Evidence map›Paper›PMID 34728711›Full record

ArticleScientific reports2021

Simultaneous expression of MMB-FOXM1 complex components enables efficient bypass of senescence.

Ruchi Kumari, Holger Hummerich, Xu Shen, Martin Fischer, Larisa Litovchick, Sibylle Mittnacht, James A DeCaprio, Parmjit S Jat

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

7 citing papers in PubMed, 14 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

8 authors at 6 institutions in 3 countries.

Ruchi KumariMRC Prion Unit at UCL, UCL Institute of Prion Diseases, 33 Cleveland Street, London, W1W 7FF, UK.
Holger Hummerich *MRC Prion Unit at UCL, UCL Institute of Prion Diseases, 33 Cleveland Street, London, W1W 7FF, UK.
Xu Shen *The UCL Cancer Institute, Paul O'Gorman Building, 72 Huntley Street, London, WC1E 6DD, UK.
Martin Fischer *Computational Biology Group, Leibniz Institute on Aging - Fritz Lipmann Institute (FLI), Beutenbergstraße 11, 07745, Jena, Germany.
Larisa LitovchickDivision of Hematology, Oncology and Palliative Care, Department of Internal Medicine, Massey Cancer Centre, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Sibylle MittnachtThe UCL Cancer Institute, Paul O'Gorman Building, 72 Huntley Street, London, WC1E 6DD, UK.
James A DeCaprioDepartment of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA, 02215, USA.
Parmjit S JatMRC Prion Unit at UCL, UCL Institute of Prion Diseases, 33 Cleveland Street, London, W1W 7FF, UK. p.jat@prion.ucl.ac.uk.
University College London · GBCRUK Lung Cancer Centre of Excellence · GBDana-Farber Cancer Institute · USLeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEMRC Prion Unit · GBVirginia Commonwealth University · US

Funding

PROJECT 4: Interrogating PP2A Signaling in Human CancersP01CA203655 · NCI · DANA-FARBER CANCER INST · PI DECAPRIO, JAMES A. · 2017 to 2021
$8.0M
The DREAM B-Myb-MuvB complex controls sensitivity to DNA replication activators and inhibitorsR35CA232128 · NCI · DANA-FARBER CANCER INST · PI DECAPRIO, JAMES A. · 2019 to 2025
$7.2M
DYRK1A signaling in control of cell growth, proliferation and DNA damage repairR01CA188571 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LITOVCHICK, LARISA · 2015 to 2019
$2.0M
Role of the DREAM Complex in Head and Neck PreneoplasiaR21DE029927 · NIDCR · VIRGINIA COMMONWEALTH UNIVERSITY · PI LITOVCHICK, LARISA · 2020 to 2021
$427k
Commonwealth Scholarship Commission PhD scholarship INCS-2014-212German Research Foundation FI 1993/2-1NCI NIH HHS P01 CA203655NCI NIH HHS R01 CA188571NCI NIH HHS R35 CA232128NIDCR NIH HHS R21 DE029927
6 · The paper itself

Abstract

Cellular senescence is a stable cell cycle arrest that normal cells undergo after a finite number of divisions, in response to a variety of intrinsic and extrinsic stimuli. Although senescence is largely established and maintained by the p53/p21

Indexed as

Cellular SenescenceGene Expression RegulationBreastCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21E2F Transcription FactorsFemaleFibroblastsForkhead Box Protein M1HumansKv Channel-Interacting ProteinsMultiprotein ComplexesPhosphorylationRepressor ProteinsRetinoblastoma Binding ProteinsTrans-ActivatorsCDKN1A protein, humanCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21E2F Transcription FactorsForkhead Box Protein M1FOXM1 protein, humanKCNIP3 protein, humanKv Channel-Interacting ProteinsMultiprotein ComplexesMYBL2 protein, humanRB1 protein, humanRepressor ProteinsRetinoblastoma Binding ProteinsTP53 protein, humanTrans-ActivatorsTumor Suppressor Protein p53Ubiquitin-Protein LigasesYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID34728711
PMCPMC8563780
OpenAlexW3210830053

What OpenQuestion 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 OpenQuestion graph.