Role of Stem Cell Elements in Chronic Myeloid Leukemia

Document Type : Review Article/ Systematic Review Article/ Meta Analysis

Authors

1 Molecular Diagnostic Unit, Research and Education Department, Razavi Hospital, Mashhad, IR Iran

2 Hematology Oncology Department, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, IR Iran

Abstract

Context: Chronic myeloid leukemia (CML) is believed to occur following the clonal expansion of haematopoietic stem cells and is maintained by expanding clones which have acquired a BCR-ABL fusion gene. The properties of untreated CML stem/progenitor cells correlate with a subsequent response to chemotherapy. Evidence Acquisition: The fifty two significant articles discussing the stem cell in chronic myeloid leukemia from 1996 to 2012 were selected according to the authors’ experience. Results: Studies have shown that primitive CML cells are less responsive to Tyrosine Kinase Inhibitors (TKIs) and are a reservoir for the relapse of multi drug resistant (MDR). Conclusions: Following that, minimal residual disease (MRD) measurement aims to detect very small numbers of leukemic cells, below the detection limit of morphology and cytogenetics with molecular techniques for patients in clinical remission.

Keywords

References

  1. 1..Jamieson CH, Ailles LE, Dylla SJ, Muijtjens M, Jones C, Zehnder JL, et al. Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML. N Engl J Med. 2004;351(7):657–67. 2. Minami Y, Kajiguchi T, Abe A, Ohno T, Kiyoi H, Naoe T. Expanded distribution of the T315I mutation among hematopoietic stem cells and progenitors in a chronic myeloid leukemia patient during imatinib treatment. Int J Hematol. 2010;92(4):664–6.

