Role of epigenetics in chronic myeloid leukemia

. 2013 Mar ; 8 (1) : 28-36.

Jazyk angličtina Země Spojené státy americké Médium print

Typ dokumentu časopisecké články, práce podpořená grantem, přehledy

Perzistentní odkaz   https://www.medvik.cz/link/pmid23296408

The efficacy of therapeutic modalities in chronic myeloid leukemia (CML) depends on both genetic and epigenetic mechanisms. This review focuses on epigenetic mechanisms involved in the pathogenesis of CML and in resistance of tumor cells to tyrosine kinase inhibitors leading to the leukemic clone escape and propagation. Regulatory events at the levels of gene regulation by transcription factors and microRNAs are discussed in the context of CML pathogenesis and therapeutic modalities.

Zobrazit více v PubMed

Nowell PC, Hungerford DA. A minute chromosome in human chronic granulocytic leukemia. Science. 1960;142:1497. PubMed

Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature. 1973;243:290–93. doi: 10.1038/243290a0. PubMed DOI

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. doi: 10.1038/nm0596-561. PubMed DOI

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. doi: 10.1126/science.1062538. PubMed DOI

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. doi: 10.1182/blood-2010-12-326405. PubMed DOI

Jenuwein T, Allis CD. Translating the histone code. Science. 2001;293:1074–80. doi: 10.1126/science.1063127. PubMed DOI

Matzke M, Matzke AJ, Kooter JM. RNA: guiding gene silencing. Science. 2001;293:1080–83. doi: 10.1126/science.1063051. PubMed DOI

Bonifer C, Cockerill PN. Chromatin mechanisms regulating gene expression in health and disease. Adv Exp Med Biol. 2011;711:12–25. doi: 10.1007/978-1-4419-8216-2_2. PubMed DOI

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. PubMed

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. PubMed

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. PubMed

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. PubMed

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. doi: 10.1371/journal.pone.0022110. PubMed DOI PMC

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. PubMed

Uchida T, Kinoshita T, Hotta T, Murate T. High-risk myelodysplastic syndromes and hypermethylation of the p15Ink4B gene. Leuk Lymphoma. 1998;32:9–18. PubMed

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. doi: 10.1046/j.1365-2141.2001.02496.x. PubMed DOI

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. PubMed

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. doi: 10.1038/leu.2010.41. PubMed DOI

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. doi: 10.1371/journal.pone.0012197. PubMed DOI PMC

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. PubMed

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. doi: 10.1002/cncr.22470. PubMed DOI

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. PubMed PMC

Avramouli A, Tsochas S, Mandala E, et al. Methylation status of RASSF1A in patients with chronic myeloid leukemia. Leuk Res. 2009;33:1130–32. doi: 10.1016/j.leukres.2009.01.003. PubMed DOI

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. doi: 10.1038/sj.onc.1207313. PubMed DOI

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. doi: 10.1186/1476-4598-9-44. PubMed DOI PMC

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. doi: 10.1111/j.1600-0609.2008.01178.x. PubMed DOI

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. PubMed

Issa JP, Zehnbauer BA, Kaufmann SH, et al. HIC1 hypermethylation is a late event in hematopoietic neoplasms. Cancer Res. 1997;57:1678–81. PubMed

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. PubMed

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. doi: 10.1158/1078-0432.CCR-07-0919. PubMed DOI

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. doi: 10.1186/1756-9966-29-54. PubMed DOI PMC

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. doi: 10.1016/S1470-2045(09)70003-8. PubMed DOI PMC

Scholz B, Marschalek R. Epigenetics and blood disorders. Br J Haematol. 2012;158:307–322. doi: 10.1111/j.1365-2141.2012.09193.x. PubMed DOI

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. doi: 10.1002/cncr.11543. PubMed DOI

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. doi: 10.1182/blood-2003-03-0687. PubMed DOI

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. doi: 10.1200/JCO.2005.11.981. PubMed DOI

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. doi: 10.1371/journal.pone.0000098. PubMed DOI PMC

Candelaria M, Herrera A, Labardini J, et al. Hydralazine and magnesium valproate as epigenetic treatment for myelodysplastic syndrome. . Ann Hematol. 2011;90:379–87. doi: 10.1007/s00277-010-1090-2. PubMed DOI

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. doi: 10.1016/j.clml.2012.01.005. PubMed DOI

Felsenfeld G, Groudine M. Controlling the double helix. Nature. 2003;421:448–53. doi: 10.1038/nature01411. PubMed DOI

Shahbazian MD, Grunstein M. Functions of site-specific histone acetylation and deacetylation. Annu Rev Biochem. 2007;76:75–100. doi: 10.1146/annurev.biochem.76.052705.162114. PubMed DOI

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. PubMed PMC

Glozak MA, Seto E. Histone deacetylases and cancer. Oncogene. 2007;26:5420–32. doi: 10.1038/sj.onc.1210610. PubMed DOI

Bolden JE, Peart MJ, Johnstone RW. Anticancer activities of histone deacetylase inhibitors. Nat Rev Drug Discov. 2006;5:769–84. doi: 10.1038/nrd2133. PubMed DOI

Mithraprabhu S, Grigoriadis G, Khong T, Spencer A. Deactylase inhibition in myeloproliferative neoplasms. Investig New Drugs. 2010;28(Suppl 1):S50–7. doi: 10.1007/s10637-010-9590-4. PubMed DOI PMC

Mann BS, Johnson JR, Cohen MH, et al. FDA approval summary: vorinostat for treatment of advanced primary cutaneous T-cell lymphoma. Oncologist. 2007;12:1247–1252. doi: 10.1634/theoncologist.12-10-1247. PubMed DOI

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. doi: 10.1182/blood-2002-08-2675. PubMed DOI

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. doi: 10.1158/1078-0432.CCR-06-0980. PubMed DOI

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. doi: 10.1074/jbc.C500186200. PubMed DOI

Hansen TB, Kjems J, Bramsen JB. Enhnacing miRNA annotation confidence in miRBase by continuous cross dataset analysis. RNA Biol. 2011;8:378–83. doi: 10.4161/rna.8.3.14333. PubMed DOI PMC

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. doi: 10.1158/1541-7786.MCR-08-0167. PubMed DOI

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. doi: 10.3324/haematol.2009.020636. PubMed DOI PMC

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. doi: 10.1186/1476-4598-10-41. PubMed DOI PMC

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. doi: 10.1186/1476-4598-8-69. PubMed DOI PMC

Venturini L, Battmer K, Castoldi M, et al. Expression of the miR-19-92 polycistron in chronic myeloid leukemia (CML) CD34+ cells. Blood. 2007;109:4399–4405. doi: 10.1182/blood-2006-09-045104. PubMed DOI

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. doi: 10.1016/j.leukres.2011.08.023. PubMed DOI

Burchert A, Wang Y, Cai D, et al. Compensatory PI3-kinase/Akt/mTor activation regulates resistance development. Leukemia. 2005;19:1774–82. doi: 10.1038/sj.leu.2403898. PubMed DOI

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. doi: 10.1371/journal.pone.0035501. PubMed DOI PMC

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;5:183–191. doi: 10.1007/s12079-011-0139-x. PubMed DOI PMC

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. doi: 10.1182/blood-2007-08-105072. PubMed DOI PMC

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. doi: 10.1016/j.cell.2010.01.007. PubMed DOI PMC

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. doi: 10.1016/j.ccr.2008.04.018. PubMed DOI

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...