Korean Journal of Clinical Pharmacy (한국임상약학회지)

Korean College Of Clinical Pharmacy (한국임상약학회)
권호 표지

ABCG2 C421A Polymorphism and Imatinib Response in Chronic Myeloid Leukemia: A Systematic Review and Meta-Analysis

ABCG2 C421A 다형성이 만성 골수성 백혈병 환자의 imatinib 치료에 미치는 영향: 체계적 문헌고찰 및 메타분석

  • Received : 2016.02.25
  • Accepted : 2016.03.11
  • Published : 2016.03.31
Download PDF
⟨ Previous Next ⟩

Abstract

Objective: To estimate the association between ABCG2 C421A polymorphism and response to imatinib in chronic myeloid leukemia. Methods: A systematic review was conducted to evaluate the effect of ABCG2 C421A polymorphism on imatinib response. The databases of PubMed, Embase, Web of science, CINAHL with FullText, and Cochrane Library were searched for all published studies from inception to December 2015. The following terms were used with functions of 'AND' and 'OR': 'chronic myeloid leukemia', 'CML', 'drug transporter', 'ABCG2', 'BCRP', 'polymorphisms', 'SNPs', and 'imatinib'. The studies reporting the association between ABCG2 polymorphism and imatinib response were evaluated. Results: A total of 7 studies were included in the present meta-analysis. The pooled analysis showed that ABCG2 c.421CC genotype was significantly associated with poor response to imatinib under the dominant model (CC vs CA+AA; OR: 0.56; 95% CI: 0.41, 0.77; p = 0.0004). The subgroup analysis of Asian studies demonstrated a significantly lower response in c.421CC genotype than in c.421CA or c.421AA genotype (OR: 0.52; 95% CI: 0.37, 0.73; p = 0.0002). In subgroup analyses of 5 studies, the patients with the c.421CC genotype exhibited higher risk for worse response than the patients with c.421CA or c.421AA genotype (heterozygote codominant model: CC vs. AC; OR: 0.49, 95% CI: 0.33, 0.73; p = 0.0006; homozygote codominant model: CC vs AA; OR: 0.43; 95% CI: 0.25, 0.75, p = 0.003). Conclusion: The ABCG2 c.421CC genotype was significantly associated with poor response to imatinib compared to the c.421CA and c.421AA genotypes in chronic myeloid leukemia, especially in Asian patients.

