Evidence map›Paper›PMID 28783166›Full record

ArticleOncogene2017

Anti-leukemic activity of microRNA-26a in a chronic lymphocytic leukemia mouse model.

L D'Abundo, E Callegari, A Bresin, A Chillemi, B K Elamin, P Guerriero, X Huang, E Saccenti, E M A A Hussein, F Casciano and 10 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  4. MicroRNAs in T Cell-Immunotherapy.International journal of molecular sciences · 2022
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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

20 authors at 9 institutions in 4 countries.

L D'AbundoDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
E CallegariDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
A BresinDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
A ChillemiLaboratory of Immunogenetics, Department of Medical Sciences, University of Torino, Torino, Italy.
B K ElaminMicrobiology Department, Faculty of Medical laboratory Sciences, University of Khartoum, Khartoum, Sudan.
P GuerrieroDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
X HuangNanoscale Science and Engineering Center for Affordable Nanoengineering of Polymeric Biomedical Devices, The Ohio State University, Columbus, OH, USA.
E SaccentiHematology Section, Department of Medical Sciences, University of Ferrara, University Hospital Arcispedale S. Anna, Ferrara, Italy.
E M A A HusseinDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
F CascianoDepartment of Morphology, Surgery, Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy.
P SecchieroDepartment of Morphology, Surgery, Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy.
G ZauliDepartment of Morphology, Surgery, Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy.
G A CalinDepartment of Experimental Therapeutics, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
G RussoLaboratorio di Oncologia Molecolare, Istituto Dermopatico dell'Immacolata, IDI-IRCCS, Rome, Italy.
L J LeeNanoscale Science and Engineering Center for Affordable Nanoengineering of Polymeric Biomedical Devices, The Ohio State University, Columbus, OH, USA.
C M CroceComprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
G MarcucciGehr Family Center For Leukemia Research Hematologic Malignancies Institute City of Hope, Duarte, CA, USA.
S SabbioniDepartment of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy.
F MalavasiLaboratory of Immunogenetics, Department of Medical Sciences, University of Torino, Torino, Italy.
M NegriniDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
University of Ferrara · ITThe Ohio State University · USAzienda Ospedaliera Citta' della Salute e della Scienza di Torino · ITIstituto Dermopatico dell'Immacolata · ITArcispedale Sant'Anna · ITCity of Hope · USThe University of Texas MD Anderson Cancer Center · USUniversity of Bisha · SAUniversity of Medical Sciences and Technology · SD

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of microRNAs (miRNAs) plays an important role in the pathogenesis of chronic lymphocytic leukemia (CLL). The Eμ-TCL1 transgenic mouse develops a form of leukemia that is similar to the aggressive type of human B-CLL, and this valuable model has been widely used for testing novel therapeutic approaches. Here, we adopted this model to investigate the potential effects of miR-26a, miR-130an and antimiR-155 in CLL therapy. Improved delivery of miRNA molecules into CLL cells was obtained by developing a novel system based on lipid nanoparticles conjugated with an anti-CD38 monoclonal antibody. This methodology has proven to be highly effective in delivering miRNA molecules into leukemic cells. Short- and long-term experiments showed that miR-26a, miR-130a and anti-miR-155 increased apoptosis after in vitro and in vivo treatment. Of this miRNA panel, miR-26a was the most effective in reducing leukemic cell expansion. Following long-term treatment, apoptosis was readily detectable by analyzing cleavage of PARP and caspase-7. These effects could be directly attributed to miR-26a, as confirmed by significant downregulation of its proven targets, namely cyclin-dependent kinase 6 and Mcl1. The results of this study are relevant to two distinct areas. The first is related to the design of a technical strategy and to the selection of CD38 as a molecular target on CLL cells, both consenting efficient and specific intracellular transfer of miRNA. The original scientific finding inferred from the above approach is that miR-26a can elicit in vivo anti-leukemic activities mediated by increased apoptosis.

Indexed as

Gene Expression Regulation, NeoplasticADP-ribosyl Cyclase 1AnimalsAntibodies, Monoclonal, Murine-DerivedApoptosisCaspase 7Cell Line, TumorCyclin-Dependent Kinase 6Down-RegulationDrug Delivery SystemsFemaleHumansLeukemia, Lymphocytic, Chronic, B-CellLipidsMembrane GlycoproteinsMiceADP-ribosyl Cyclase 1Antibodies, Monoclonal, Murine-DerivedCasp7 protein, mouseCaspase 7Cd38 protein, mouseCdk6 protein, mouseCyclin-Dependent Kinase 6LipidsMcl1 protein, mouseMembrane GlycoproteinsMicroRNAsMIRN130 microRNA, mouseMirn155 microRNA, mouseMirn26 microRNA, mouseMyeloid Cell Leukemia Sequence 1 ProteinPoly(ADP-ribose) PolymerasesProto-Oncogene ProteinsTcl1 protein, mouse

Identifiers

PMID28783166
OpenAlexW2744185357

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.