ABSTRACT
Objective To explore whether alcohol promotes the development of breast cancer in TA2 mice and the possible potential mechanism. Methods Thirty-two 6-8-week old nulliparous female TA2 mice were randomly divided into control and ethanol-exposure groups, 16 mice in each group. The mice of the ethanol-exposure group were given 2%ethanol in drinking water, and the mice of control group received regular drinking water. Serum ethanol concentration in the TA2 mice was measured using an ANALOX AM1 alcohol analyzer. The incidence of breast cancer, tumor growth rate and tumor size of the ethanol-exposure and control groups were observed and compared. The estrogen levels of the two groups was detected by enzyme-linked immunosorbent assay ( ELASA) . Results Compared with the control group, the tumor for-mation rate of spontaneous breast cancer in the alcohol-exposure group was significantly increased (62. 5% vs. 43. 75%, P<0. 05), the average number of days of tumor formation was shortened (285 days vs. 335 days, P<0. 05), the tumor weight and volume were increased but not significant ( P>0. 05 ) , and the level of estrogen in the ethanol-exposure mice was significantly higher than that in the control group ( P>0. 05 ) . Conclusions Alcohol promotes the tumorigenesis of spontaneous breast cancer in TA2 mice, which may be associated to the increase of estrogen levels.
ABSTRACT
Objective To explore whether alcohol promotes the development of breast cancer in TA2 mice and the possible potential mechanism. Methods Thirty-two 6-8-week old nulliparous female TA2 mice were randomly divided into control and ethanol-exposure groups, 16 mice in each group. The mice of the ethanol-exposure group were given 2%ethanol in drinking water, and the mice of control group received regular drinking water. Serum ethanol concentration in the TA2 mice was measured using an ANALOX AM1 alcohol analyzer. The incidence of breast cancer, tumor growth rate and tumor size of the ethanol-exposure and control groups were observed and compared. The estrogen levels of the two groups was detected by enzyme-linked immunosorbent assay ( ELASA) . Results Compared with the control group, the tumor for-mation rate of spontaneous breast cancer in the alcohol-exposure group was significantly increased (62. 5% vs. 43. 75%, P<0. 05), the average number of days of tumor formation was shortened (285 days vs. 335 days, P<0. 05), the tumor weight and volume were increased but not significant ( P>0. 05 ) , and the level of estrogen in the ethanol-exposure mice was significantly higher than that in the control group ( P>0. 05 ) . Conclusions Alcohol promotes the tumorigenesis of spontaneous breast cancer in TA2 mice, which may be associated to the increase of estrogen levels.
ABSTRACT
In eukaryotic cells, histones are packaged into octameric core particles with DNA wrapping around to form nucleosomes, which are the basic units of chromatin (Kornberg and Thomas, 1974). Multicellular organisms utilise chromatin marks to translate one single genome into hundreds of epigenomes for their corresponding cell types. Inheritance of epigenetic status is critical for the maintenance of gene expression profile during mitotic cell divisions (Allis et al., 2006). During S phase, canonical histones are deposited onto DNA in a replication-coupled manner (Allis et al., 2006). To understand how dividing cells overcome the dilution of epigenetic marks after chromatin duplication, DNA replication coupled (RC) nucleosome assembly has been of great interest. In this review, we focus on the potential influence of RC nucleosome assembly processes on the maintenance of epigenetic status.