Evidence map›Paper›PMID 28707321›Full record

ArticleBritish journal of haematology2017

Expansion of BCR/ABL1

Leo Edlinger, Angelika Berger-Becvar, Ingeborg Menzl, Gregor Hoermann, Georg Greiner, Eva Grundschober, Zsuzsanna Bago-Horvath, Wael Al-Zoughbi, Gerald Hoefler, Christine Brostjan and 5 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of haematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

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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

15 authors at 4 institutions in 2 countries.

Leo EdlingerInstitute of Pharmacology and Toxicology, Department of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Angelika Berger-BecvarInstitute of Pharmacology and Toxicology, Department of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Ingeborg MenzlInstitute of Pharmacology and Toxicology, Department of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Gregor HoermannDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Georg GreinerDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Eva GrundschoberInstitute of Pharmacology and Toxicology, Department of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Zsuzsanna Bago-HorvathInstitute of Pharmacology and Toxicology, Department of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Wael Al-ZoughbiInstitute of Pathology, Medical University of Graz, Graz, Austria.
Gerald HoeflerInstitute of Pathology, Medical University of Graz, Graz, Austria.
Christine BrostjanDepartment of Surgery, Research Laboratories, Medical University of Vienna, Vienna General Hospital, Vienna, Austria.
Lars GilleInstitute of Pharmacology and Toxicology, Department of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Richard MorigglLudwig Boltzmann Institute for Cancer Research (LBI-CR), Vienna, Austria.
Andreas SpittlerCore Facility Flow Cytometry & Department of Surgery, Research Laboratories, Medical University of Vienna, Vienna, Austria.
Veronika SexlInstitute of Pharmacology and Toxicology, Department of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Andrea Hoelbl-KovacicInstitute of Pharmacology and Toxicology, Department of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.ORCID 0000-0001-6219-8794
University of Veterinary Medicine Vienna · ATMedical University of Vienna · ATMedical University of Graz · ATVienna General Hospital · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p21-activated kinases (PAKs) are key nodes in oncogenic signalling pathways controlling growth, survival, and motility of cancer cells. Their activity is increased in many human cancers and is associated with poor prognosis. To date, PAK deregulation has mainly been studied in solid tumours, where PAK1 and PAK4 are the main isoforms deregulated. We show that PAK1 and PAK2 are the critical isoforms in a BCR/ABL1

Indexed as

Cell ProliferationAnimalsCell Line, TumorEndothelial CellsExosomesExtracellular MatrixFusion Proteins, bcr-ablHematologic NeoplasmsHumansLeukemiaLymphomaMiceMice, Inbred NODNeovascularization, Pathologicp21-Activated KinasesBCR-ABL1 fusion protein, humanFusion Proteins, bcr-ablp21-Activated KinasesPAK1 protein, humanPAK2 protein, humanBCR/ABL1CMLexosomeslymphomap21-activated kinasesPAK2

Identifiers

PMID28707321
PMCPMC5655792
OpenAlexW2735470706

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.