Relevant bibliographies by topics / Methylation frequencies

Academic literature on the topic 'Methylation frequencies'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Methylation frequencies"

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Cusack, Martin, and Paul Scotting. "DNA methylation in germ cell tumour aetiology: current understanding and outstanding questions." REPRODUCTION 146, no. 2 (August 2013): R49—R60. http://dx.doi.org/10.1530/rep-12-0382.

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Germ cell tumours (GCTs) are a diverse group of neoplasms that can be histologically subclassified as either seminomatous or non-seminomatous. These two subtypes have distinct levels of differentiation and clinical characteristics, the non-seminomatous tumours being associated with poorer prognosis. In this article, we review how different patterns of aberrant DNA methylation relate to these subtypes. Aberrant DNA methylation is a hallmark of all human cancers, but particular subsets of cancers show unusually high frequencies of promoter region hypermethylation. Such a ‘methylator phenotype’ has been described in non-seminomatous tumours. We discuss the possible cause of distinct methylation profiles in GCTs and the potential of DNA methylation to provide new targets for therapy. We also consider how recent developments in our understanding of this epigenetic modification and the development of genome-wide technologies are shedding new light on the role of DNA methylation in cancer aetiology.
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Jeong, D. H., M. Y. Youm, Y. N. Kim, K. B. Lee, M. S. Sung, H. K. Yoon, and K. T. Kim. "Promoter methylation of p16, DAPK, CDH1, and TIMP-3 genes in cervical cancer: correlation with clinicopathologic characteristics." International Journal of Gynecologic Cancer 16, no. 3 (2006): 1234–40. http://dx.doi.org/10.1136/ijgc-00009577-200605000-00043.

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This study was conducted to investigate the promoter methylation status of the p16, DAPK, CDH1, and TIMP-3 genes in primary cervical cancer and its correlation with clinicopathologic characteristics. Promoter methylation was evaluated using a methylation-specific polymerase chain reaction in 78 cervical cancer tissue specimens and 24 control, normal cervical tissue specimens. Clinicopathologic parameters were obtained from medical records, and the relationship between the discrete variables and the methylation status was evaluated. The frequencies of promoter methylation of p16, DAPK, CDH1, and TIMP-3 in cervical cancer were 57%, 44.9%, 52.6%, and 9%, respectively. Primary cervical cancer had significantly higher methylation frequencies for the p16 and DAPK promoters than did the control, normal cervix (P < 0.0001). The promoter methylation of TIMP-3 was significantly higher in adenocarcinoma than in squamous cell carcinoma (41.7% vs 3%, respectively, P = 0.0175). High-stage cancers exhibited an increased promoter methylation frequency for p16 (P = 0.0061). The promoter methylation of the p16 gene is a frequent event in cervical carcinogenesis and may have potential clinical application as a marker for the progression and prognosis of cancer.
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Jabbari, Kamel, and Giorgio Bernardi. "Cytosine methylation and CpG, TpG (CpA) and TpA frequencies." Gene 333 (May 2004): 143–49. http://dx.doi.org/10.1016/j.gene.2004.02.043.

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Yates, Phillip A., Robert Burman, James Simpson, Olga N. Ponomoreva, Mathew J. Thayer, and Mitchell S. Turker. "Silencing of Mouse Aprt Is a Gradual Process in Differentiated Cells." Molecular and Cellular Biology 23, no. 13 (July 1, 2003): 4461–70. http://dx.doi.org/10.1128/mcb.23.13.4461-4470.2003.

