Evidence map›Paper›PMID 24782508›Full record

ArticleBlood2014

TBLR1 fuses to retinoid acid receptor α in a variant t(3;17)(q26;q21) translocation of acute promyelocytic leukemia.

Yirui Chen, Shouyun Li, Chunlin Zhou, Chengwen Li, Kun Ru, Qing Rao, Haiyan Xing, Zheng Tian, Kejing Tang, Yingchang Mi and 3 more

Open access · bronzeAbstract readCase Reports
PubMed Publisher
In one paragraph

Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
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  8. [To construct Chinese hematology community].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2024
    Article
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  16. Case report: A rare case ofFrontiers in oncology · 2022
    Article
  17. Review
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  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Yirui ChenState Key Laboratory of Experimental Hematology.
Shouyun LiState Key Laboratory of Experimental Hematology.
Chunlin ZhouDepartment of Clinical Hematology, and.
Chengwen LiDepartment of Hematopathology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China; and.
Kun RuDepartment of Hematopathology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China; and.
Qing RaoState Key Laboratory of Experimental Hematology.
Haiyan XingState Key Laboratory of Experimental Hematology.
Zheng TianState Key Laboratory of Experimental Hematology.
Kejing TangState Key Laboratory of Experimental Hematology.
Yingchang MiDepartment of Clinical Hematology, and.
Baohong WangDepartment of Clinical Hematology, Weifang People's Hospital, Shandong, China.
Min WangState Key Laboratory of Experimental Hematology.
Jianxiang WangState Key Laboratory of Experimental Hematology, Department of Clinical Hematology, and.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNInstitute of Hematology & Blood Diseases Hospital · CNWeifang People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The majority of acute promyelocytic leukemia (APL) cases are characterized by the PML-RARα fusion gene. Although the PML-RARα fusion gene can be detected in >98% of APL cases, RARα is also found to be fused with other partner genes, which are also related to all-trans retinoic acid (ATRA)-dependent transcriptional activity and cell differentiation. In this study, we identified a novel RARα fusion gene, TBLR1-RARα (GenBank KF589333), in a rare case of APL with a t(3;17)(q26;q21),t(7;17)(q11.2;q21) complex chromosomal rearrangement. To our knowledge, TBLR1-RARα is the 10th RARα chimeric gene that has been reported up to now. TBLR1-RARα contained the B-F domains of RARα and exhibited a distinct subcellular localization. It could form homodimers and also heterodimers with retinoid X receptor α. As a result, TBLR1-RARα exhibited diminished transcriptional activity by recruitment of more transcriptional corepressors compared with RARα. In the presence of pharmacologic doses of ATRA, TBLR1-RARα could be degraded, and its homodimerization was abrogated. Moreover, when treated with ATRA, TBLR1-RARα could mediate the dissociation and degradation of transcriptional corepressors, consequent transactivation of RARα target genes, and cell differentiation induction in a dose- and time-dependent manner.

Indexed as

Amino Acid SequenceAntineoplastic AgentsBase SequenceCell DifferentiationChromosomes, Human, Pair 17Chromosomes, Human, Pair 3Cloning, MolecularDNA, NeoplasmHEK293 CellsHumansKaryotypingLeukemia, Promyelocytic, AcuteMaleMiddle AgedMolecular Sequence DataNuclear ProteinsAntineoplastic AgentsDNA, NeoplasmNuclear ProteinsOncogene Proteins, FusionRARA protein, humanReceptors, Cytoplasmic and NuclearReceptors, Retinoic AcidRepressor ProteinsRetinoic Acid Receptor alphaTBL1XR1 protein, humanTrans-ActivatorsTretinoin

Identifiers

PMID24782508
OpenAlexW2006243709

What OpenQuestion holds

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Registered trials

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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.