No abstract available.
Carboplatin* ; Cytarabine* ; Cytosine* ; Etoposide*

No abstract available.
Cytosine Deaminase* ; Cytosine* ; Genetic Therapy* ; Osteocalcin* ; Prostate* ; Prostatic Neoplasms*

No abstract available.
Child* ; Cytarabine* ; Cytosine* ; Humans ; Leukemia*

To observe mtDNA length heteroplasmy in a homoploymeric cytosine tract of the mitochondrial HV2 region, we carried out size-based separation of PCR products, which was produced by using primers designed to minimize the stutter production. Blood and hair shaft samples were collected from 25 individuals. The result showed significant qualitative/quantitative peak pattern variations among blood and hair shaft mtDNA profiles. Based on the results of this study, an exclusion depended solely on differences in length of the major C-tract variant could thus be an erroneous interpretation. Therefore, differences in the number of cytosine or qualitative/quantitative peak pattern variations in the C-tract of the mtDNA HV2 region cannot be used alone to support an interpretation of exclusion.
Cytosine ; DNA, Mitochondrial* ; Hair* ; Polymerase Chain Reaction

No abstract available.
Adult* ; Cytarabine* ; Cytosine* ; Humans ; Leukemia* ; Mitoxantrone*

No abstract available.
Bone Marrow* ; Cytosine Deaminase* ; Cytosine* ; Homicide* ; Mesenchymal Stromal Cells* ; Prostate* ; Prostatic Neoplasms*

No abstract available.
Cytarabine* ; Cytosine* ; Drug Therapy, Combination* ; Idarubicin* ; Leukemia, Myeloid, Acute*

No abstract available.
Cytarabine* ; Cytosine* ; Humans ; Idarubicin* ; Induction Chemotherapy* ; Leukemia, Myeloid, Acute*

OBJECTIVETo compare the DNA methylation-related alteration induced by trichloroethylene (TCE) in human hepatic L-02 cells (L-02 cells) and SET deficient cells, and reveal the role of SET on the mechanisms in TCE-induced epigenetic pathway.

METHODSThe L-02 cells and pre-established SET deficient cells were treated with different TCE concentrations, and the changes of total cell viability, DNA methylation level and DNA methyltransferases (DNMTs) activity were measured, respectively. In addition, the TCE-induced alteration in the protein expression of DNMT1, DNMT3a and DNMT3b were analyzed by Western blotting.

RESULTSAfter treatment with TCE for 24 h, the cell proliferation level was significantly decreased in both cell lines. When concentrations of TCE were 0, 1.0, 2.0, 4.0 and 8.0 mmol/L, the proliferation levels of L-02 cells were 100.00±2.70, 83.34±2.38, 75.56±4.51, 71.67±2.77 and 66.67±1.63, respectively (F = 58.29, P < 0.001); the cell proliferation levels of SET deficient cells were 101.12±1.67, 85.01±2.33, 79.44±1.67, 78.337±3.89 and 76.11±3.33, respectively (F = 42.41, P < 0.001). When concentration of TCE reached 4.0 mmol/L, the difference of cell proliferation level between two groups was statistically significant (t = -3.51; P = 0.013). After treated by TCE for 24 h, the global DNA methylation significantly decreased in both cell lines (F value was 212.87 and 79.32, respectively, P < 0.001). The difference between two groups was not statistically significant. After treated by TCE for 24 h, the methyltransferases activities were significantly decreased in both cell cells (F values were 77.92 and 113.80, respectively, P-0.001). The SET deficiency could inhibit the decrease of methyltransferases activity under TCE treatment. When the concentration of TCE reached 8.0 mmol/L, the enzymatic activity of L-02 cells and SET deficient cells decreased to 67.61%±2.85% and 72.97%± 1.94%, respectively. The difference between two groups was statistically significant (t = -3.94, P = 0.008). After treated with TCE for 24 h, concentrations of TCE were 0, 1.0, 2.0, 4.0 and 8.0 mmol/L, and the relative protein levels of DNMT1 in normal L-02 cells increased significantly to 1.00±0.03, 1.28±0.04, 1.20±0.04, 1.62±0.05, 1.43±0.04 (F = 103.00, P < 0.001); In SET deficient cells, the expressions of DNMT1 were 1.00±0.04, 0.96±0.02, 1.19±0.05, 0.85±0.03, 0.83±0.03, which was significantly down-regulated under TCE treatment (F = 44.18, P < 0.001).

CONCLUSIONSET deficiency can significantly attenuate the TCE-induced decreases of cell viability and DNMTs activity, as well as alteration of protein expression of DNMT1 in L-02 cells, which indicated that SET was involved in the mechanism of TCE-induced cytotoxicity and epigenetic pathway in L-02 cells.

OBJECTIVE: To examine the expression of DNMT1, DNMT3a, and DNMT3b in the eutopic and ectopic endometrium in women with endometriosis. METHODS: RT-PCR and real-time RT-PCR were used to examine the expression of DNMT1, DNMT3a, and DNMT3b in the eutopic and ectopic endometrium in 20 women with endometriosis and the endometrium in 20 women without endometriosis. Immunofluorescene staining was used to detect the expression of DNMT1 in these tissues. RESULTS: The expression levels of DNMT1, DNMT3a, and DNMT3b were significantly lower in the ectopic endometrium and eutopic endometrium than those of the control endometium (P<0.05). The changes in the ectopic endometium compared with the control endometium were 0.44, 0.12, and 0.27 folds for DNMT1, DNMT3a, and DNMT3b, respectively, and these in the eutopic endometrium were 0.27, 0.13, and 0.15 folds for DNMT1,DNMT3a, and DNMT3b, respectively. The expression level of DNMT1, DNMT3a, and DNMT3b between the ectopic endometrium and eutopic endometrium was not significantly different (P>0.05 ). Immunofluorescence staining that DNMT1 protein level significantly decreased in the ectopic endometrium and eutopic endometrium of endometriosis patients. CONCLUSION Decreased expression levels of DNMT1, DNMT3a, and DNMT3b in the ectopic endometrium and eutopic endometrium may play a role in patients with abnormal epigenetics which may lead to endometriosis.
Adult ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases ; metabolism ; Endometriosis ; enzymology ; genetics ; Endometrium ; enzymology ; Epigenomics ; Female ; Humans