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ABSTRACT Mouse Aprt constructs that are highly susceptible to DNA methylation-associated inactivation in embryonal carcinoma cells were transfected into differentiated cells, where they were expressed. Construct silencing was induced by either whole-cell fusion of the expressing differentiated cells with embryonal carcinoma cells or by treatment of the differentiated cells with the DNA demethylating agent 5-aza-2′-deoxycytidine. Induction of silencing was enhanced significantly by the presence of a methylation center fragment positioned upstream of a truncated promoter comprised of two functional Sp1 binding sites. Initial silencing of the Aprt constructs was unstable, as evidenced by high spontaneous reversion frequencies (≈10−2). Stably silenced subclones with spontaneous reversion frequencies of <10−5 were isolated readily from the unstably silenced clones. These reversion frequencies were enhanced significantly by treatment of the cells with 5-aza-2′-deoxycytidine. A bisulfite sequence analysis demonstrated that CpG methylation initiated within the methylation center region on expressing alleles and that the induction of silencing allowed methylation to spread towards and eventually into the promoter region. Combined with the induction of revertants by 5-aza-2′-deoxycytidine, this result suggested that stabilization of silencing was due to an increased density of CpG methylation. All allelic methylation patterns were variegated, which is consistent with a gradual and evolving process. In total, our results demonstrate that silencing of mouse Aprt is a gradual process in the differentiated cells.
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Piras, Ignazio Stefano, Anna Costa, Maria Cristina Tirindelli, Andrea Stoccoro, Matthew J. Huentelman, Roberto Sacco, Fabio Coppedè, and Carla Lintas. "Genetic and epigenetic MTHFR gene variants in the mothers of attention-deficit/hyperactivity disorder affected children as possible risk factors for neurodevelopmental disorders." Epigenomics 12, no. 10 (May 2020): 813–23. http://dx.doi.org/10.2217/epi-2019-0356.

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Aim: To assess promoter methylation levels, gene expression levels and 677C>T/1298A>C genotype and allele frequencies of the MTHFR gene in 45 mothers of attention-deficit/hyperactivity disorder affected child/children (ADHDM) and compare it with age matched healthy control mothers (HCM). Materials & methods: High resolution melting analysis, quantitative real time PCR and PCR-RFLP were performed to assess methylation, gene expression and genotyping, respectively. Significance between ADHDM and HCM was assessed by linear (methylation and gene expression) and logistic regression (genotypes). Results: MTHFR gene expression levels were significantly higher in the ADHDM compared with the HCM group (adj-p < 7.7E-04). No differences in MTHFR promoter methylation level and 677C>T/1298A>C genotype frequencies were detected between ADHDM and HCM. Conclusion: We observed increased MTHFR expression levels not resulting from promoter methylation changes in ADHDM respect to HMC, potentially contributing to the ADHD condition in their children and deserving further investigation.
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Goyon, C., C. Barry, A. Grégoire, G. Faugeron, and J. L. Rossignol. "Methylation of DNA repeats of decreasing sizes in Ascobolus immersus." Molecular and Cellular Biology 16, no. 6 (June 1996): 3054–65. http://dx.doi.org/10.1128/mcb.16.6.3054.

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In Ascobolus immersus, DNA duplications are subject to the process of methylation induced premeiotically (MIP), which methylates the cytosine residues within the repeats and results in reversible gene silencing. The triggering of MIP requires pairing of the repeats, and its detection requires maintenance of the resulting methylation. MIP of kilobase-size duplications occurs frequently and leads to the methylation of all C residues in the repeats, including those belonging to non-CpG sequences. Using duplications of decreasing sizes, we observed that tandem repeats never escaped MIP when larger than 630 bp and showed a sudden and drastic drop in MIP frequencies when their sizes decreased from 630 to 317 bp. This contrasted with the progressive decrease of MIP frequencies observed with ectopic repeats, in which apparently the search for homology influences the MIP triggering efficiency. The minimal size actually required for a repeat to undergo detectable MIP was found to be close to 300 bp. Genomic sequencing and Southern hybridization analyses using restriction enzymes sensitive to C methylation showed a loss of methylation at non-CpG sites in short DNA segments, methylation being restricted to a limited number of CpG dinucleotides. Our data suggest the existence of two distinct mechanisms underlying methylation maintenance, one responsible for methylation at CpG sites and the other responsible for methylation at non-CpG sites.
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Derks, Sarah, Cindy Postma, Peter T. M. Moerkerk, Sandra M. van den Bosch, Beatriz Carvalho, Mario A. J. A. Hermsen, Walter Giaretti, et al. "Promoter Methylation Precedes Chromosomal Alterations in Colorectal Cancer Development." Analytical Cellular Pathology 28, no. 5-6 (January 1, 2006): 247–57. http://dx.doi.org/10.1155/2006/846251.

