The effects of co-exposure to methyl ethyl ketone on the biological monitoring of occupational exposure to N,N-dimethylformamide

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Title:	The effects of co-exposure to methyl ethyl ketone on the biological monitoring of occupational exposure to N,N-dimethylformamide
Authors:	Chang, HY;Shih, TS;Cheng, CC;Tsai, CY;Lai, SJ;Wang, VS
Contributors:	公共衛生學院職安系;China Med Coll, Dept Occupat Safety & Hlth, Taichung, Taiwan;Natl Cheng Kung Univ, Coll Med, Grad Sch Environm & Occupat Hlth, Tainan 70101, Taiwan;Council Labor Affairs, Inst Occupat Safety & Hlth, Taipei, Taiwan
Date:	2003
Issue Date:	2010-09-24 14:00:55 (UTC+8)
Publisher:	SPRINGER-VERLAG
Abstract:	JunB is a component of the Jun family genes of the activating protein-1 transcription factors that are important in the control of cell growth and differentiation and neoplastic transformation. Recently, it was demonstrated that transgenic mice specifically lacking JunB expression in the myeloid lineage developed a myeloproliferative disease, eventually progressing to blast crisis that resembled human chronic myeloid leukemia (CML). To gain further insights into the role of JunB in human CML, we examined peripheral blood from 17 healthy individuals and CML patients (11 in blastic crisis and 21 in chronic phase) by real-time quantitative reverse transcription-polymerase chain reaction analysis for the expression of JunB. The results showed the expression levels of JunB were significantly impaired in CML cases (blastic crisis < chronic phase < normal). Mutational analysis of the whole gene and methylation analysis of cytosine-phosphate guanosine (CpG) sites at the promoter area were further performed to investigate the possible mechanisms. However, no mutation was found within the coding region or the 9 flanking evolutionarily conserved regions in all CML cases. Interestingly, in the promoter area of JunB gene, most of the CpG sites were methylated in CML cases; in contrast, none of these CpG sites were methylated in normal cases. Demethylation by treatment of hypermethylated K562 cells with 5'-aza-2'-deoxycytidine resulted in partial reactivation of JunB expression. Our results suggest that the downregulated JunB expression in CML was due to the inactivation of JunB gene by methylation and the differential expression was correlated to the ratio of cells being methylated. (C) 2003 by The American Society of Hematology.
Relation:	INTERNATIONAL ARCHIVES OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH 76(2):121-128
Appears in Collections:	[Department and Graduate of Health Services Administration] Journal articles

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