Perfil de metilación en pacientes con leucemia mieloide crónica: revisión sistemática

Juliana Pérez Mejía; Jaiberth Antonio Cardona Arias; Paola Andrea Acevedo Toro

doi:10.17533/udea.hm.335030

Authors

Juliana Pérez Mejía University of Antioquia
Jaiberth Antonio Cardona Arias University of Antioquia
Paola Andrea Acevedo Toro University of Antioquia

DOI:

https://doi.org/10.17533/udea.hm.335030

Keywords:

chronic myeloid leukemia, epigenetics, methylation

Abstract

Introduction: DNA hypermethylation is involved in the transcriptional regulation of tumor suppressor genes in different types of hematological neoplasms including chronic myeloid leukemia (CML). A system-atic review was carried out following the indications proposed in the PRISMA guide (Preferred Report-ing Items for Systematic Reviews and Meta-Analyzes) aiming at identifying the main hypermethylated genes in patients with CML in the three clinical phases of the disease according to the scientific literature pub-lished between 2003 and 2013.

Methods: date and type of publication were taken into account as part of the eligibility criteria of the different studies. Only original articles, with the search terms in title, summary, and keywords were included, together with the studies that mentioned the clinical phase of patients’ illness. There was no filter applied per publication language. Lastly, 15 articles were ob-tained. A descriptive analysis of the same was then conducted, in which absolute and relative frequencies of place, person and time variables were calculated, with emphasis on the country, the clinical phase and the year of publication.

Results: during the hypermethylation analysis in patients with CML, a total of 39 genes classified as tumor suppressors, circadian cycle regulators, coding for transcription factors/receptors involved in DNA repair, pathways signaling and nucleotide metabolism, among others, were evaluated. In addition, a value of p = 0.000 was obtained in the multiple comparisons of the proportion of hypermethylation according to the clinical phase of the disease, establishing then a possible relationship between the progression of the disease and the percentage of methylation of those genes in patients with CML.

Conclusions :our results corroborate the absence of marker genes for progression by hypermethylation in CML and suggest individual gene studies to be fur-ther analyzed, in order to establish a causal relation-ship between the proportion of methylation and the progression of the disease.

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Author Biographies

Juliana Pérez Mejía, University of Antioquia

Bacteriologist and Clinical Laboratory Technician. Master's Student in Microbiology and Bioanalysis, emphasis in Hematology. Molecular Hematopathology Research Group (HEMO). School of Microbiology, University of Antioquia.

Jaiberth Antonio Cardona Arias, University of Antioquia

Microbiologist and Bioanalyst, MSc in Epidemiology, University of Antioquia.

Paola Andrea Acevedo Toro, University of Antioquia

Microbiologist and Bioanalyst. MSc in Basic Biomedical Sciences. Professor at the School of Microbiology. Molecular Hematopathology Research Group (HEMO), University of Antioquia.

References

Orazi A, Benett JM, Germing U, Brunnin RD, Baing BJ, Thiele J. Myelodysplastic/myeloproliferative neo-plasms. En: WHO Classification of Tumours of Haema-topoietic and Lymphoid Tissues. 4.a ed. Lyon: Interna-tional Agency for Research on Cancer; 2008. p. 76-86.

Vardiman J. Myloproliferative neoplasms. En: Hema-topathology. Philadelphia: Elsevier Saunders; 2011. p. 698-732

Pérez-Mejía J, Acevedo-Toro PA. Epigenética: una nueva herramienta para el estudio de la leucemia mie-loide crónica. Medicina & Laboratorio. 2013;19:243-255.

Lavallade H de. Chronic myeloid leukaemia. Medicine. 2013;41:275-277.

Morales C, Cárdena VT, Valencia JE, Ribón G, Darío R, Manrique H. Leucemia Mieloide Crónica: diagnósti-co y tratamiento. CES Medicina. 2010;24:97-108.

Zhang Y, Rowley JD. Chronic myeloid leukemia: cu-rrent perspectives. Clin Lab Med. 2011;31:687-698.

