Article in Nature communications, 2022. 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, 9 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
15 authors at 2 institutions in 2 countries.
R C NayakHoxworth Blood Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA. ramesh.nayak@uc.edu.ORCID 0000-0002-3206-8152
K H ChangDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
A K SinghHoxworth Blood Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
M KotliarEpigenomics Data Analysis Core, Divisions of Allergy & Immunology and Human Genetics, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.ORCID 0000-0002-6486-3898
M DesaiDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
A M WellendorfDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
M WunderlichDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
J BartramDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
B MizukawaDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.ORCID 0000-0002-3312-2982
M CuadradoInstituto de Biología Molecular y Celular del Cáncer, Centro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain.ORCID 0000-0001-9410-1205
P DexheimerDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.ORCID 0000-0003-3965-6894
A BarskiEpigenomics Data Analysis Core, Divisions of Allergy & Immunology and Human Genetics, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.ORCID 0000-0002-1861-5316
X R BusteloInstituto de Biología Molecular y Celular del Cáncer, Centro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain.ORCID 0000-0001-9398-6072
N N NassarDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.ORCID 0000-0003-0481-4784
J A CancelasHoxworth Blood Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA. jose.cancelas@uc.edu.ORCID 0000-0002-1291-7233
Cincinnati Children's Hospital Medical Center · USConsejo Superior de Investigaciones Científicas · ES
Funding
Xenotransplant and Genome Editing CoreU54DK126108 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Daniel Starczynowski, YI ZHENG · 2021 to 2026
$5.0M
Targeted Inhibition in LeukemiaR01CA237016 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI CANCELAS, JOSE A., NASSAR, NICOLAS · 2020 to 2023
$2.0M
Therapeutic insights through patient derived leukemia xenograftsR50CA211404 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI Mark Wunderlich · 2016 to 2026
$1.9M
SciDAP: Scientific Data Analysis PlatformR42HG011219 · NHGRI · DATIRIUM, LLC · PI BARSKI, ARTEM, KARTASHOV, ANDREY · 2022 to 2023
$1.6M
SciDAP: a next generation universal platform for collaborative data analysisR41HG011219 · NHGRI · DATIRIUM, LLC · PI BARSKI, ARTEM, KARTASHOV, ANDREY · 2020 to 2021
Acute B-cell lymphoblastic leukemia (B-ALL) results from oligo-clonal evolution of B-cell progenitors endowed with initiating and propagating leukemia properties. The activation of both the Rac guanine nucleotide exchange factor (Rac GEF) Vav3 and Rac GTPases is required for leukemogenesis mediated by the oncogenic fusion protein BCR-ABL. Vav3 expression becomes predominantly nuclear upon expression of BCR-ABL signature. In the nucleus, Vav3 interacts with BCR-ABL, Rac, and the polycomb repression complex (PRC) proteins Bmi1, Ring1b and Ezh2. The GEF activity of Vav3 is required for the proliferation, Bmi1-dependent B-cell progenitor self-renewal, nuclear Rac activation, protein interaction with Bmi1, mono-ubiquitination of H2A(K119) (H2AK119Ub) and repression of PRC-1 (PRC1) downstream target loci, of leukemic B-cell progenitors. Vav3 deficiency results in de-repression of negative regulators of cell proliferation and repression of oncogenic transcriptional factors. Mechanistically, we show that Vav3 prevents the Phlpp2-sensitive and Akt (S473)-dependent phosphorylation of Bmi1 on the regulatory residue S314 that, in turn, promotes the transcriptional factor reprogramming of leukemic B-cell progenitors. These results highlight the importance of non-canonical nuclear Rho GTPase signaling in leukemogenesis.
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.
Nuclear Vav3 is required for polycomb repression complex-1 activity in B-cell lymphoblastic leukemogenesis. · full record | OpenQuestion