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Background: Colorectal cancers are characterized by genetic and epigenetic alterations. This study aimed to explore the timing of promoter methylation and relationship with mutations and chromosomal alterations in colorectal carcinogenesis. Methods: In a series of 47 nonprogressed adenomas, 41 progressed adenomas (malignant polyps), 38 colorectal carcinomas and 18 paired normal tissues, we evaluated promoter methylation status of hMLH1, O6MGMT, APC, p14ARF, p16INK4A, RASSF1A, GATA-4, GATA-5, and CHFR using methylation-specific PCR. Mutation status of TP53, APC and KRAS were studied by p53 immunohistochemistry and sequencing of the APC and KRAS mutation cluster regions. Chromosomal alterations were evaluated by comparative genomic hybridization. Results: Our data demonstrate that nonprogressed adenomas, progressed adenomas and carcinomas show similar frequencies of promoter methylation for the majority of the genes. Normal tissues showed significantly lower frequencies of promoter methylation of APC, p16INK4A, GATA-4, and GATA-5 (P-values: 0.02, 0.02, 1.1×10−5 and 0.008 respectively). P53 immunopositivity and chromosomal abnormalities occur predominantly in carcinomas (P values: 1.1×10−5 and 4.1×10−10). Conclusions: Since promoter methylation was already present in nonprogressed adenomas without chromosomal alterations, we conclude that promoter methylation can be regarded as an early event preceding TP53 mutation and chromosomal abnormalities in colorectal cancer development.
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Caban, Omar L., Aimee Pons, Nilka J. Barrios, and Adriana Baez. "Hypermethylation Status of Cancer-Associated Genes in Pediatric Acute Lymphoblastic Leukemia (ALL): Incidence and Potential Implications in Therapy." Blood 114, no. 22 (November 20, 2009): 4422. http://dx.doi.org/10.1182/blood.v114.22.4422.4422.

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Abstract Abstract 4422 Introduction Acute Lymphoblastic Leukemia (ALL) is the most common malignancy diagnosed in children, representing nearly one third of all pediatric cancers. Aberrant methylation of CpG island of the promoter region of genes causes gene silencing and could be critical in the initiation and progression ALL. Patients and Methods The study included a group of 10 de novo pediatric cases of ALL and 18 healthy control children. The cases were treated according to the University Children Hospital protocol and followed-up for 28 days. In the present study we assessed the methylation frequency of p14ARF, p15CDKN2B, p16CDKN2A, MLH1, CTNNB1, and APAF1 genes before cases started therapy (Day 0) and after completing the induction phase at Day 28. DNA was extracted from peripheral blood cells from cases and controls. Methylation status was performed using the MethyLight technique. The methylation index (MI; ratio between the number of genes methylated and the number of genes analyzed) was calculated and results were correlated to minimal residual disease (MRD) status of the cases. Results The gene most frequently methylated was p15CDKN2B (90% of cases on Day 0). Frequencies of p16CDKN2A, MLH1, CTNNB1 gene methylation were 80%, 70%, and 10% respectively. A coexistence of p15CDKN2B, p16CDKN2A and MLH1 gene methylation was observed. No patient showed methylation in p14ARF and APAF1 genes. The methylation index ranged from 0 to 0.67 with a median of 0.5. After induction therapy was completed (Day 28) the most frequently methylated gene was p15CDKN2B (80% of cases on Day 28). Frequencies of MLH1, p16CDKN2A, p14ARF and CTNNB1 gene methylation were 40%, 30%, 20% and 10% respectively. No patient showed methylation of the APAF1 genes on Day 28. The methylation index ranged from 0 to 0.67 with a median of 0.17 on Day 28. We found that after the induction treatment methylation of p15CDKN2B, p16CDKN2A, and MLH1 is a frequent event. Interestingly methylation of p14ARF was detected after induction. No significant differences in the frequencies of gene methylation and presence of minimal residual disease between patients with and without aberrant methylation, respectively, were found. We found that the methylation status was not associated with patient age at diagnosis, sex, FAB classification and cytogenetic changes. Conclusions Our findings suggest that aberrant methylation of p15CDKN2B gene is a frequent event in this pathology. The relationship between methylation of p15CDKN2B and leukemia has been reported previously. It appears that methylation of p15CDKN2B is an early event in ALL and continue to be present even after patients completed the induction treatment. Simultaneously, our data would confirm that, in our cohort, the methylation of p16CDKN2A and MLH1 gene promoters is a frequent event in pediatric ALL. However, to assess the impact of promoter methylation of these tumor suppressor genes on disease prognosis longer follow-up and a larger patient population is warranted. Disclosures: No relevant conflicts of interest to declare.
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Skeldal, Sune, Annelise Krogdahl, Jens Ahm Sørensen, Peter A. Andreasen, and Shan Gao. "CpG methylation of the PAI-1 gene 5’-flanking region is inversely correlated with PAI-1 mRNA levels in human cell lines." Thrombosis and Haemostasis 94, no. 09 (2005): 651–60. http://dx.doi.org/10.1160/th05-02-0114.

