Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.8field-weighted citation impact, top 16% 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
6 citing papers in PubMed, 15 citations in OpenAlex.
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
13 authors at 3 institutions in 2 countries.
Rainer HubmannDepartment of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-6792-3876
Susanne SchnablDepartment of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, 1090 Vienna, Austria.
Mohammad AraghiDepartment of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, 1090 Vienna, Austria.
Christian SchmidlCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090 Vienna, Austria.ORCID 0000-0002-0522-202X
André F RendeiroCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090 Vienna, Austria.
Martin HilgarthDepartment of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, 1090 Vienna, Austria.
Dita DemirtasDepartment of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, 1090 Vienna, Austria.
Farghaly AliDepartment of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-4714-9710
Philipp B StaberDepartment of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, 1090 Vienna, Austria.
Peter ValentDepartment of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-0456-5095
Christoph ZielinskiDepartment of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, 1090 Vienna, Austria.
Ulrich JägerDepartment of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0001-9826-1062
Medhat ShehataDepartment of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0001-6891-646X
Medical University of Vienna · ATComprehensive Cancer Center Vienna · ATAustrian Academy of Sciences · AT
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
NOTCH signaling represents a promising therapeutic target in chronic lymphocytic leukemia (CLL). We compared the anti-neoplastic effects of the nuclear NOTCH2 inhibitor gliotoxin and the pan-NOTCH γ-secretase inhibitor RO4929097 in primary CLL cells with special emphasis on the individual roles of the different NOTCH receptors. Gliotoxin rapidly induced apoptosis in all CLL cases tested, whereas RO4929097 exerted a variable and delayed effect on CLL cell viability. Gliotoxin-induced apoptosis was associated with inhibition of the
Indexed as
AdultAgedAged, 80 and overAmyloid Precursor Protein SecretasesAntineoplastic AgentsApoptosisBenzazepinesCell SurvivalDose-Response Relationship, DrugDown-RegulationFemaleFluorocarbonsGliotoxinHumansLectins, C-TypeLeukemia, Lymphocytic, Chronic, B-Cell2,2-dimethyl-N-(6-oxo-6,7-dihydro-5H-dibenzo(b,d)azepin-7-yl)-N'-(2,2,3,3,3-pentafluoropropyl)malonamideAmyloid Precursor Protein SecretasesAntineoplastic AgentsBenzazepinesFCER2 protein, humanFluorocarbonsGliotoxinLectins, C-TypeNOTCH2 protein, humanNOTCH3 protein, humanNR4A1 protein, humanNuclear Receptor Subfamily 4, Group A, Member 1Receptor, Notch2Receptor, Notch3Receptors, IgERNA, MessengerATAC-seqbinary cell fate decisionCD5+ B-cell homeostasischronic lymphocytic leukemia (CLL)FCER2 (CD23)gliotoxinNOTCH2NOTCH3NR4A1positive/negative selectionRO4929097γ-secretase inhibitors
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.
Targeting Nuclear NOTCH2 by Gliotoxin Recovers a Tumor-Suppressor NOTCH3 Activity in CLL. · full record | Socratic