Role of epigenetics in chronic myeloid leukemia

Current Hematologic Malignancy Reports

Volumn 8, Issue 1, 2013, Pages 28-36

  MacHova Polakova, Katerina ^a   Koblihova, Jitka ^a   Stopka, Tomas ^b  

^a INSTITUTE OF HEMATOLOGY AND BLOOD TRANSFUSION   (Czech Republic)

^b CHARLES UNIVERSITY   (Czech Republic)

Author keywords

CML; Epigenetics; microRNA; Tyrosine kinase inhibitors

Indexed keywords

5 AZA 2' DEOXYCYTIDINE; ABELSON KINASE; BCR ABL PROTEIN; CELL PROTEIN; DEATH ASSOCIATED PROTEIN KINASE; DEATH ASSOCIATED PROTEIN KINASE 1; DNA; EARLY B CELL FACTOR 2; HYDRALAZINE; IMATINIB; MICRORNA; MICRORNA 146A; RAS ASSOCIATION DOMAIN FAMILY PROTEIN 1A; TRANSCRIPTION FACTOR AP 2; TRANSCRIPTION FACTOR AP 2 ALPHA; UNCLASSIFIED DRUG; VALPROIC ACID; VORINOSTAT;

ACUTE GRANULOCYTIC LEUKEMIA; ACUTE LYMPHOBLASTIC LEUKEMIA; ARTICLE; BONE MARROW SUPPRESSION; CANCER CHEMOTHERAPY; CANCER PATIENT; CHROMATIN CONDENSATION; CHRONIC MYELOID LEUKEMIA; CPG ISLAND; DNA METHYLATION; DRUG EFFICACY; DRUG RESPONSE; EPIGENETICS; GENE EXPRESSION PROFILING; GENE EXPRESSION REGULATION; GENE FUNCTION; GENE TARGETING; HISTONE METHYLATION; HISTONE MODIFICATION; HUMAN; LOW DRUG DOSE; MYELODYSPLASTIC SYNDROME; PROTEIN EXPRESSION; PROTEIN FUNCTION;

ANTINEOPLASTIC AGENTS; DNA METHYLATION; DRUG RESISTANCE, NEOPLASM; EPIGENOMICS; FUSION PROTEINS, BCR-ABL; GENE EXPRESSION REGULATION, LEUKEMIC; HUMANS; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; MICRORNAS; PROTEIN KINASE INHIBITORS;

EID: 84874261693     PISSN: 15588211     EISSN: 1558822X     Source Type: Journal    
DOI: 10.1007/s11899-012-0152-z     Document Type: Article

References (62)

