The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Combined DNA Methyltransferase and Histone Deacetylase Inhibition in the Treatment of Myeloid Neoplasms
Open accessAbstract
Optimal reexpression of most genes silenced through promoter methylation requires the sequential application of DNA methyltransferase inhibitors followed by histone deacetylase inhibitors in tumor cell cultures. Patients with myelodysplastic syndrome or acute myeloid leukemia (AML) were treated with the methyltransferase inhibitor 5-azacitidine (aza-CR) followed by the histone deacetylase inhibitor sodium phenylbutyrate. Major responses associated with cytogenetic complete response developed in patients receiving prolonged dosing schedules of aza-CR. Bisulfite sequencing of the p15 promoter in marrow DNA during the first cycle of treatment showed heterogeneous allelic demethylation in three responding patients, suggesting ongoing demethylation within the tumor clone, but no demethylation in two nonresponders. Six of six responding patients with pretreatment methylation of p15 or CDH-1 promoters reversed methylation during the first cycle of therapy (methylation-specific PCR), whereas none of six nonresponders showed any demethylation. Gene demethylation correlated with the area under the aza-CR plasma concentration-time curve. Administration of both drugs was associated with induction of acetylation of histones H3 and H4. This study provides the first demonstration that molecular mechanisms responsible for responses to DNA methyltransferase/histone deacetylase inhibitor combinations may include reversal of aberrant epigenetic gene silencing. The promising percentage of major hematologic responses justifies the testing of such combinations in prospective randomized trials. (Cancer Res 2006; 66(12): 6361-9)
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DNA methylation patterns and epigenetic memory
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Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands.
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Self-citationInternational scoring system for evaluating prognosis in myelodysplastic syndromes
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Gene Silencing in Cancer in Association with Promoter Hypermethylation
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Self-citationCameron, E. E., Bachman, K. E., Myöhänen, S., Herman, J. G., & Baylin, S. B. (1999) · Nature Genetics · doi:10.1038/5047 · Cited by 1,857
Self-citationMethylation-Induced Repression— Belts, Braces, and Chromatin
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DNMT1 binds HDAC2 and a new co-repressor, DMAP1, to form a complex at replication foci
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Cited by
A decade of exploring the cancer epigenome—biological and translational implications
Baylin, S. B., & Jones, P. A. (2011) · Nature Reviews Cancer · doi:10.1038/nrc3130 · Cited by 2,871
Self-citationAnticancer activities of histone deacetylase inhibitors
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Fenaux, P., Mufti, G. J., Hellstrom-Lindberg, E., Santini, V., Finelli, C., Giagounidis, A., Schoch, R., Gattermann, N., Sanz, G., List, A., et al. (2009) · The Lancet Oncology · doi:10.1016/s1470-2045(09)70003-8 · Cited by 2,663
Self-citationEpigenetic Determinants of Cancer
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Self-citationReversal of H3K9me2 by a Small-Molecule Inhibitor for the G9a Histone Methyltransferase
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Metadata
- Authors
- Gore, S. D., Baylin, S., Sugar, E., Carraway, H., Miller, C. B., Carducci, M., Grever, M., Galm, O., Dauses, T., Karp, J. E., Rudek, M. A., Zhao, M., Smith, B. D., Manning, J., Jiemjit, A., Dover, G., Mays, A., Zwiebel, J., Murgo, A., Weng, L.-J., & Herman, J. G.
- Venue
- Cancer Research
- Published
- 2006-06-15
- Volume
- 66
- Issue
- 12
- Pages
- 6361-6369
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2163583950
- Cited by
- 474
- References
- 42
- FWCI
- 20.01
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Gore, S. D., Baylin, S., Sugar, E., Carraway, H., Miller, C. B., Carducci, M., Grever, M., Galm, O., Dauses, T., Karp, J. E., Rudek, M. A., Zhao, M., Smith, B. D., Manning, J., Jiemjit, A., Dover, G., Mays, A., Zwiebel, J., Murgo, A., . . . Herman, J. G. (2006). Combined DNA Methyltransferase and Histone Deacetylase Inhibition in the Treatment of Myeloid Neoplasms. Cancer Research. https://doi.org/10.1158/0008-5472.can-06-0080
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.