5 methylcytosine/breast neoplasms

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Accurate quantification of 5-Methylcytosine, 5-Hydroxymethylcytosine, 5-Formylcytosine, and 5-Carboxylcytosine in genomic DNA from breast cancer by chemical derivatization coupled with ultra performance liquid chromatography- electrospray quadrupole time of flight mass spectrometry analysis.

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The DNA demethylation pathway has been discovered to play a significant role in DNA epigenetics. This pathway removes the methyl group from cytosine, which is involved in the oxidation of 5-methylcytosine to 5-hydroxymethylcytosine (5-hmC) by ten-eleven translocation (TET) proteins. Then, 5-hmC can

Absence of methylation of CpG dinucleotides within the promoter of the breast cancer susceptibility gene BRCA2 in normal tissues and in breast and ovarian cancers.

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Germline mutations of the BRCA2 gene on chromosome 13q12-q13 predispose to the development of early-onset breast cancer and ovarian cancer. Loss of heterozygosity detected using chromosome 13q markers in the vicinity of BRCA2 is observed in most cancers arising in carriers of germline BRCA2

Methylation and silencing of the retinoic acid receptor-beta2 gene in breast cancer.

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BACKGROUND A growing body of evidence supports the hypotheses that the retinoic acid receptor beta2 (RAR-beta2) gene is a tumor suppressor gene and that the chemopreventive effects of retinoids are due to induction of RAR-beta2. RAR-beta2 expression is reduced in many malignant tumors, and we

Increased protein stability causes DNA methyltransferase 1 dysregulation in breast cancer.

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We report that DNA methyltransferase 1 (DNMT1) expression is dysregulated in breast cancer. The elevated protein levels are not a result of increased mRNA levels, but rather an increase in protein half-life. We found that DNMT1 protein levels were elevated in breast cancer tissues and in MCF-7

Genomic sequencing indicates a correlation between DNA hypomethylation in the 5' region of the pS2 gene and its expression in human breast cancer cell lines.

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The methylation status of the cytosines located on the 5' region of the pS2 gene have been investigated in two human breast cancer cell lines. The genomic sequencing method used is based on an oxydative deamination by NaHSO3 of the unmethylated cytosines, but not 5-methylcytosine. Data obtained

5-Carboxylcytosine levels are elevated in human breast cancers and gliomas.

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BACKGROUND DNA methylation (5-methylcytosine (5mC)) patterns are often altered in cancers. Ten-eleven translocation (Tet) proteins oxidise 5mC to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC). In addition to their presumptive specific biological roles, these

Hypermethylation of calcitonin gene regulatory sequences in human breast cancer as revealed by genomic sequencing.

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DNA methylation has been studied intensively during the past years in order to elucidate its role in the regulation of gene expression, gene imprinting and cancer progression. Earlier studies have shown that a general genomic under-methylation is associated with chronic lymphocytic leukemia and

Chromosome X genomic and epigenomic aberrations and clinical implications in breast cancer by base resolution profiling.

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OBJECTIVE Abnormal inactivation or loss of inactivated X chromosome (Xi) is implicated in women's cancer. However, the underlying mechanisms and clinical relevance are little known. METHODS High-throughput sequencing was conducted on breast cancer cell lines for copy number, RNA expression and

Homozygous deletion, rearrangement and hypermethylation implicate chromosome region 3p14.3-3p21.3 in sporadic breast-cancer development.

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DNAs from 19 malignant human breast tumors and 2 benign fibroadenomas were analyzed for heterozygosity at 5 polymorphic loci on the short arm of chromosome 3. One homozygous deletion and one rearrangement were identified using probe D3S2 which maps to 3p14.3-3p21.1. This probe also detected novel

Methylated DNA immunoprecipitation and microarray-based analysis: detection of DNA methylation in breast cancer cell lines.

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The methylated DNA immunoprecipitation microarray (MeDIP-chip) is a genome-wide, high-resolution approach to detect DNA methylation in whole genome or CpG (cytosine base followed by a guanine base) islands. The method utilizes anti-methylcytosine antibody to immunoprecipitate DNA that contains

DNA methylation of retinoic acid receptor beta in breast cancer and possible therapeutic role of 5-aza-2'-deoxycytidine.

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The retinoic acid receptor beta (RARbeta), a putative tumor suppressor gene, has been reported to be poorly expressed in breast cancer. In this report using the methylation-specific PCR reaction we observed DNA methylation in the promoter region of RARbeta in several primary breast tumors. DNA

Role of TET1 and 5hmC in an obesity-linked pathway driving cancer stem cells in triple-negative breast cancer

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Triple negative breast cancer (TNBC) is a subtype of breast cancer that lacks expression of estrogen receptor, progesterone receptor and the epidermal growth factor receptor 2 (HER2) but is enriched with cancer stem cell-like cells (CSCs). CSCs are the fraction of cancer cells recognized as the

Hypoxia Drives Breast Tumor Malignancy through a TET-TNFα-p38-MAPK Signaling Axis.

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Hypoxia is a hallmark of solid tumors that drives malignant progression by altering epigenetic controls. In breast tumors, aberrant DNA methylation is a prevalent epigenetic feature associated with increased risk of metastasis and poor prognosis. However, the mechanism by which hypoxia alters DNA

HMGA2/TET1/HOXA9 signaling pathway regulates breast cancer growth and metastasis.

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The ten-eleven translocation (TET) family of methylcytosine dioxygenases initiates demethylation of DNA and is associated with tumorigenesis in many cancers; however, the mechanism is mostly unknown. Here we identify upstream activators and downstream effectors of TET1 in breast cancer using human

Analysis of 5-methylcytosine in DNA of breast and colon cancer tissues.

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5-methylcytosine (m(5)C) can be used as a sensitive marker of progress of the tumor formation induced by the oxidative damage reactions. We have analyzed the amount of m(5)C in DNA of patients with breast and colon cancers. Two dimensional thin layer chromatography (TLC) has been used to monitor

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