    1. Jiang X, Fujisaki T, Nicolini F, Berger M, Holyoake T, Eisterer W, et al. Autonomous multi-lineage differentiation in vitro of primitive CD34+ cells from patients with chronic myeloid leukemia. Leukemia. 2000;14(6):1112–21.
    2. Barnes DJ, Palaiologou D, Panousopoulou E, Schultheis B, Yong AS, Wong A, et al. Bcr-Abl expression levels determine the rate of development of resistance to imatinib mesylate in chronic myeloid leukemia. Cancer Res. 2005;65(19):8912–9.
    3. Hamilton A, Elrick L, Myssina S, Copland M, Jorgensen H, Melo JV, et al. BCR-ABL activity and its response to drugs can be determined in CD34+ CML stem cells by CrkL phosphorylation status using flow cytometry. Leukemia. 2006;20(6):1035–9. Ghayoor Karimiani E et al. 4 Razavi Int J Med. 2015;3(1):e25247
    4. Deininger MW, Vieira S, Mendiola R, Schultheis B, Goldman JM, Melo JV. BCR-ABL tyrosine kinase activity regulates the expression of multiple genes implicated in the pathogenesis of chronic myeloid leukemia. Cancer Res. 2000;60(7):2049–55.
    5. Vigneri P, Wang JY. Induction of apoptosis in chronic myelogenous leukemia cells through nuclear entrapment of BCR-ABL tyrosine kinase. Nat Med. 2001;7(2):228–34.
    6. Radford IR. Imatinib. Novartis. Curr Opin Investig Drugs. 2002;3(3):492–9.
    7. Kantarjian HM, Cortes JE, O'Brien S, Giles F, Garcia-Manero G, Faderl S, et al. Imatinib mesylate therapy in newly diagnosed patients with Philadelphia chromosome-positive chronic myelogenous leukemia: high incidence of early complete and major cytogenetic responses. Blood. 2003;101(1):97–100.
    8. Druker BJ, Talpaz M, Resta DJ, Peng B, Buchdunger E, Ford JM, 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(14):1031–7.
    9. Copland M, Hamilton A, Elrick LJ, Baird JW, Allan EK, Jordanides N, et al. Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction. Blood. 2006;107(11):4532–9.
    10. Bhatia R, Holtz M, Niu N, Gray R, Snyder DS, Sawyers CL, et al. Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment. Blood. 2003;101(12):4701–7.
    11. Merx K, Muller MC, Kreil S, Lahaye T, Paschka P, Schoch C, et al. Early reduction of BCR-ABL mRNA transcript levels predicts cytogenetic response in chronic phase CML patients treated with imatinib after failure of interferon alpha. Leukemia. 2002;16(9):1579–83.
    12. Hughes T, Deininger M, Hochhaus A, Branford S, Radich J, Kaeda J, et al. Monitoring CML patients responding to treatment with tyrosine kinase inhibitors: review and recommendations for harmonizing current methodology for detecting BCR-ABL transcripts and kinase domain mutations and for expressing results. Blood. 2006;108(1):28–37.
    13. Weisberg E, Manley PW, Breitenstein W, Bruggen J, Cowan-Jacob SW, Ray A, et al. Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. Cancer Cell. 2005;7(2):129–41.
    14. O'Hare T, Walters DK, Stoffregen EP, Jia T, Manley PW, Mestan J, et al. In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants. Cancer Res. 2005;65(11):4500–5.
    15. Branford S, Rudzki Z, Walsh S, Parkinson I, Grigg A, Szer J, 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(1):276–83.
    16. Hochhaus A, Kreil S, Corbin AS, La Rosee P, Muller MC, Lahaye T, et al. Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy. Leukemia. 2002;16(11):2190–6.
    17. Gambacorti-Passerini CB, Gunby RH, Piazza R, Galietta A, Rostagno R, Scapozza L. Molecular mechanisms of resistance to imatinib in Philadelphia-chromosome-positive leukaemias. Lancet Oncol. 2003;4(2):75–85.
    18. Apperley JF. Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia. Lancet Oncol. 2007;8(11):1018–29.
    19. Mahon FX, Deininger MW, Schultheis B, Chabrol J, Reiffers J, Goldman JM, et al. Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: diverse mechanisms of resistance. Blood. 2000;96(3):1070–9.
    20. Berman E. Genetic mutations in chronic myelogenous leukemia: when to check and what to do? Curr Opin Hematol. 2012;19(2):110–6.
    21. Oehler VG, Radich JP. Monitoring bcr-abl by polymerase chain reaction in the treatment of chronic myeloid leukemia. Curr Oncol Rep. 2003;5(5):426–35.
    22. Gabert J, Beillard E, van der Velden VH, Bi W, Grimwade D, Pallisgaard N, et al. Standardization and quality control studies of 'real-time' quantitative reverse transcriptase polymerase chain reaction of fusion gene transcripts for residual disease detection in leukemia - a Europe Against Cancer program. Leukemia. 2003;17(12):2318–57.
    23. Asnafi V, Rubio MT, Delabesse E, Villar E, Davi F, Damaj G, et al. Prediction of relapse by day 100 BCR-ABL quantification after allogeneic stem cell transplantation for chronic myeloid leukemia. Leukemia. 2006;20(5):793–9.
    24. Hochhaus A, Reiter A, Saussele S, Reichert A, Emig M, Kaeda J, et al. Molecular heterogeneity in complete cytogenetic responders after interferon-alpha therapy for chronic myelogenous leukemia: low levels of minimal residual disease are associated with continuing remission. German CML Study Group and the UK MRC CML Study Group. Blood. 2000;95(1):62–6.
    25. Emig M, Saussele S, Wittor H, Weisser A, Reiter A, Willer A, et al. Accurate and rapid analysis of residual disease in patients with CML using specific fluorescent hybridization probes for real time quantitative RT-PCR. Leukemia. 1999;13(11):1825–32.