Valencia J, Gul-Uludağ, H, Mahdipoor P. Jiang, X, Uludağ H. Investigating siRNA delivery to chronic myeloid leukemia K562 cells with lipophilic polymers for therapeutic BCR-ABL down-regulation. J Control Release. 2013;172:495-503.

Roychowdhury S & Talpaz M. Managing resistan-ce in chronic myeloid leukemia. Blood Reviews. 2011;25:279-290.

Pesach J & Ben-Yehuda D. Molecular evolution of chronic myeloid leukaemia. Semin Cancer Biol. 2001;11:313.322.

Arpinati M, Tolomelli G, Bochicchio M, Castagnetti F, Amabile M, Bandini G, et al. Molecular Monito-ring of BCR-ABL Transcripts after Allogeneic Stem Cell Transplantation for Chronic Myeloid Leukemia. Biol Blood Marrow Transplant. 2013;19:735-740.

Sastry P. Prevention of progression in chronic myeloid leukemia by altering DNA methylation with a pyridoxi-ne analogue. Medical Hypotheses. 1999;53:488-489.

Waddington CH. An introduction to modern genetics. London: Allen and Unwin; 1939.

Esteller M. Epigenetics in cancer. N Engl J Med. 2008;358:1148-59.

Wilting RH, Dannenberg JH. Epigenetic mechanisms in tumorigenesis, tumor cell heterogeneity and drug resistance. Drug Resist Updat. 2012;2:21-38.

Melki JR, Clark SJ. DNA methylation changes in leu-kaemia. Semin Cancer Biol. 2002;12:347-57.

Rush LJ, Plass C. Alterations of DNA methylation in hematologic malignancies. Cancer Lett. 2002;185:1-12

.17. Tsai HC, Baylin SB. Cancer epigenetics: linking basic biology to clinical medicine. Cell Res. 2011;21:502-517.

Bixby D, Talpaz M. Mechanisms of resistance to tyro-sine kinase inhibitors in chronic myeloid leukemia and recent therapeutic strategies to overcome resis-tance. Hematology Am Soc Hematol Educ Program. 2009;1:461-76.

Urrutia G, Bonfill X. PRISMA declaration: A proposal to improve the publication of systematic reviews and meta-analyses. Med Clin. 2010;135:507-11.

Strobe Statement. Strobe Statement Strengthning reporting of observational studies in epidemiology. Strobe checklists [nternet]. [Consultado 2013 May 04]. Disponible en: http://www.strobe-statement.org/in-dex.php?id=available-checklists.

Jelinek J, Gharibyan V, Estecio MR, Kondo K, He R, Chung W, et al. Aberrant DNA methylation is associa-ted with disease progression, resistance to imatinib and shortened survival in chronic myelogenous leuke-mia. PLoS One. 2011;6:1-9.

Uehara E, Takeuchi S, Yang Y, Fukumoto T, Mat-suhashi Y, Tamura T, et al. Aberrant methylation in promoter-associated CpG islands of multiple genes in chronic myelogenous leukemia blast crisis. Oncol Lett. 2012;3:190-192.

Qian J, Wang YL, Lin J, Yao DM, Xu WR, Wu CY. Abe-rrant methylation of the death-associated protein ki-nase 1 (DAPK1) CpG island in chronic myeloid leuke-mia. Eur J Hematol. 2008;82:119-123.

Gomez J, Castillejo JA, Jiménez A, Cervantes F, Bo-que C, Hermosin L, et al. Cadherin-13, a Mediator of Calcium-Dependent Cell-Cell Adhesion, Is Silenced by Methylation in Chronic Myeloid Leukemia and Correla-tes With Pretreatment Risk Profile and Cytogenetic Res-ponse to Interferon Alfa. J Clin Oncol. 21;2003:1472-9.

Yang MY, Chang JG, Lin PM, Tang KP, Chen YH, Lin HY, et al. Downregulation of circadian clock genes in chronic myeloid leukemia: Alternative methylation pattern of hPER3. Cancer Sci. 2006;97:1298-1307.

Yang H, Liang H, Yan JS, Tao R, Hao SG, Ma LY. Down-regulation of hematopoiesis master regulator PU.1 via aberrant methylation in chronic myeloid leukemia. Int J Hematol. 2012;96:65-73.

