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We began analyzing https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1007/s13148-011-0041-7, but it redirected us to https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1007/s13148-011-0041-7. The analysis below is for the second page.

Title[redir]:
Epigenetic regulation of prostate cancer | Clinical Epigenetics | Full Text
Description:
Prostate cancer is a commonly diagnosed cancer in men and a leading cause of cancer deaths. Whilst the underlying mechanisms leading to prostate cancer are still to be determined, it is evident that both genetic and epigenetic changes contribute to the development and progression of this disease. Epigenetic changes involving DNA hypo- and hypermethylation, altered histone modifications and more recently changes in microRNA expression have been detected at a range of genes associated with prostate cancer. Furthermore, there is evidence that particular epigenetic changes are associated with different stages of the disease. Whilst early detection can lead to effective treatment, and androgen deprivation therapy has a high response rate, many tumours develop towards hormone-refractory prostate cancer, for which there is no successful treatment. Reliable markers for early detection and more effective treatment strategies are, therefore, needed. Consequently, there is a considerable interest in the potential of epigenetic changes as markers or targets for therapy in prostate cancer. Epigenetic modifiers that demethylate DNA and inhibit histone deacetylases have recently been explored to reactivate silenced gene expression in cancer. However, further understanding of the mechanisms and the effects of chromatin modulation in prostate cancer are required. In this review, we examine the current literature on epigenetic changes associated with prostate cancer and discuss the potential use of epigenetic modifiers for treatment of this disease.

Matching Content Categories {๐Ÿ“š}

  • Health & Fitness
  • Education
  • Science

Content Management System {๐Ÿ“}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {๐Ÿ“ˆ}

What is the average monthly size of doi.org audience?

๐Ÿš„ Respectable Traffic: 10k - 20k visitors per month


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How Does Doi.org Make Money? {๐Ÿ’ธ}

We see no obvious way the site makes money.

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Keywords {๐Ÿ”}

cancer, prostate, pubmed, google, scholar, dna, cell, expression, methylation, gene, cells, hypermethylation, histone, study, genes, tumour, lines, found, gstp, treatment, human, promoter, res, samples, central, epigenetic, studies, mirnas, hypomethylation, progression, tumours, growth, lncap, individuals, combination, potential, levels, modifications, androgen, cpg, patients, effects, metastatic, vivo, metastasis, hkme, mice, clin, cancers, inhibitors,

Topics {โœ’๏ธ}

pi-class glutathione s-transferase ฯ€-class glutathione-s-transferase promote androgen-receptor-dependent transcription tnfalpha-related apoptosis-inducing ligand post-prostate massage-voided urine tumor suppressor pten/mmac1 lymph-node-positive prostate cancers prostate-tumour-bearing mouse model cyclin-dependent kinase 2a hormone-independent cell lines stimulating ar-dependent transcription hormone-refractory prostate cancer ar-positive cell lines androgen-independent cell lines hormone-refractory prostate cancers s100 calcium-binding protein cd44โ€‰+โ€‰alpha2beta1+ cell population free prostate-specific antigen retinoid-resistant prostate cancer castration-resistant prostate cancer ar-negative cell lines hif-1alpha/hif-1beta p53-defective cell lines hormone-independent prostate cancer cell-free circulating dna open access article increased cell-free dna quantitative methylation-specific pcr prostate cancer-related proteins androgen-independent prostate cancer develop androgen-independent status gene-specific hypermethylation events gene-specific hypomethylation events cell-free plasma dna cell-free dna hypermethylation cell-free dna appears rarฮฒ2 promoter-luciferase gene multi-platform mirna screening cancer-related genomic regions polycomb repression signature late-stage prostate cancer demonstrated anti-tumourigenic activities privacy choices/manage cookies prostate cancer-specific genes prostate-cancer-specific genes ectopic mir-34a expression demethylating agent 5-aza-2โ€ฒdeoxycitidine nucleoside inhibitor 5-aza-2โ€ฒ-deoxycytidine decitabine-mediated gene expression human cell lines

Questions {โ“}

  • Brothman AR, Swanson G, Maxwell TM, Cui J, Murphy KJ, Herrick J, Speights VO, Isaac J, Rohr LR (2005) Global hypomethylation is common in prostate cancer cells: a quantitative predictor for clinical outcome?
  • Halliwell B (2006) Oxidative stress and neurodegeneration: where are we now?
  • Schwartz G, Hulka B (1990) Is vitamin D deficiency a risk factor for prostate cancer?

Schema {๐Ÿ—บ๏ธ}

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         headline:Epigenetic regulation of prostate cancer
         description:Prostate cancer is a commonly diagnosed cancer in men and a leading cause of cancer deaths. Whilst the underlying mechanisms leading to prostate cancer are still to be determined, it is evident that both genetic and epigenetic changes contribute to the development and progression of this disease. Epigenetic changes involving DNA hypo- and hypermethylation, altered histone modifications and more recently changes in microRNA expression have been detected at a range of genes associated with prostate cancer. Furthermore, there is evidence that particular epigenetic changes are associated with different stages of the disease. Whilst early detection can lead to effective treatment, and androgen deprivation therapy has a high response rate, many tumours develop towards hormone-refractory prostate cancer, for which there is no successful treatment. Reliable markers for early detection and more effective treatment strategies are, therefore, needed. Consequently, there is a considerable interest in the potential of epigenetic changes as markers or targets for therapy in prostate cancer. Epigenetic modifiers that demethylate DNA and inhibit histone deacetylases have recently been explored to reactivate silenced gene expression in cancer. However, further understanding of the mechanisms and the effects of chromatin modulation in prostate cancer are required. In this review, we examine the current literature on epigenetic changes associated with prostate cancer and discuss the potential use of epigenetic modifiers for treatment of this disease.
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      headline:Epigenetic regulation of prostate cancer
      description:Prostate cancer is a commonly diagnosed cancer in men and a leading cause of cancer deaths. Whilst the underlying mechanisms leading to prostate cancer are still to be determined, it is evident that both genetic and epigenetic changes contribute to the development and progression of this disease. Epigenetic changes involving DNA hypo- and hypermethylation, altered histone modifications and more recently changes in microRNA expression have been detected at a range of genes associated with prostate cancer. Furthermore, there is evidence that particular epigenetic changes are associated with different stages of the disease. Whilst early detection can lead to effective treatment, and androgen deprivation therapy has a high response rate, many tumours develop towards hormone-refractory prostate cancer, for which there is no successful treatment. Reliable markers for early detection and more effective treatment strategies are, therefore, needed. Consequently, there is a considerable interest in the potential of epigenetic changes as markers or targets for therapy in prostate cancer. Epigenetic modifiers that demethylate DNA and inhibit histone deacetylases have recently been explored to reactivate silenced gene expression in cancer. However, further understanding of the mechanisms and the effects of chromatin modulation in prostate cancer are required. In this review, we examine the current literature on epigenetic changes associated with prostate cancer and discuss the potential use of epigenetic modifiers for treatment of this disease.
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