ReviewBriefings in functional genomics2011
Dynamics of epigenetic modifications in leukemia.
Review in Briefings in functional genomics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- KCTD15 deregulation is associated with alterations of the NF-κB signaling in both pathological and physiological model systems.Scientific reports · 2021Trial
- Deciphering the role of Wnt signaling in acute myeloid leukemia prognosis: how alterations in DNA methylation come into play in patients' prognosis.Journal of cancer research and clinical oncology · 2020Review
- Epimutational profile of hematologic malignancies as attractive target for new epigenetic therapies.Oncotarget · 2016Review
- Characterising the epigenome as a key component of the fetal exposome in evaluating in utero exposures and childhood cancer risk.Mutagenesis · 2015Review
- Targeting Histone Deacetylases in Diseases: Where Are We?Antioxidants & redox signaling · 2015Review
- ZRF1 controls the retinoic acid pathway and regulates leukemogenic potential in acute myeloid leukemia.Oncogene · 2014Article
- Inhibition of histone methyltransferase EZH2 depletes leukemia stem cell of mixed lineage leukemia fusion leukemia through upregulation of p16.Cancer science · 2014Article
- HDAC3 is essential for DNA replication in hematopoietic progenitor cells.The Journal of clinical investigation · 2013Article
- TET proteins: on the frenetic hunt for new cytosine modifications.Briefings in functional genomics · 2013Review
- Mechanisms of epigenetic regulation of leukemia onset and progression.Advances in immunology · 2013Review
- Chromatin remodeling in cancer: a gateway to regulate gene transcription.Molecular oncology · 2012Review
- The HARE-HTH and associated domains: novel modules in the coordination of epigenetic DNA and protein modifications.Cell cycle (Georgetown, Tex.) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromatin modifications at both histones and DNA are critical for regulating gene expression. Mis-regulation of such epigenetic marks can lead to pathological states; indeed, cancer affecting the hematopoietic system is frequently linked to epigenetic abnormalities. Here, we discuss the different types of modifications and their general impact on transcription, as well as the polycomb group of proteins, which effect transcriptional repression and are often mis-regulated. Further, we discuss how chromosomal translocations leading to fusion proteins can aberrantly regulate gene transcription through chromatin modifications within the hematopoietic system. PML-RARa, AML1-ETO and MLL-fusions are examples of fusion proteins that mis-regulate epigenetic modifications (either directly or indirectly), which can lead to acute myeloblastic leukemia (AML). An in-depth understanding of the mechanisms behind the mis-regulation of epigenetic modifications that lead to the development and progression of AMLs could be critical for designing effective treatments.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.