    26. Ostergaard M, Nyvold CG, Jovanovic JV, Andersen MT, Kairisto V, Morgan YG, et al. Development of standardized approaches to reporting of minimal residual disease data using a reporting software package designed within the European LeukemiaNet. Leukemia. 2011;25(7):1168–73.
    27. Goldman J. Monitoring minimal residual disease in BCR-ABLpositive chronic myeloid leukemia in the imatinib era. Curr Opin Hematol. 2005;12(1):33–9.
    28. Scheuring UJ, Pfeifer H, Wassmann B, Bruck P, Gehrke B, Petershofen EK, et al. Serial minimal residual disease (MRD) analysis as a predictor of response duration in Philadelphia-positive acute lymphoblastic leukemia (Ph+ALL) during imatinib treatment. Leukemia. 2003;17(9):1700–6.
    29. Hughes TP, Kaeda J, Branford S, Rudzki Z, Hochhaus A, Hensley ML, et al. Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia. N Engl J Med. 2003;349(15):1423–32.
    30. Chung NG, Buxhofer-Ausch V, Radich JP. The detection and significance of minimal residual disease in acute and chronic leukemia. Tissue Antigens. 2006;68(5):371–85.
    31. Jovanovic JV, Score J, Waghorn K, Cilloni D, Gottardi E, Metzgeroth G, et al. Low-dose imatinib mesylate leads to rapid induction of major molecular responses and achievement of complete molecular remission in FIP1L1-PDGFRA-positive chronic eosinophilic leukemia. Blood. 2007;109(11):4635–40.
    32. Lane S, Saal R, Mollee P, Jones M, Grigg A, Taylor K, et al. A >or=1 log rise in RQ-PCR transcript levels defines molecular relapse in core binding factor acute myeloid leukemia and predicts subsequent morphologic relapse. Leuk Lymphoma. 2008;49(3):517–23.
    33. Pavlovsky C, Giere I, Moiraghi B, Pavlovsky MA, Aranguren PN, Garcia J, et al. Molecular monitoring of imatinib in chronic myeloid leukemia patients in complete cytogenetic remission: does achievement of a stable major molecular response at any time point identify a privileged group of patients? A multicenter experience in Argentina and Uruguay. Clin Lymphoma Myeloma Leuk. 2011;11(3):280–5.
    34. Cross NC. Standardisation of molecular monitoring for chronic myeloid leukaemia. Best Pract Res Clin Haematol. 2009; 22(3):355–65.
    35. Rabin K, Man TK, Lau CC. Personalized care of pediatric cancer patients. Nestle Nutr Workshop Ser Pediatr Program. 2008;62:173–85.
    36. Bruggemann M, Gokbuget N, Kneba M. Acute lymphoblastic leukemia: monitoring minimal residual disease as a therapeutic principle. Semin Oncol. 2012;39(1):47–57.
    37. Viprey VF, Burchill SA. Gene expression profiling for discovery of novel markers of minimal disease. Clin Cancer Res. 2009;15(21):6742.
    38. Pine SR, Moy FH, Wiemels JL, Gill RK, Levendoglu-Tugal O, Ozkaynak MF, et al. Real-time quantitative PCR: standardized detection of minimal residual disease in pediatric acute lymphoblastic leukemia. Polymerase chain reaction. J Pediatr Hematol Oncol. 2003;25(2):103–8.
    39. Day PJ. Miniaturization applied to analysis of nucleic acids in heterogeneous tissues. Expert Rev Mol Diagn. 2006;6(1):23–8. Ghayoor Karimiani E et al. Razavi Int J Med. 2015;3(1):e25247 5
    40. Stahlberg A, Andersson D, Aurelius J, Faiz M, Pekna M, Kubista M, et al. Defining cell populations with single-cell gene expression profiling: correlations and identification of astrocyte subpopulations. Nucleic Acids Res. 2011;39(4).
    41. Bengtsson M, Stahlberg A, Rorsman P, Kubista M. Gene expression profiling in single cells from the pancreatic islets of Langerhans reveals lognormal distribution of mRNA levels. Genome Res. 2005;15(10):1388–92.
    42. Fialkow PJ, Jacobson RJ, Papayannopoulou T. Chronic myelocytic leukemia: clonal origin in a stem cell common to the granulocyte, erythrocyte, platelet and monocyte/macrophage. Am J Med. 1977;63(1):125–30.
    43. Groffen J, Stephenson JR, Heisterkamp N, de Klein A, Bartram CR, Grosveld G. Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22. Cell. 1984;36(1):93–9.
    44. Kurzrock R, Kantarjian HM, Druker BJ, Talpaz M. Philadelphia chromosome-positive leukemias: from basic mechanisms to molecular therapeutics. Ann Intern Med. 2003;138(10):819–30.
    45. Nowell PC, Hungerford DA. Chromosome studies in human leukemia. II. Chronic granulocytic leukemia. J Natl Cancer Inst. 1961;27:1013–35.
    46. Jorgensen HG, Holyoake TL. A comparison of normal and leukemic stem cell biology in Chronic Myeloid Leukemia. Hematol Oncol. 2001;19(3):89–106.
    47. Shah NP, Nicoll JM, Nagar B, Gorre ME, Paquette RL, Kuriyan J, 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):117–25.
    48. Bazzoni G, Carlesso N, Griffin JD, Hemler ME. Bcr/Abl expression stimulates integrin function in hematopoietic cell lines. J Clin Invest. 1996;98(2):521–8.
    49. Simanovsky M, Berlinsky S, Sinai P, Leiba M, Nagler A, Galski H. Phenotypic and gene expression diversity of malignant cells in human blast crisis chronic myeloid leukemia. Differentiation. 2008;76(8):908–22.
    50. Damiano JS, Hazlehurst LA, Dalton WS. Cell adhesion-mediated drug resistance (CAM-DR) protects the K562 chronic myelogenous leukemia cell line from apoptosis induced by BCR/ABL inhibition, cytotoxic drugs, and gamma-irradiation. Leukemia. 2001;15(8):1232–9.
Razavi International Journal of Medicine
Volume 3, Issue 1
January 2015
Pages 1-5

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