Keywords

References

  1. Groffen J, Stephenson JR, Heisterkamp N, et al. Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22. Cell 1984;36:93-9. https://doi.org/10.1016/0092-8674(84)90077-1
  2. Ren R. Mechanisms of BCR-ABL in the pathogenesis of chronic myelogenous leukaemia. Nat Rev Cancer 2005;5:172-83. https://doi.org/10.1038/nrc1567
  3. Baccarani M, Deininger MW, Rosti G, et al. European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013. Blood 2013;122:872-84. https://doi.org/10.1182/blood-2013-05-501569
  4. National Institute for Health and Care Excellence. Guidance on the use of imatinib for chronic myeloid leukaemia. Available from https://www.nice.org.uk/guidance/ta70/chapter/1-guidance. Accessed January 25, 2016.
  5. Schindler T, Bornmann W, Pellicena P, et al. Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. Science 2000;289:1938-42. https://doi.org/10.1126/science.289.5486.1938
  6. Kantarjian HM, Talpaz M, Giles F, et al. New insights into the pathophysiology of chronic myeloid leukemia and imatinib resistance. Ann Intern Med 2006;145:913-23. https://doi.org/10.7326/0003-4819-145-12-200612190-00008
  7. 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;104:2940-42. https://doi.org/10.1182/blood-2004-04-1398
  8. Brendel C, Scharenberg C, Dohse M, et al. Imatinib mesylate and nilotinib (AMN107) exhibit high-affinity interaction with ABCG2 on primitive hematopoietic stem cells. Leukemia 2007;21:1267-75. https://doi.org/10.1038/sj.leu.2404638
  9. Shukla S, Sauna ZE, Ambudkar SV. Evidence for the interaction of imatinib at the transport-substrate site(s) of the multidrug-resistancelinked ABC drug transporters ABCB1 (P-glycoprotein) and ABCG2. Leukemia 2008;22:445-7. https://doi.org/10.1038/sj.leu.2404897
  10. Kondo C, Suzuki H, Itoda M, et al. Functional analysis of SNPs variants of BCRP/ABCG2. Pharm Res 2004;21:1895-903. https://doi.org/10.1023/B:PHAM.0000045245.21637.d4
  11. Stacy AE, Jansson PJ, Richardson DR. Molecular pharmacology of ABCG2 and its role in chemoresistance. Mol Pharmacol 2013;84:655-69. https://doi.org/10.1124/mol.113.088609
  12. Kawabata S, Oka M, Soda H, et al. Expression and functional analyses of breast cancer resistance protein in lung cancer. Clin Cancer Res 2003;9:3052-7.
  13. Jordanides NE, Jorgensen HG, Holyoake TL, et al. Functional ABCG2 is overexpressed on primary CML CD34+ cells and is inhibited by imatinib mesylate. Blood 2006;108:1370-3. https://doi.org/10.1182/blood-2006-02-003145
  14. Shah NP. Medical management of CML. Hematology Am Soc Hematol Educ Program 2007:371-5.
  15. Skoglund K, Boiso Moreno S, Jonsson JI, et al. Single-nucleotide polymorphisms of ABCG2 increase the efficacy of tyrosine kinase inhibitors in the K562 chronic myeloid leukemia cell line. Pharmacogenet Genomics 2014;24:52-61. https://doi.org/10.1097/FPC.0000000000000022
  16. Nambu T, Hamada A, Nakashima R, et al. Association of SLCO1B3 polymorphism with intracellular accumulation of imatinib in leukocytes in patients with chronic myeloid leukemia. Biol Pharm Bull 2011;34:114-9. https://doi.org/10.1248/bpb.34.114
  17. Yamakawa Y, Hamada A, Nakashima R, et al. Association of genetic polymorphisms in the influx transporter SLCO1B3 and the efflux transporter ABCB1 with imatinib pharmacokinetics in patients with chronic myeloid leukemia. Ther Drug Monit 2011;33:244-50.
  18. Wells GA, Shea B, O'Connell D, et al. The Newcastle-Ottawa scale (NOS) for assessing the quality of nonrandomised studies in meta-analysis. Ottawa Hospital Research Institute. Available from http://www.ohri.ca/programs/clinical_epidemiology/oxford.asp. Accessed January 20, 2016.
  19. Zheng JS, Hu XJ, Zhao YM, et al. Intake of fish and marine n-3 polyunsaturated fatty acids and risk of breast cancer: meta-analysis of data from 21 independent prospective cohort studies. BMJ 2013;346:f3706. https://doi.org/10.1136/bmj.f3706
  20. Anthony A, Ankathil R, Ai-Sim G, et al. Influence of ABCB1 C3435T and ABCG2 C421A Gene Polymorphisms in Response to Imatinib Mesylate in Chronic Myeloid Leukemia Patients. International Journal of Environmental Science and Development 2012;3:274-8.
  21. Shinohara Y, Takahashi N, Nishiwaki K, et al. A multicenter clinical study evaluating the confirmed complete molecular response rate in imatinib-treated patients with chronic phase chronic myeloid leukemia by using the international scale of real-time quantitative polymerase chain reaction. Haematologica 2013;98:1407-13. https://doi.org/10.3324/haematol.2013.085167
  22. Takahashi N, Miura M, Scott SA, et al. Influence of CYP3A5 and drug transporter polymorphisms on imatinib trough concentration and clinical response among patients with chronic phase chronic myeloid leukemia. J Hum Genet 2010;55:731-7. https://doi.org/10.1038/jhg.2010.98
  23. Seong SJ, Lim M, Sohn SK, et al. Influence of enzyme and transporter polymorphisms on trough imatinib concentration and clinical response in chronic myeloid leukemia patients. Ann Oncol 2013;24:756-60. https://doi.org/10.1093/annonc/mds532
  24. Au A, Aziz Baba A, Goh AS, et al. Association of genotypes and haplotypes of multi-drug transporter genes ABCB1 and ABCG2 with clinical response to imatinib mesylate in chronic myeloid leukemia patients. Biomed Pharmacother 2014;68:343-9. https://doi.org/10.1016/j.biopha.2014.01.009
  25. de Lima LT, Vivona D, Bueno CT, et al. Reduced ABCG2 and increased SLC22A1 mRNA expression are associated with imatinib response in chronic myeloid leukemia. Med Oncol 2014;31:851. https://doi.org/10.1007/s12032-014-0851-5
  26. Salimizand H, Amini S, Abdi M, et al. Concurrent effects of ABCB1 C3435T, ABCG2 C421A, and XRCC1 Arg194Trp genetic polymorphisms with risk of cancer, clinical output, and response to treatment with imatinib mesylate in patients with chronic myeloid leukemia. Tumour Biol 2015; DOI 10.1007/s13277-015-3874-4
  27. Bixby D, Talpaz M. Mechanisms of resistance to tyrosine kinase inhibitors in chronic myeloid leukemia and recent therapeutic strategies to overcome resistance. Hematology Am Soc Hematol Educ Program 2009:461-7.
  28. Eechoute K, Sparreboom A, Burger H, et al. Drug transporters and imatinib treatment: implications for clinical practice. Clin Cancer Res 2011;17:406-15. https://doi.org/10.1158/1078-0432.CCR-10-2250
  29. Koo DH, Ryu MH, Ryoo BY, et al. Association of ABCG2 polymorphism with clinical efficacy of imatinib in patients with gastrointestinal stromal tumor. Cancer Chemother Pharmacol 2015;75:173-82. https://doi.org/10.1007/s00280-014-2630-6
  30. Zu B, Li Y, Wang X, et al. MDR1 gene polymorphisms and imatinib response in chronic myeloid leukemia: a meta-analysis. Pharmacogenomics 2014;15:667-77. https://doi.org/10.2217/pgs.13.222