical Cancer Research

Volumn 15, Issue 14, 2009, Pages 4750-4758

  Dong, Hwan Kim ^a,c,d   Sriharsha, Lakshmi ^a   Xu, Wei ^a   Kamel Reid, Suzanne ^b   Liu, Xiangdong ^b   Siminovitch, Katherine ^b   Messner, Hans A ^a   Lipton, Jeffrey H ^a  

^a UNIVERSITY OF TORONTO   (Canada)

^b UNIVERSITY HEALTH NETWORK   (Canada)

^c Sungkyunkwan University School of Medicine   (South Korea)

^d Sungkyunkwan University   (South Korea)

Author keywords

[No Author keywords available]

Indexed keywords

BCR ABL PROTEIN; BREAST CANCER RESISTANCE PROTEIN; CYTOCHROME P450 3A5; DNA; IMATINIB; MULTIDRUG RESISTANCE PROTEIN 1; ORGANIC CATION TRANSPORTER 1; OROSOMUCOID;

ADOLESCENT; ADULT; ADVANCED CANCER; AGED; ARTICLE; BLOOD SAMPLING; CANCER STAGING; CHRONIC MYELOID LEUKEMIA; CONTROLLED STUDY; CYTOGENETICS; DRUG DOSE ESCALATION; DRUG EFFICACY; FEMALE; GENE FREQUENCY; GENOTYPE; HUMAN; MAJOR CLINICAL STUDY; MALE; PHARMACOGENETICS; PRIORITY JOURNAL; SINGLE NUCLEOTIDE POLYMORPHISM; TREATMENT FAILURE; TREATMENT RESPONSE;

ADOLESCENT; ADULT; AGED; ANTINEOPLASTIC AGENTS; ATP-BINDING CASSETTE TRANSPORTERS; CYTOCHROME P-450 CYP3A; DRUG RESISTANCE, NEOPLASM; FEMALE; FUSION PROTEINS, BCR-ABL; GENE FREQUENCY; GENETIC PREDISPOSITION TO DISEASE; GENOTYPE; GLYCOPROTEINS; HUMANS; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; MALE; MIDDLE AGED; NEOPLASM PROTEINS; OCTAMER TRANSCRIPTION FACTOR-1; P-GLYCOPROTEIN; PHARMACOGENETICS; PIPERAZINES; POLYMORPHISM, SINGLE NUCLEOTIDE; PROGNOSIS; PYRIMIDINES; TREATMENT OUTCOME; YOUNG ADULT;

EID: 68049087941     PISSN: 10780432     EISSN: None     Source Type: Journal    
DOI: 10.1158/1078-0432.CCR-09-0145     Document Type: Article

References (48)