Liu T, Lin SF, Chang JG, Yang MY, Hung SY, Chang CS. Epigenetic alteration of the SOCS1 gene in chronic myeloid leukaemia. Br J Haematol. 2003;123:654-661.

San Jose-Eneriz E, Agirre X, Jiménez-Velasco, Cor-deu L, Martín V, Arqueros V, et al. Epigenetic down-regulation of BIM expression is associated with redu-ced optimal responses to imatinib treatment in chronic myeloid leukaemia. Eur J Cancer. 2009;45:1877-1889.

Song J. Epigenetic inactivation of PLCD1 in chronic myeloid leukemia. Int J Mol Med. 2012;30:179-84.

Nagy E, Beck Z, Kiss A, Csoma E, Telek B, Konya J, et al. Frequent methylation of p16INK4A and p14ARF genes implicated in the evolution of chronic myeloid leukaemia from its chronic to accelerated phase. Eur J Cancer. 2003;39:2298-2305

.31. Strathdee G, Holyoake TL, Sim A, Parker A, Oscier DG, Melo JV, et al. Inactivation of HOXA Genes by Hy-permethylation in Myeloid and Lymphoid Malignancy is Frequent and Associated with Poor Prognosis. Clin Cancer Res. 2007;13:5048-55.

Yang M, Liu TC, Chang JG, Lin, PM, Lin SF. JunB gene expression is inactivated by methylation in chronic myeloid leukemia. Blood. 2003; 101:3205-11.

Wang YL, Qian J, Lin J, Yao DM, Qian Z, Zhu ZH, et al. Methylation status of DDIT3 gene in chronic myeloid leukemia. Exp Clin Cancer Res. 2010:29-54.

Pena M, Pardini MI,Colturato VA, Pinheiro NA. Methylation status of the SOCS 1 and JUNB genes in chronic myeloid leukemia patients. Rev Bras Hematol Hemoter. 2009;31:147-152.

Pehlivan M, Sercan Z, Sercan HO. sFRP1 promoter methylation is associated with persistent Philadelphia chromosome in chronic myeloid leukemia. Leuk Res. 2009; 33:1062-7.

You R, Ho CL, Hung HM, Hsieh YF, Ju JC, Chao TY. Identification of DNA methylation biomarkers in imati-nib-resistant chronic myeloid leukemia cells. Genomic Med Biomarkers Heath Sci. 2012;4:12-15.

Joha S, Dauphin V, Leprêtre F, Corm S, Nicolini FE, Roumier C, et al. Genomic characterization of Imati-nib resistance in CD34+ cell populations from chronic myeloid leukaemia patients. Leuk Res. 2011;35:448-58.

Sardina J, López-Ruano G, Sánchez-Sánchez B, Lla-nillo M, Hernández-Hernández A. Reactive oxygen species: Are they important for haematopoiesis?Crit Rev Oncol Hematol. 2012;81:57-274.

Sallmyr A, Fan J, Rassool FV. Genomic instability in myeloid malignancies: Increased reactive oxygen spe-cies (ROS), DNA double strand breaks (DSBs) and error-prone repair. Cancer Lett. 2008;270:1-9.

Gutierrez S, de la Rica L, Ballestar E, Santamaría C, Sánchez-Abarca LI, Caballero-Velazquez T, et al. Epigenetic regulation of PRAME in acute myeloid leukemia is different compared to CD34+ cells from healthy donors: Effect of 5-AZA treatment. Leuk Res. 2012;36:895-899.

How A, Nielsen, HM, Tost J. DNA methylation based biomarkers: Practical considerations and applications. Biochimie. 2012;94:2314-2337

.42. American Type Culture Collection. K562 cell line [Internet]. [Consultado 2014 May 18] Disponible en: https://www.atcc.org/products/all/CCL-243.aspx

Leone G, Voso MT, Teofili L, Lubbert M. Inhibitors of DNA methylation in the treatment of hematological malignancies and MDS. Clin Immunol. 2003;109: 89-102.