본문 바로가기
KERD
논문KCI 등재

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

1

조회

0

다운로드

0

인용

0

참고문헌

키워드

주제분류약학

초록

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.

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.

참고문헌 (30)

  1. Groffen J, "Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22", Cell, 36, pp.93~99 (1984)
  2. Ren R, "Mechanisms of BCR-ABL in the pathogenesis of chronic myelogenous leukaemia", Nat Rev Cancer, 5, pp.172~183 (2005)
  3. Baccarani M, "European LeukemiaNet recommendations for the management of chronic myeloid leukemia:2013", Blood, 122, pp.872~884 (2013)
  4. "Guidance on the use of imatinib for chronic myeloid leukaemia"[URL]
  5. Schindler T, "Structural mechanism for STI-571 inhibition of abelson tyrosine kinase", Science, 289, pp.1938~1942 (2000)
  6. Kantarjian HM, "New insights into the pathophysiology of chronic myeloid leukemia and imatinib resistance", Ann Intern Med, 145, pp.913~923 (2006)
  7. Burger H, "Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)", ABCG2drug pump, 2004, pp.104, 2940~2942
  8. Brendel C, "Imatinib mesylate and nilotinib (AMN107) exhibit high-affinity interaction with ABCG2 on primitive hematopoietic stem cells", Leukemia, 21, pp.1267~1275 (2007)
  9. Shukla S, "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, 22, pp.445~447 (2008)
  10. Kondo C, "Functional analysis of SNPs variants of BCRP", ABCG2, 2004, pp.21, 1895~1903
  11. Stacy AE, "Molecular pharmacology of ABCG2 and its role in chemoresistance", Mol Pharmacol, 84, pp.655~669 (2013)
  12. Kawabata S, "Expression and functional analyses of breast cancer resistance protein in lung cancer", Clin Cancer Res, 9, pp.3052~3057 (2003)
  13. Jordanides NE, "Functional ABCG2is overexpressed on primary CML CD34+ cells and is inhibited by imatinib mesylate", Blood, 108, pp.1370~1373 (2006)
  14. Shah NP, "Medical management of CML", Hematology Am Soc Hematol Educ Program, pp.371~375 (2007)
  15. Skoglund K, "Single-nucleotide polymorphisms of ABCG2 increase the efficacy of tyrosine kinase inhibitors in the K562 chronic myeloid leukemia cell line", Pharmacogenet Genomics, 24, pp.52~61 (2014)
  16. Nambu T, "Association of SLCO1B3polymorphism with intracellular accumulation of imatinib in leukocytes in patients with chronic myeloid leukemia", Biol Pharm Bull, 34, pp.114~119 (2011)
  17. Yamakawa Y, "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, 33, pp.244~250 (2011)
  18. "The Newcastle-Ottawa scale (NOS) for assessing the quality of nonrandomised studies in meta-analysis"[URL]
  19. Zheng JS, "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, 346, pp.f3706~ (2013)
  20. Anthony A, "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, 3, pp.274~278 (2012)
  21. Shinohara Y, "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, 98, pp.1407~1413 (2013)
  22. Takahashi N, "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, 55, pp.731~737 (2010)
  23. Seong SJ, "Influence of enzyme and transporter polymorphisms on trough imatinib concentration and clinical response in chronic myeloid leukemia patients", Ann Oncol, 24, pp.756~760 (2013)
  24. Au A, "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, 68, pp.343~349 (2014)
  25. de Lima LT, "Reduced ABCG2 and increased SLC22A1 mRNA expression are associated with imatinib response in chronic myeloid leukemia", Med Oncol, 31, pp.851~ (2014)
  26. Hana Salimizand, "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", Tumor Biology, 37(1), pp.791~798 (2016), Springer Nature[DOI]
  27. Bixby D, "Mechanisms of resistance to tyrosine kinase inhibitors in chronic myeloid leukemia and recent therapeutic strategies to overcome resistance", Hematology Am Soc Hematol Educ Program, pp.461~467 (2009)
  28. Eechoute K, "Drug transporters and imatinib treatment: implications for clinical practice", Clin Cancer Res, 17, pp.406~415 (2011)
  29. Koo DH, "Association of ABCG2 polymorphism with clinical efficacy of imatinib in patients with gastrointestinal stromal tumor", Cancer Chemother Pharmacol, 75, pp.173~182 (2015)
  30. Zu B, "MDR1 gene polymorphisms and imatinib response in chronic myeloid leukemia: a meta-analysis", Pharmacogenomics, 15, pp.667~677 (2014)

관련 논문AI추천

Coexisting with Clonal Evolution and BCR-ABL Mutant in CML Patients Treated with Second-generation Tyrosine Kinase Inhibitors Predict the Discrepancy of in vitro Drug Sensitivity김여경, 김형준, 배우균, 신명근, 심현정, 안재숙, 양덕환, 이세련, 이제중, 정익주, 조상희, Li Yu대한암학회 · Cancer Research and Treatment2010 · 제42권 제1호만성골수성백혈병 치료제의 효과: 메타분석유기연한국병원약사회 · 병원약사회지2013 · 제30권 제4호Survival impact of adherence to tyrosine kinase inhibitor in chronic myeloid leukemiaJaeyeon Jang, Jee Hyun Kong, Jii Bum Lee, Jong In Lee, Kwang Yong Shim, Seungtaek Lim, Tae-Hwa Go, Yundeok Kim대한내과학회 · The Korean Journal of Internal Medicine2021 · 제36권 제6호Rapid Sequential Gain of ABL1 Kinase Domain Mutations with a Complex Karyotype in the Progression of Chronic Myelogenous Leukemia공선영, 박선섭, 심효은, 엄혜석, 이혜원, 정유선, 조은해대한진단검사의학회 · Annals of Laboratory Medicine2014 · 제34권 제5호BCR-ABL1 transcripts (MR4.5) at post-transplant 3 months as an early predictor for long-term outcomes in chronic myeloid leukemia강기훈, 김동욱, 김수현, 송혜영, 유혜련, 이미영, 이성은, 장은정, 최수영, 황희정대한내과학회 · The Korean Journal of Internal Medicine2017 · 제32권 제1호The role of early molecular predictor in transplant-eligible chronic myelogenous leukemia김성현대한내과학회 · The Korean Journal of Internal Medicine2017 · 제32권 제1호

이 간행물의 다른 논문 (12건)