ReviewOncogene2001
Avian erythroleukemia: a model for corepressor function in cancer.
Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
14 citing papers in PubMed, 30 citations in OpenAlex.
- Shrinking to bird size with dinosaur-level cancer defences: Evolution of cancer suppression over macroevolutionary time.PLoS computational biology · 2025Article
- Molecular Landscapes and Models of Acute Erythroleukemia.HemaSphere · 2021Review
- The effect of oncoprotein v-erbA on thyroid hormone-regulated genes in hepatocytes and their potential role in hepatocellular carcinoma.Molecular biology reports · 2011Article
- Thyroid hormone receptor mutations in cancer and resistance to thyroid hormone: perspective and prognosis.Journal of thyroid research · 2011Article
- A conserved lysine in the thyroid hormone receptor-alpha1 DNA-binding domain, mutated in hepatocellular carcinoma, serves as a sensor for transcriptional regulation.Molecular cancer research : MCR · 2010Article
- Thyroid hormone receptor mutants implicated in human hepatocellular carcinoma display an altered target gene repertoire.Oncogene · 2009Article
- Thyroid hormone receptor mutations found in renal clear cell carcinomas alter corepressor release and reveal helix 12 as key determinant of corepressor specificity.Molecular endocrinology (Baltimore, Md.) · 2009Article
- Association of v-ErbA with Smad4 disrupts TGF-beta signaling.Molecular biology of the cell · 2009Article
- Erythroid and megakaryocytic transformation.Oncogene · 2007Review
- Article
- In vivo repression of an erythroid-specific gene by distinct corepressor complexes.The EMBO journal · 2002Article
- Critical residues within the BTB domain of PLZF and Bcl-6 modulate interaction with corepressors.Molecular and cellular biology · 2002Article
- Histone deacetylase inhibitors induce remission in transgenic models of therapy-resistant acute promyelocytic leukemia.The Journal of clinical investigation · 2001Article
- Chromatin remodeling: why it is important in cancer.Oncogene · 2001Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional regulation at the level of chromatin plays crucial roles during eukaryotic development and differentiation. A plethora of studies revealed that the acetylation status of histones is controlled by multi-protein complexes containing (de)acetylase activities. In the current model, histone deacetylases and acetyltransferases are recruited to chromatin by DNA-bound repressors and activators, respectively. Shifting the balance between deacetylation, i.e. repressive chromatin and acetylation, i.e. active chromatin can lead to aberrant gene transcription and cancer. In human acute promyelocytic leukemia (APL) and avian erythroleukemia (AEL), chromosomal translocations and/or mutations in nuclear hormone receptors, RARalpha [NR1B1] and TRalpha [NR1A1], yielded oncoproteins that deregulate transcription and alter chromatin structure. The oncogenic receptors are locked in their 'off' mode thereby constitutively repressing transcription of genes that are critical for differentiation of hematopoietic cells. AEL involves an oncogenic version of the chicken TRalpha, v-ErbA. Apart from repression by v-ErbA via recruitment of corepressor complexes, other repressors and corepressors appear to be involved in repression of v-ErbA target genes, such as carbonic anhydrase II (CAII). Reactivation of repressed genes in APL and AEL by chromatin modifying agents such as inhibitors of histone deacetylase or of methylation provides new therapeutic strategies in the treatment of acute myeloid leukemia.
Indexed as
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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.