Evidence map›Paper›PMID 28596283›Full record

ArticleHaematologica2017

Combined targeting of STAT3 and STAT5: a novel approach to overcome drug resistance in chronic myeloid leukemia.

Karoline V Gleixner, Mathias Schneeweiss, Gregor Eisenwort, Daniela Berger, Harald Herrmann, Katharina Blatt, Georg Greiner, Konstantin Byrgazov, Gregor Hoermann, Marina Konopleva and 9 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

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  11. [Mechanism of STAT3 phosphorylation mediated leukemia cells resistance to doxorubicin].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2020
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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

19 authors at 7 institutions in 4 countries.

Karoline V GleixnerDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Austria karoline.gleixner@meduniwien.ac.at.
Mathias SchneeweissLudwig Boltzmann Cluster Oncology, Medical University of Vienna, Austria.
Gregor EisenwortLudwig Boltzmann Cluster Oncology, Medical University of Vienna, Austria.
Daniela BergerDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Austria.
Harald HerrmannLudwig Boltzmann Cluster Oncology, Medical University of Vienna, Austria.
Katharina BlattDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Austria.
Georg GreinerDepartment of Laboratory Medicine, Medical University of Vienna, Austria.
Konstantin ByrgazovChildren's Cancer Research Institute (CCRI), Vienna, Austria.
Gregor HoermannLudwig Boltzmann Cluster Oncology, Medical University of Vienna, Austria.
Marina KonoplevaDepartment of Leukemia, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Islam WaliulInstitute of Drug Delivery Sciences, Sojo University, Kumamoto and BioDynamics Research Laboratory, Kumamoto, Japan.
Abbarna A CumaraswamyDepartment of Chemistry, University of Toronto, Canada.
Patrick T GunningDepartment of Chemistry, University of Toronto, Canada.
Hiroshi MaedaInstitute of Drug Delivery Sciences, Sojo University, Kumamoto and BioDynamics Research Laboratory, Kumamoto, Japan.
Richard MorigglLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Michael DeiningerDivision of Hematology and Hematologic Malignancies, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA.
Thomas LionChildren's Cancer Research Institute (CCRI), Vienna, Austria.
Michael AndreeffDepartment of Leukemia, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Peter ValentDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Austria.
Medical University of Vienna · ATLudwig Boltzmann Cluster for Cardiovascular Research · ATSojo University · JPThe University of Texas MD Anderson Cancer Center · USUniversity of Toronto · CALudwig Boltzmann Institute for Cancer Research · ATUniversity of Utah · US

Funding

Mechanisms of resistance to ponatinib therapy in chronic myeloid leukemiaR01CA178397 · NCI · UNIVERSITY OF UTAH · PI DEININGER, MICHAEL W., O'HARE, THOMAS J. · 2014 to 2018
$2.6M
NCI NIH HHS R01 CA178397
6 · The paper itself

Abstract

In chronic myeloid leukemia, resistance against BCR-ABL1 tyrosine kinase inhibitors can develop because of

Indexed as

Drug Delivery SystemsAdultAgedAged, 80 and overCell Line, TumorDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiddle AgedNeoplastic Stem CellsProtein Kinase InhibitorsSTAT3 Transcription FactorSTAT5 Transcription FactorBCR-ABL1 fusion protein, humanFusion Proteins, bcr-ablProtein Kinase InhibitorsSTAT3 protein, humanSTAT3 Transcription FactorSTAT5 Transcription Factor

Identifiers

PMID28596283
PMCPMC5685220
OpenAlexW2624005914

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.