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SummaryThe physiological and pathophysiological functions of PAI-1 are related to its expression by specific cell types in normal and diseased tissues. We analysed the contribution of DNA methylation to the variation in PAI-1 mRNA levels in five cell lines. We found varying frequencies of methylation of 25 CpGs in the -805/+152 region of the PAI-1 gene in Bowes, MCF-7 and U937 cells, while little or no methylation was detected in Hep2 and HT-1080 cells. The methylation frequency was inversely correlated with PAI-1 mRNA level within its 20-fold range in Bowes, MCF-7,U937,and Hep2 cells, while the lack of methylation in both Hep2 and HT- 1080 cells suggested another mechanism behind the 150-fold higher level in HT-1080 cells than in Hep2 cells. However, all cell lines exhibited a high frequency of methylation of 10 CpGs in a CpG island at about -1800. Treatment with 5-aza-2‘-deoxycytidine led up to circa a 40-fold increase in the PAI-1 mRNA level and a strong decrease in the frequency of methylation in the -805/+152 region in Bowes, MCF-7 and U937. The histone deacetylase inhibitor trichostatin A induced a several fold increase of the PAI-1 mRNA level in cells with a high methylation frequency of the -805/+152 region. As compared with matched normal tissue, three samples of oral squamous cell carcinomas displayed decreased frequencies of methylation of the PAI-1 5' flanking region and increased levels of PAI-1 mRNA. These results for the first time implicate DNA methylation and histone acetylation in regulation of the PAI-1 gene, and indicate that without proper CpG islands in 5’-flanking region, trancription may be regulated by methylation of less dense CpGs in the 5’-flanking region rather than methylation of upstream CpG island.
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Zaletaev, Dmitry V., Vladimir V. Strelnikov, Tatiana V. Kekeeva, Valeria V. Zemliakova, Ekaterina B. Kuznetsova, and Dmitri S. Mikhaylenko. "Methylation anomalies in cancerogenesis: search for new genes, development of methods and DNA-markers for diagnosis." Ecological genetics 9, no. 3 (September 15, 2011): 27–32. http://dx.doi.org/10.17816/ecogen9327-32.

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The report considers the epigenetic defects and their diagnostics in tumors. Aberrant methylation of the promoter or regulatory region of a gene results in its functional inactivation, which is phenotypically similar to structural deletion. Cancerogenesis-associated genes are often methylated in tumors. Tumors differ in methylation frequencies, allowing differential diagnostics. Aberrant methylation of tumor suppressor genes occurs in early cancerogenesis, and its detection may be employed in presymptomatic and noninvasive diagnostics of tumors.
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Book chapters on the topic "Methylation frequencies"

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Boyko, Alex, and Igor Kovalchuk. "Analysis of Mutation/Rearrangement Frequencies and Methylation Patterns at a Given DNA Locus Using Restriction Fragment Length Polymorphism." In Plant Epigenetics, 49–62. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-646-7_6.

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