1. Kantarjian HM, Cortes JE, O'Brien S, et al. Long-term survival benefit and improved complete cytogenetic and molecular response rates with imatinib mesylate in Philadelphia chromosome-positive chronic-phase chronic myeloid leukemia after failure of interferon-á. Blood 2004;104:1979-1988 (Pubitemid 39297846)
2. Kantarjian HM, Talpaz M, Giles F, O'Brien S, Cortes J. New insights into the pathophysiology of chronic myeloid leukemia and imatinib resistance. Ann Intern Med 2006;145:913-923 (Pubitemid 351639967)
3. 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 (Pubitemid 32743979)
4. Mahon FX, Belloc F, Lagarde V, et al. MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models. Blood 2003;101: 2368-2373 (Pubitemid 36304670)
5. Haiat S, Decleves X, Mittaine B, et al. Determination of imatinib plasma levels by high performance liquid chromatography (HPLC): evaluation of pharmacokinetic variability and haematological consequences. Blood 2006;108:1375a.
6. Gardner ER, Burger H, van Schaik RH, et al. Association of enzyme and transporter genotypes with the pharmacokinetics of imatinib. Clin Pharmacol Ther 2006;80:192-201. (Pubitemid 44160695)
7. Illmer T, Schuler US, Thiede C, et al. MDR1 gene polymorphisms affect therapy outcome in acute myeloid leukemia patients. Cancer Res 2002;62:4955-4962 (Pubitemid 34984419)
8. Kim DH, Park JY, Sohn SK, et al. Multidrug resistance-1 gene polymorphisms associated with treatment outcomes in de novo acute myeloid leukemia. Int J Cancer 2006;118:2195-2201
9. Gurney H, Wong M, Balleine RL, et al. Imatinib disposition and ABCB1 (MDR1, P-glycoprotein) genotype. Clin PharmacolTher 2007;82:33-40. (Pubitemid 46944197)
10. Yanase K, Tsukahara S, Mitsuhashi J, Sugimoto Y. Functional SNPs of the breast cancer resistance protein-therapeutic effects and inhibitor development. Cancer Lett 2006;234:73-80. (Pubitemid 43343941)
11. Morisaki K, Robey RW, Ozvegy-Laczka C, et al. Single nucleotide polymorphisms modify the transporter activity of ABCG2. Cancer Chemother Pharmacol 2005;56:161-172 (Pubitemid 40884271)
12. Honjo Y, Morisaki K, Huff LM, et al. Single-nucleotide polymorphism (SNP) analysis in the ABC half-transporter ABCG2 (MXR/BCRP/ABCP1). Cancer Biol Ther 2002;1:696-702.
13. Sakata T, Anzai N, Shin HJ, et al. Novel single nucleotide polymorphisms of organic cation transporter 1 (SLC22A1) affecting transport functions. Biochem Biophys Res Commun 2004;313:789-793 (Pubitemid 38021900)
14. Schinkel AH, Jonker JW. Polymorphisms affecting function of the human organic cation transporter hOCT1 (SLC22A1): what are the consequences ? Pharmacogenetics 2002;12:589-590
15. Kerb R, Brinkmann U, Chatskaia N, et al. Identification of genetic variations of the human organic cation transporter hOCT1 and their functional consequences. Pharmacogenetics 2002;12:591-595 (Pubitemid 36005667)
16. Itoda M, Saito Y, Maekawa K, et al. Seven novel single nucleotide polymorphisms in the human SLC22A1 gene encoding organic cation transporter 1 (OCT1). Drug Metab Pharmacokinet 2004;19: 308-312
17. Bolton AE, Peng B, Hubert M, et al. Effect of rifampicin on the pharmacokinetics of imatinib mesylate (Gleevec, STI571) in healthy subjects. Cancer Chemother Pharmacol 2004;53:102-106 (Pubitemid 38186987)
18. Dutreix C, Peng B, Mehring G, et al. Pharmacokinetic interaction between ketoconazole and imatinib mesylate (Glivec) in healthy subjects. Cancer Chemother Pharmacol 2004;54:290-294 (Pubitemid 39304422)
19. Fitos I, Visy J, Zsila F, Mady G, Simonyi M. Selective binding of imatinib to the genetic variants of human alpha1-acid glycoprotein. Biochim Biophys Acta 2006;1760:1704-1712 (Pubitemid 44667264)
20. Gambacorti-Passerini C, Zucchetti M, Russo D, et al. Alpha1 acid glycoprotein binds to imatinib (STI571) and substantially alters its pharmacokinetics in chronic myeloid leukemia patients. Clin Cancer Res 2003;9:625-632 (Pubitemid 36182594)
21. Gambacorti-Passerini C, le Coutre P, Zucchetti M, D'Incalci M. Binding of imatinib by alpha(1)-acid glycoprotein. Blood 2002;100:367-8; author reply 8-9.
22. Gambacorti-Passerini C, Barni R, le Coutre P, et al. Roleofalpha1acidglycoproteininthe in vivo resistance of human BCR-ABL(+) leukemic cells to the abl inhibitor STI571. J Natl Cancer Inst 2000;92:1641-1650
23. Branford S, Fletcher L, Cross NC, et al. Desirable performance characteristics for BCR-ABL measurement on an international reporting scale to allow consistent interpretation of individual patient response and comparison of response rates between clinical trials. Blood 2008;112:3330-3338
