Evidence map›Paper›PMID 29367757›Full record

ArticleOncogene2018

The miR-17/92 cluster is involved in the molecular etiology of the SCLL syndrome driven by the BCR-FGFR1 chimeric kinase.

Tianxiang Hu, Yating Chong, Haiyan Qin, Eiko Kitamura, Chang-Sheng Chang, Jeane Silva, Mingqiang Ren, John K Cowell

Abstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Review
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  5. Article
  6. Deciphering the role of microRNAs in mustard gas-induced toxicity.Annals of the New York Academy of Sciences · 2021
    Review
  7. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Tianxiang HuGeorgia Cancer Center, Augusta University, Augusta, GA, USA.
Yating ChongGeorgia Cancer Center, Augusta University, Augusta, GA, USA.
Haiyan QinGeorgia Cancer Center, Augusta University, Augusta, GA, USA.
Eiko KitamuraGeorgia Cancer Center, Augusta University, Augusta, GA, USA.
Chang-Sheng ChangGeorgia Cancer Center, Augusta University, Augusta, GA, USA.
Jeane SilvaGeorgia Cancer Center, Augusta University, Augusta, GA, USA.
Mingqiang RenGeorgia Cancer Center, Augusta University, Augusta, GA, USA.
John K CowellGeorgia Cancer Center, Augusta University, Augusta, GA, USA. jcowell@augusta.edu.

Funding

GENETIC ANALYSIS OF MYELOPROLIFERATIVE DISEASER01CA076167 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI COWELL, JOHN K · 1999 to 2024
$6.2M
NCI NIH HHS R01 CA076167
6 · The paper itself

Abstract

MicroRNAs (miRNAs) have pathogenic roles in the development of a variety of leukemias. Here we identify miRNAs that have important roles in the development of B lymphomas resulting from the expression of the chimeric BCR-FGFR1 kinase. The miR-17/92 cluster was particularly implicated and forced expression resulted in increased cell proliferation, while inhibiting its function using miRNA sponges reduced cell growth and induced apoptosis. Cells treated with the potent BGJ389 FGFR1 inhibitor led to miR-17/92 downregulation, suggesting regulation by FGFR1. Transient luciferase reporter assays and qRT-PCR detection of endogenous miR-17/92 expression in stable transduced cell lines demonstrated that BCR-FGFR1 can regulate miR-17/92 expression. This positive association of miR-17/92 with BCR-FGFR1 was also confirmed in primary mouse SCLL tissues and primary human CLL samples. miR-17/92 promotes cell proliferation and survival by targeting CDKN1A and PTEN in B-lymphoma cell lines and primary tumors. An inverse correlation in expression levels was seen between miR-17/92 and both CDKN1A and PTEN in two cohorts of CLL patients. Finally, in vivo engraftment studies demonstrated that manipulation of miR-17/92 was sufficient to affect BCR-FGFR1-driven leukemogenesis. Overall, our results define miR-17/92 as a downstream effector of FGFR1 in BCR-FGFR1-driven B-cell lymphoblastic leukemia.

Indexed as

AnimalsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHEK293 CellsHumansLymphomaMiceMice, Inbred BALB CMicroRNAsMultigene FamilyOncogene Proteins, FusionProto-Oncogene Proteins c-bcrReceptor, Fibroblast Growth Factor, Type 1SyndromeBCR protein, humanFGFR1 protein, humanMicroRNAsMIRN17 microRNA, humanMIRN92 microRNA, humanOncogene Proteins, FusionProto-Oncogene Proteins c-bcrReceptor, Fibroblast Growth Factor, Type 1

Identifiers

PMID29367757
PMCPMC5889328

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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.