1. Nowell PC, Hungerford DA. A minute chromosome in human chronic granulocytic leukemia. Science. 1960;142:1497.
2. Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature. 1973;243:290-93.
3. Druker BJ, Tamura S, Buchdunger E, et al. Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells. Nat Med. 1996;2:561-66.
4. 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;293:876-80.
5. Soverini S, Hochhaus A, Nicolini FE, et al. BCR-ABL kinase domain mutation analysis in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors: recommendations from an expert panel on behalf of European LeukemiaNet. Blood. 2011;118:1208-15.
6. Jenuwein T, Allis CD. Translating the histone code. Science. 2001;293:1074-80.
7. Matzke M, Matzke AJ, Kooter JM. RNA: guiding gene silencing. Science. 2001;293:1080-83.
8. Bonifer C, Cockerill PN. Chromatin mechanisms regulating gene expression in health and disease. Adv Exp Med Biol. 2011;711:12-25.
9. Asimakopoulos FA, Shteper PJ, Krichevsky S, et al. ABL1 methylation is a distinct molecular event associated with clonal evolution of chronic myeloid leukemia. Blood. 1999;94:2452-60.
10. Issa JP, Kantarjian H, Mohan A, et al. Methylation of the ABL1 promoter in chronic myelogenous leukemia: lack of prognostic significance. Blood. 1999;93:2075-80.
11. Ben-Yehuda D, Krichevsky S, Rachmilewitz EA, et al. Molecular follow-up of disease progression and interferon therapy in chronic myelocytic leukemia. Blood. 1997;90:4918-23.
12. Nguyen TT, Mohrbacher AF, Tsai YC, et al. Quantitative measure of c-abl and p15 methylation in chronic myelogenous leukemia: biological implications. Blood. 2000;95:2990-92.
13. • Jelinek J, Gharibyan V, Estecio MR, et al. Aberrant DNA methylation is associated with disease progression, resistance to imatinib and shortened survival in chronic myelogenous leukemia. PLoS One. 2011;6:e22110. This report comprehensively describes aberrant DNA methylation of selected genes in CML.
14. Sun B, Jiang G, Zaydan MA, et al. ABL1 promoter methylation can exist independently of BCR-ABL transcription in chronic myeloid leukemia hematopoietic progenitors. Cancer Res. 2001;61:6931-37.
15. Uchida T, Kinoshita T, Hotta T, Murate T. High-risk myelodysplastic syndromes and hypermethylation of the p15Ink4B gene. Leuk Lymphoma. 1998;32:9-18.
16. Tien HF, Tang JH, Tsay W, et al. Methylation of the p15(INK4B) gene in myelodysplastic syndrome: it can be detected early at diagnosis or during disease progression and is highly associated with leukaemic transformation. Br J Haematol. 2001;112:148-54.
17. Wong IH, Ng MH, Huang DP, Lee JC. Aberrant p15 promoter methylation in adult and childhood acute leukemias of nearly all morphologic subtypes: potential prognostic implications. Blood. 2000;95:1942-49.
18. Deneberg S, Grövdal M, Karimi M, et al. Gene-specific and global methylation patterns predict outcome in patients with acute myeloid leukemia. Leukemia. 2010;24:932-41.
19. Alvarez S, Suela J, Valencia A, et al. DNA methylation profiles and their relationship with cytogenetic status in adult acute myeloid leukemia. PLoS One. 2010;5:e12197.
20. Herman JG, Civin CI, Issa JP, et al. Distinct patterns of inactivation of p15INK4B and p16INK4A characterize the major types of hematological malignancies. Cancer Res. 1997;57:837-41.
21. Oki Y, Kantarjian HM, Gharibyan V, et al. Phase II study of low-dose decitabine in combination with imatinib mesylate in patients with accelerated or myeloid blastic phase of chronic myelogenous leukemia. Cancer. 2007;109:899-906.
22. Uehara E, Takeuchi S, Yang Y, et al. Aberrant methylation in promoter-associated CpG islands of multiple genes in chronic myelogenous leukemia blast crisis. Oncol Lett. 2012;3:190-92.
23. Avramouli A, Tsochas S, Mandala E, et al. Methylation status of RASSF1A in patients with chronic myeloid leukemia. Leuk Res. 2009;33:1130-32.
24. Murray PG, Qiu GH, Fu L, et al. Frequent epigenetic inactivation of the RASSF1A tumor suppressor gene in Hodgkin's lymphoma. Oncogene. 2004;23:1326-31.
25. Dunwell T, Hesson L, Rauch TA, et al. A genome-wide screen identifies frequently methylated genes in haematological and epithelial cancers. Mol Cancer. 2010;9:44.
26. Qian J, Wang YL, Lin J, et al. Aberrant methylation of the death-associated protein kinase 1 (DAPK1) CpG island in chronic myeloid leukemia. Eur J Haematol. 2009;82:119-23.
27. Nelkin BD, Przepiorka D, Burke PJ, et al. Abnormal methylation of the calcitonin gene marks progression of chronic myelogenous leukemia. Blood. 1991;77:2431-34.
28. Issa JP, Zehnbauer BA, Kaufmann SH, et al. HIC1 hypermethylation is a late event in hematopoietic neoplasms. Cancer Res. 1997;57:1678-81.
29. Issa JP, Zehnbauer BA, Civin CI, et al. The estrogen receptor CpG island is methylated in most hematopoietic neoplasms. Cancer Res. 1996;56:973-77.
30. Strathdee G, Holyoake TL, Sim A, et al. Inactivation of HOXA genes by hypermethylation in myeloid and lymphoid malignancy is frequent and associated with poor prognosis. Clin Cancer Res. 2007;13:5048-55.
31. Wang YL, Qian J, Lin J, et al. Methylation status of DDIT3 gene in chronic myeloid leukemia. J Exp Clin Cancer Res. 2010;29:54.
32. Fenaux P, Mufti GJ, Hellstrom-Lindberg E, et al. Efficacy of azacitidine compared with that of conventional care regimens in the treatment of higher-risk myelodysplastic syndromes: a randomised, open-label, phase III study. Lancet Oncol. 2009;10:223-32.
33. Scholz B, Marschalek R. Epigenetics and blood disorders. Br J Haematol. 2012;158:307-22. doi: 10.1111/j.1365-2141.2012.09193.x.
