Next-generation sequencing identifies major DNA methylation changes during progression of Ph+ chronic myeloid leukemia

Heller, Gerwin; Topakian, Thaïs; Altenberger, Corinna; Cerny-Reiterer, Sabine; Herndlhofer, Susanne; Ziegler, Barbara; Datlinger, Paul; Byrgazov, Konstantin; Bock, Christoph; Mannhalter, Christine; Hörmann, Georg; Sperr, Wolfgang R.; Lion, Thomas; Zielinski, Christoph; Valent, Peter; Zöchbauer‐Müller, Sabine

doi:10.1038/leu.2016.143

Cited by 52 publications

(55 citation statements)

References 57 publications

(71 reference statements)

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“…This technique has also been used to analyze differences in CpG site methylation in DNA from chronic phase (CP), accelerated phase (AP), and blast crisis (BC) of chronic myeloid leukemia (CML) patients and control individuals. The RRBS analysis showed a higher numbers of methylated CpGs in BC‐CML samples compared with other samples (Heller et al, ). In a recent study using RRBS, Ashktorab et al () reported a list of differentially methylated genes in colorectal neoplasia, tubulovillous adenoma, tubular adenoma, and normal samples.…”

Section: Bisulfite Conversion‐based Methodsmentioning

confidence: 99%

Comparison of genome‐wide analysis techniques to DNA methylation analysis in human cancer

Soozangar

Sadeghi

Jeddi

et al. 2017

Journal Cellular Physiology

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DNA methylation was the first epigenetic modification to be detected in human cancers with specific relation to aberrant gene expression. Herein, DNA methylation analysis explains how epigenetic patterns affect gene expression level. Hypermethylation at tumor suppressor gene loci leads to increased tumorigenesis due to tumor suppressor gene silencing, whereas global hypomethylation of CpG islands (CGIs) is followed by genomic instability and aberrant activation of multiple oncogenes. Therefore, characterization of the genes which silenced or activated epigenetically in human tumor cells can improve our understanding of cancer biology. Different genome-wide methodologies are applied to evaluate methylation status. Various commonly conducted techniques for this evaluation are reviewed in this paper. We provided comparative description of the procedures, advantages, and drawbacks of genome-wide DNA methylation analysis methods and biological applications, to give information on selecting the appropriate method for different methylation studies.

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Section: Bisulfite Conversion‐based Methodsmentioning

confidence: 99%

Comparison of genome‐wide analysis techniques to DNA methylation analysis in human cancer

Soozangar

Sadeghi

Jeddi

et al. 2017

Journal Cellular Physiology

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“…It has been reported for years that DNA-level epigenetic regulation plays a causative role in cancer and can thus be targeted for treatment of the disorder (19). In CML, Heller et al observed downregulated expression of many of these genes in BC-CML compared with CP-CML samples, using RNA-sequencing (20). However, a single DNA methylation change may act as a precipitating event in CML progression (21) and may provide a useful basis for revealing new targets of therapy in advanced CML.…”

Section: Discussionmentioning

confidence: 99%

The epigenetic effect of microRNA in BCR-ABL1-positive microvesicles during the transformation of normal hematopoietic transplants

Shen

Jiang

et al. 2017

Oncology Reports

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Epigenetics have been demonstrated to play a pivotal role in the progression of multiple cancers. Our previous study has demonstrated that microvesicles (MVs) derived from K562 cells could malignantly transform normal hematopoietic cells. The aim of this section was to elucidate the epigenetic effects of RNA in K562-MVs. We altered some epigenetic RNAs (miR-106a-5p, miR-106b-5p and lincPOU3F3) in K562-MVs and followed the process of transformation. Global DNA methylation and DNA methyltransferase (DNMT) levels were observed respectively. Our findings revealed that increased miR-106a/b in K562-MVs accelerated the transformation process (8.33±0.94 vs. 13.29±1.28 days; P<0.01) whereas decreased lincPOU3F3 delayed the transformation (17.83±0.29 days; P<0.05). The targets of miR-106a/b and lincPOU3F3 in the recipient cells were DNMT3a and DNMT3b. We found that lincPOU3F3 directly increased the DNMT3a/b while miR-106a/b only in part by targeting RB. However, global DNA methylation and special gene methylation was altered due to the concurrent regulation of DNMT3a and DNMT3b. Consequently, we demonstrated that tumor-derived MVs represent a notable intercellular epigenetic communication between cancer cells and recipient cells.

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“…Researchers investigate the mutations in IDH1 and IDH2 in acute myeloid leukemia (AML), chondrosarcoma, myelodysplastic syndromes, and cholangiocarcinoma (25)(26). Mutant IDH (mutIDH), and its associated molecular pathways can be an attractive therapeutic targets for AML due to limited treatment option (27). But their prevalence and prognostic impact remain to be explored in large extensively characterized CML and AML.…”

Section: E J M Rmentioning

confidence: 99%

A Comprehensive Review on the Role of Cell Growth and Apoptotic Genes Towards the Progression of CML

Fatima¹,

Mahdi²,

Afreen³

et al. 2019

EJMR

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Imatinib is a tyrosin kinase inhibitor, which has proven to be very effective in achieving high remission rates and improving prediction of treatment outcome. However a fraction of CML patients presents with resistance to this drug. Imatinib-based therapies were discontinued due to resistance and intolerance/noncompliance. the resistance for imatinib is developed due to the occurrence of point mutations in the BCR-ABL KD(kinase domain), although BCR-ABL amplification and impaired signaling pathways may contribute to the resistance. Other possible BCR-ABL independent mechanisms that influence resistance include reduced bioavailability of imatinib within Ph-positive cells, cytogenetic changes, disfunctionality of p53, and activation of alternative signaling pathways that promote cell survival and proliferation and reduced apoptosis. The achievement of Chronic myeloid leukemia (CML) is one of the most common leukemia. CML is described by a balanced genetic translocation, t(9;22)(q34;q11.2), in which the Abelson gene (ABL1) from chromosome 9q34 fused with the breakpoint cluster region (BCR) gene on chromosome 22q11.2. This genetic translocation is known as the Philadelphia chromosome. The molecular consequence of this translocation is the generation of a BCR-ABL1 fusion oncogene, which in turn translates into a BCR-ABL1 oncoprotein , which is the type of protein called a tyrosine kinase. This protein causes CML cells to grow and divide out of control. In a very small number of CML cases, the leukemia cells have the BCR-ABL oncogene but not the Philadelphia chromosome. It's thought that the BCR-ABL gene must form in a different way in these people. In an even smaller number of people who seem to have CML, neither the Philadelphia chromosome nor the BCR-ABL oncogene can be found. They might have other, unknown oncogenes causing their disease and are not considered to truly have CML.

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Next-generation sequencing identifies major DNA methylation changes during progression of Ph+ chronic myeloid leukemia

Cited by 52 publications

References 57 publications

Comparison of genome‐wide analysis techniques to DNA methylation analysis in human cancer

Comparison of genome‐wide analysis techniques to DNA methylation analysis in human cancer

The epigenetic effect of microRNA in BCR-ABL1-positive microvesicles during the transformation of normal hematopoietic transplants

A Comprehensive Review on the Role of Cell Growth and Apoptotic Genes Towards the Progression of CML

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