Methylation status of RASSF1A in patients with chronic myeloid leukemia

被引：14

作者：

Avramouli, Antigoni ^{[1
]}

Tsochas, Stefanos ^{[1
]}

Mandala, Eudokia ^{[2
]}

Katodritou, Eirini ^{[3
]}

Ioannou, Maria ^{[4
]}

Ritis, Konstantinos ^{[5
]}

Speletas, Matthaios ^{[1
]}

机构：

[1] Univ Thessaly, Sch Med, Dept Immunol & Histocompatibil, Larisa 41110, Greece

[2] Aristotle Univ Thessaloniki, Dept Internal Med D, Thessaloniki, Greece

[3] Theagen Anticanc Inst, Dept Hematol, Thessaloniki, Greece

[4] Univ Thessaly, Sch Med, Dept Pathol, Larisa 41110, Greece

[5] Democritus Univ Thrace, Dept Internal Med A, Alexandroupolis, Greece

来源：

LEUKEMIA RESEARCH | 2009年 / 33卷 / 08期

关键词：

Chronic myeloid leukemia; RASSF1A; Methylation; HEMATOLOGIC MALIGNANCIES; GENE;

D O I：

10.1016/j.leukres.2009.01.003

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

RASSF1A, a key cell cycle related gene, is expressed in all hematopoietic cells, it is implicated in ras signaling pathway and its promoter hypermethylation is observed in a wide variety of solid tumors. Till now, RASSF1A methylation status has not been investigated in patients with chronic myeloid leukemia (CML). In this study, we analyzed 41 patients carrying the BCR-ABL rearrangement, in different stages of the disease. No patient displayed RASSF1A promoter methylation, although the K562 erythroleukemia cell line, bearing the BCR-ABL rearrangement, was found methylated. Thus, our findings indicate that RASSF1A methylation does not appear to represent a critical step in the pathogenesis and/or the progression of CML. (C) 2009 Elsevier Ltd. All rights reserved.

引用

页码：1130 / 1132

页数：3

共 10 条

[1] The RASSF1A tumor suppressor [J].

Donninger, Howard ;

Vos, Michele D. ;

Clark, Geoffrey J. .

JOURNAL OF CELL SCIENCE, 2007, 120 (18) :3163-3172

[2] Aberrant promoter methylation and silencing of the RASSF1A gene in pediatric tumors and cell lines [J].

Harada, K ;

Toyooka, S ;

Maitra, A ;

Maruyama, R ;

Toyooka, KO ;

Timmons, CF ;

Tomlinson, GE ;

Mastrangelo, D ;

Hay, RJ ;

Minna, JD ;

Gazdar, AF .

ONCOGENE, 2002, 21 (27) :4345-4349

[3] Aberrant methylation of the negative regulators RASSFIA, SHP-1 and SOCS-1 in myelodysplastic syndromes and acute myeloid leukaemia [J].

Johan, MF ;

Bowen, DT ;

Frew, ME ;

Goodeve, AC ;

Reilly, JT .

BRITISH JOURNAL OF HAEMATOLOGY, 2005, 129 (01) :60-65

[4] Epigenetic alterations complement mutation of JAK2 tyrosine kinase in patients with BCR/ABL-negative myeloproliferative disorders [J].

Jost, E. ;

do O, N. ;

Dahl, E. ;

Maintz, C. E. ;

Jousten, P. ;

Habets, L. ;

Wilop, S. ;

Herman, J. G. ;

Osieka, R. ;

Galm, O. .

LEUKEMIA, 2007, 21 (03) :505-510

[5] Philadelphia chromosome-positive leukemias: From basic mechanisms to molecular therapeutics [J].

Kurzrock, R ;

Kantarjian, HM ;

Druker, BJ ;

Talpaz, M .

ANNALS OF INTERNAL MEDICINE, 2003, 138 (10) :819-830

[6] Analysis of relative gene expression data using real-time quantitative PCR and the 2-ΔΔCT method [J].

Livak, KJ ;

Schmittgen, TD .

METHODS, 2001, 25 (04) :402-408

[7] Phase II study of low-dose decitabine in combination with imatinib mesylate in patients with accelerated or myeloid blastic phase of chronic myelogenous leukemia [J].

Oki, Yasuhiro ;

Kantarjian, Hagop M. ;

Gharibyan, Vazganush ;

Jones, Dan ;

O'Brien, Susan ;

Verstovsek, Srdan ;

Cortes, Jorge ;

Morris, Gail M. ;

Garcia-Manero, Guillermo ;

Issa, Jean-Pierre J. .

CANCER, 2007, 109 (05) :899-906

[8] Alterations of DNA methylation in hematologic malignancies [J].

Rush, LJ ;

Plass, C .

CANCER LETTERS, 2002, 185 (01) :1-12

[9]

Speletas M, 2001, HAEMATOLOGICA, V86, P918

[10] Methylation profiling of twenty promoter-CpG islands of genes which may contribute to hepatocellular carcinogenesis [J].

Yu, J ;

Ni, M ;

Xu, J ;

Zhang, HY ;

Gao, BM ;

Gu, JR ;

Chen, JG ;

Zhang, LS ;

Wu, MC ;

Zhen, SS ;

Zhu, JD .

BMC CANCER, 2002, 2 (1)

← 1 →