34. Kantarjian HM, O'Brien S, Cortes J, et al. Results of decitabine (5-aza-2'deoxycytidine) therapy in 130 patients with chronic myelogenous leukemia. Cancer. 2003;98:522-28.
35. Issa JP, Garcia-Manero G, Giles FJ, et al. Phase 1 study of low-dose prolonged exposure schedules of the hypomethylating agent 5-aza-2'-deoxycytidine (decitabine) in hematopoietic malignancies. Blood. 2004;103:1635-40.
36. Issa JP, Gharibyan V, Cortes J, et al. Phase II study of low-dose decitabine in patients with chronic myelogenous leukemia resistant to imatinib mesylate. J Clin Oncol. 2005;23:3948-56.
37. Arce C, Pérez-Plasencia C, González-Fierro A, et al. A proof-of-principle study of epigenetic therapy added to neoadjuvant doxorubicin cyclophosphamide for locally advanced breast cancer. PLoS One. 2006;1:e98.
38. Candelaria M, Herrera A, Labardini J, et al. Hydralazine and magnesium valproate as epigenetic treatment for myelodysplastic syndrome. Ann Hematol. 2011;90:379-87.
39. Cervera E, Candelaria M, López-Navarro O, et al. Epigenetic therapy with hydralazine and magnesium valproate reverses imatinib resistance in patients with chronic myeloid leukemia. Clin Lymphoma Myeloma Leuk. 2012;12:207-12.
40. Felsenfeld G, Groudine M. Controlling the double helix. Nature. 2003;421:448-53.
41. Shahbazian MD, Grunstein M. Functions of site-specific histone acetylation and deacetylation. Annu Rev Biochem. 2007;76:75-100.
42. Gronbaek K, Muller-Tidow C, Perini G, et al. A critical appraisal of tools available for monitoring epigenetic changes in clinical samples from patients with myeloid malignancies. Haematologica. 2012 Apr 4.
43. Glozak MA, Seto E. Histone deacetylases and cancer. Oncogene. 2007;26:5420-32.
44. Bolden JE, Peart MJ, Johnstone RW. Anticancer activities of histone deacetylase inhibitors. Nat Rev Drug Discov. 2006;5:769-84.
45. Mithraprabhu S, Grigoriadis G, Khong T, Spencer A. Deactylase inhibition in myeloproliferative neoplasms. Investig New Drugs. 2010;28 Suppl 1:S50-7.
46. Mann BS, Johnson JR, Cohen MH, et al. FDA approval summary: vorinostat for treatment of advanced primary cutaneous T-cell lymphoma. Oncologist. 2007;12:1247-52.
47. Nimmanapalli R, Fuino L, Stobaugh C, et al. Cotreatment with the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) enhances imatinib-induced apoptosis of Bcr-Abl-positive human acute leukemia cells. Blood. 2003;101:3236-39.
48. Fiskus W, Pranpat M, Balasis M, et al. Cotreatment with vorinostat (suberoylanilide hydroxamic acid) enhances activity of dasatinib (BMS-354825) against imatinib mesylate-sensitive or imatinib mesylate-resistant chronic myelogenous leukemia cells. Clin Cancer Res. 2006;12:5869-78.
49. Bali P, Pranpat M, Bradner J, et al. Inhibition of histone deacetylase 6 acetylates and disrupts the chaperone function of heat shock protein 90: a novel basis for antileukemia activity of histone deacetylase inhibitors. J Biol Chem. 2005;280:26729-734.
50. Hansen TB, Kjems J, Bramsen JB. Enhnacing miRNA annotation confidence in miRBase by continuous cross dataset analysis. RNA Biol. 2011;8:378-83.
51. Agirre X, Jiménez-Velasco A, José-Enériz ES, et al. Down-regulation of hsa-miR-10a in chronic myeloid leukemia CD34+ cells increases USF2-mediated cell growth. Mol Cancer Res. 2008;6:1830-40.
52. Flamant S, Ritchie W, Guilhot J, et al. Micro-RNA response to imatinib mesylate in patients with chronic myeloid leukemia. Haematologica. 2010;95:1325-33.
53. • Machová Poláková K, Lopotová T, Klamová H, et al. Expression patterns of microRNAs associated with CML phases and their disease related targets. Mol Cancer. 2011;10:41. First complex study about microRNA expression profiles with clinically-defined CML stages or therapeutic responses to imatinib and in silico prediction of microRNA targets underlying their importance in CML.
54. • José-Enériz ES, Román-Gómez J, Jiménez-Velaso A, et al. MicroRNA expression profiling in imatinib-resistant chronic myeloid leukemia patients without clinically significant ABL1-mutations. Mol Cancer. 2009;8:69. First report about microRNAs that are associated with imatinib resistant patients with CML.
55. Venturini L, Battmer K, Castoldi M, et al. Expression of the miR-19-92 polycistron in chronic myeloid leukemia (CML) CD34+ cells. Blood. 2007;109:4399-405.
56. Scholl V, Hassan R, Zalcberg IR. miRNA-451: A putative predictor marker of Imatinib therapy response in chronic myeloid leukemia. Leuk Res. 2012;36:119-21.
57. Burchert A, Wang Y, Cai D, et al. Compensatory PI3-kinase/Akt/mTor activation regulates resistance development. Leukemia. 2005;19:1774-82.
58. Rokah OH, Granot G, Ovcharenko A, et al. Downregulation of miR-31, miR-155, and miR-564 in chronic myeloid leukemia cells. PLoS One. 2012;7:e35501.
59. Suresh S, McCallum L, Lu W, et al. MicroRNAs 130a/b are regulated by BCR-ABL and downregulate expression of CCN3 in CML. J Cell Commun Signal. 2011;5:183-91.
60. Lidonnici MR, Corradini F, Waldron T. Requirement of c-Myb for p210BCR/ABL-dependent transformation of hematopoietic progenitors and leukemogenesis. Blood. 2008;111:4771-79.
61. Eiring AM, Harb JG, Neviani P, et al. miR-328 functions as an RNA decoy to modulate hnRNP E2 regulation of mRNA translation in leukemic blasts. Cell. 2010;140:652-65.
62. Bueno MJ, Castro IP. Gómez de Cedrón M, et al. Genetic and epigenetic silencing of microRNA-203 enhances ABL1 and BCR-ABL1 oncogene expression. Cancer Cell. 2008;13:496-506.