24. Muller MC, Saglio G, Lin F, et al. An international study to standardize the detection and quantitation of BCR-ABL transcripts from stabilized peripheral blood preparations by quantitative RT-PCR. Haematologica 2007;92:970-973 (Pubitemid 350144244)
25. Branford S, Cross NC, Hochhaus A, et al. Rationale for the recommendations for harmonizing current methodology for detecting BCR-ABL transcripts in patients with chronic myeloid leukaemia. Leukemia 2006;20:1925-1930 (Pubitemid 44614879)
26. Druker BJ, Talpaz M, Resta DJ, et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med 2001;344:1031-1037 (Pubitemid 32267972)
27. Baccarani M, Saglio G, Goldman J, et al. Evolving concepts in the management of chronic myeloid leukemia: recommendations from an expert panel on behalf of the European Leukemia Net. Blood 2006; 108:1809-1820 (Pubitemid 44394987)
28. Picard S, Titier K, Etienne G, etal. Trough imatinib plasma levels are associated with both cytogenetic and molecular responses to standard-dose imatinib in chronic myeloid leukemia. Blood 2007;109:3496-9.
29. 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;104:2940-2942
30. Robey RW, Polgar O, Deeken J, To KW, Bates SE. ABCG2: determining its relevance in clinical drug resistance. Cancer Metastasis Rev 2007;26:39-57. (Pubitemid 46452182)
31. Doyle LA, Ross DD. Multidrug resistance mediated by the breast cancer resistance protein BCRP (ABCG2). Oncogene 2003;22:7340-7358 (Pubitemid 37487163)
32. Brendel C, Scharenberg C, DohseM, et al. Imatinib mesylate and nilotinib (AMN107) exhibit high-affinity interaction with ABCG2 on primitive hematopoietic stem cells. Leukemia 2007;21:1267-1275 (Pubitemid 46831816)
33. Houghton PJ, Germain GS, Harwood FC, et al. Imatinib mesylate is a potent inhibitor of the ABCG2 (BCRP) transporter and reverses resistance to topotecan and SN-38 in vitro. Cancer Res 2004;64:2333-2337
34. Jordanides NE, Jorgensen HG, Holyoake TL, Mountford JC. Functional ABCG2 is overexpressed on primary CML CD34+ cells and is inhibited by imatinib mesylate. Blood 2006;108:1370-1373
35. Nakanishi T, Shiozawa K, Hassel BA, Ross DD. Complex interaction of BCRP/ABCG2 and imatinib in BCRABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression. Blood 2006;108:678-684 (Pubitemid 44061370)
36. Ozvegy-Laczka C, Hegedus T, Varady G, et al. High-affinity interaction of tyrosine kinase inhibitors with the ABCG2 multidrug transporter. Mol Pharmacol 2004;65:1485-1495 (Pubitemid 38668306)
37. Thomas J, Wang L, Clark RE, Pirmohamed M. Active transport of imatinib into and out of cells: implications for drug resistance. Blood 2004;104:3739-3745 (Pubitemid 39564452)
38. White D, SaundersV, Dang P, et al. Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity. Blood 2007;110:4064-4072 (Pubitemid 350248463)
39. White D, Saunders V, Dang P, et al. OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib. Blood 2006;108:697-704. (Pubitemid 44061372)
40. Crossman LC, Druker BJ, Deininger MW, Pirmohamed M, Wang L, Clark RE. hOCT 1 and resistance to imatinib. Blood 2005;106:1133-4; author reply 4.
41. Wang L, Giannoudis A, Lane S, Williamson P, Pirmohamed M, Clark R. Expression of the uptake drug transporter hOCT1 is an important clinical determinant of the response to imatinib in chronic myeloid leukemia. Clin Pharmacol Ther 2008;83:258-264
42. White DL, Saunders VA, Dang P, et al. Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity; higher doses of imatinib may overcome the negative impact of low OCT-1 activity. Blood 2007;110:4064-4072 (Pubitemid 350248463)
43. Peng B, Lloyd P, Schran H. Clinical pharmacokinetics of imatinib. Clin Pharmacokinet 2005;44:879-894
44. Marin D, Marktel S, Bua M, et al. The use of imatinib (STI571) in chronic myelod leukemia: some practical considerations. Haematologica 2002;87:979-988
45. Juranka PF, Zastawny RL, LingV. P-glycoprotein: multidrug-resistance and a superfamily of membrane associated transport proteins. FASEB J 1989;3: 2583-2592 (Pubitemid 20013272)
46. Illmer T, Schaich M, Platzbecker U, et al. P-glycoprotein-mediated drug efflux is a resistance mechanism of chronic myelogenous leukemia cells to treatment with imatinib mesylate. Leukemia 2004;18:401-408 (Pubitemid 38425851)
47. Fromm MF. The influence of MDR1 polymorphisms on P-glycoprotein expression and function in humans. Adv Drug Deliv Rev 2002;54:1295-1310
48. Kimchi-Sarfaty C, Oh JM, Kim IW, et al. A "silent" polymorphism in the MDR1 gene changes substrate specificity. Science 2007;315:525-528