Restriction landmark genome scanning for aberrant methylation in primary refractory and relapsed acute myeloid leukemia; involvement of the WIT-1 gene

@article{Plass1999RestrictionLG,
  title={Restriction landmark genome scanning for aberrant methylation in primary refractory and relapsed acute myeloid leukemia; involvement of the WIT-1 gene},
  author={Christoph Plass and Feng Yu and Li Yu and Matthew P Strout and Wa'el El‐Rifai and Erkki Elonen and Sakari Knuutila and Guido Marcucci and Donn C. Young and William A. Held and Clara Derber Bloomfield and Michael A. Caligiuri},
  journal={Oncogene},
  year={1999},
  volume={18},
  pages={3159-3165}
}
There is substantial evidence to suggest that aberrant DNA methylation in the regulatory regions of expressed genes may play a role in hematologic malignancy. In the current report, the Restriction Landmark Genomic Scanning (RLGS) method was used to detect aberrant DNA methylation (M) in acute myeloid leukemia (AML). RLGS-M profiles were initially performed using DNA from diagnostic, remission, and relapse samples from a patient with AML. Rp18, one of the eight spots found that was absent in… 
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63 Citations

DNA methylation patterns at relapse in adult acute lymphocytic leukemia.

DNA methylation patterns are stable in a majority of patients with relapsed ALL, but a subset of patients acquire new methylation changes, in particular affecting cell cycle regulatory genes.

Novel methylation targets in de novo acute myeloid leukemia with prevalence of chromosome 11 loci.

Evidence for widespread aberrant methylation in AML is provided, with identification of novel methylation targets, epigenetic changes that appear unique to AML, and apparent preferential methylation on chromosome 11.

Early aberrant DNA methylation events in a mouse model of acute myeloid leukemia

This study identified early aberrantly methylated genes as potential contributors to onset and progression of AML, underscoring the relevance of the mouse model for human AML.

Restriction landmark genomic scanning for DNA methylation in cancer: past, present, and future applications.

Minimal Residual Disease in Acute Myeloid Leukemia

Because the fusion transcripts are thought to be specific to the leukemic cells, their detection in BM or blood from AML patients who achieve CR following intensive treatment has been used as a surrogate marker for minimal residual disease (MRD).

Quantitative analyses of DAPK1 methylation in AML and MDS

A refined DAPK1 methylation analysis in a large representative patient cohort of AML and MDS patients proofing almost complete absence of elevated DNA methylation is presented.

DNA methylation profiling in acute myeloid leukemia: from recent technological advances to biological and clinical insights.

An overview of current advances in deciphering the leukemic epigenome and its clinical relevance is provided and high-throughput analyses and genome-wide studies provide an optimal starting point for future epigenetic and integrative analyses that will further the development and use of predictive and prognostic epigenetic markers in acute myeloid leukemia.

DNA Methylation Markers in Patients with Gastrointestinal Cancers

The progress in the understanding of methylation in gastrointestinal tumors, the potential clinical applications ofmethylation-based markers and the process for the discovery and validation of highly specific and sensitive markers for the use in these applications are reviewed.

DNA methylation profiling: a new tool for evaluating hematologic malignancies.

These findings highlight the importance of DNA methylation in epigenetic control of early mammalian development as well as the role ofDNA methylation following embryogenesis, which is not resolved.

Hypermethylation of CpG sites at the promoter region is associated with deregulation of mitochondrial ATPsyn-β and chemoresistance in acute myeloid leukemia.

5-azacitidine(5-Aza)- a demethylating agent, could restore ATPsyn-β mRNA expression and increase the adriamycin sensitivity of primary leukemic cells from seven relapsed/ refractory AML patients.
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