Evidence map›Paper›PMID 37082139›Full record

ArticleCell genomics2023

Escape from oncogene-induced senescence is controlled by POU2F2 and memorized by chromatin scars.

Ricardo Iván Martínez-Zamudio, Alketa Stefa, José Américo Nabuco Leva Ferreira Freitas, Themistoklis Vasilopoulos, Mark Simpson, Gregory Doré, Pierre-François Roux, Mark A Galan, Ravi J Chokshi, Oliver Bischof and 1 more

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

Article in Cell genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 42 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

11 authors at 3 institutions in 2 countries.

Ricardo Iván Martínez-ZamudioCenter for Cell Signaling, Department of Microbiology, Biochemistry, and Molecular Genetics, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
Alketa StefaCenter for Cell Signaling, Department of Microbiology, Biochemistry, and Molecular Genetics, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
José Américo Nabuco Leva Ferreira FreitasSorbonne Université, UMR 8256, Biological Adaptation and Ageing - IBPS, 75005 Paris, France.
Themistoklis VasilopoulosCenter for Cell Signaling, Department of Microbiology, Biochemistry, and Molecular Genetics, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
Mark SimpsonCenter for Cell Signaling, Department of Microbiology, Biochemistry, and Molecular Genetics, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
Gregory DoréInstitut Pasteur, Plasmodium RNA Biology Unit, 25 Rue du Docteur Roux, 75724 Cedex 15 Paris, France.
Pierre-François RouxIRCM, Institut de Recherche en Cancérologie de Montpellier, INSERM U1194, Université de Montpellier, Institut Régional du Cancer de Montpellier, Montpellier, France.
Mark A GalanDepartment of Pathology and Laboratory Medicine, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
Ravi J ChokshiDepartment of Surgery, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
Oliver BischofIMRB, Mondor Institute for Biomedical Research, INSERM U955 - Université Paris Est Créteil, UPEC, Faculté de Médecine de Créteil 8, rue du Général Sarrail, 94010 Créteil, France.
Utz HerbigCenter for Cell Signaling, Department of Microbiology, Biochemistry, and Molecular Genetics, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
Rutgers, The State University of New Jersey · USInserm · FRInstitut Pasteur · FR

Funding

Tumor Suppression by Telomere Dysfunction Induced SenescenceR01CA136533 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI HERBIG, UTZ · 2010 to 2021
$3.7M
NCI NIH HHS R01 CA136533
6 · The paper itself

Abstract

Although oncogene-induced senescence (OIS) is a potent tumor-suppressor mechanism, recent studies revealed that cells could escape from OIS with features of transformed cells. However, the mechanisms that promote OIS escape remain unclear, and evidence of post-senescent cells in human cancers is missing. Here, we unravel the regulatory mechanisms underlying OIS escape using dynamic multidimensional profiling. We demonstrate a critical role for AP1 and POU2F2 transcription factors in escape from OIS and identify senescence-associated chromatin scars (SACSs) as an epigenetic memory of OIS detectable during colorectal cancer progression. POU2F2 levels are already elevated in precancerous lesions and as cells escape from OIS, and its expression and binding activity to

Indexed as

AP-1cellular senescencecolorectal cancerOct-2OISOIS escapeoncogene-induced senescencePOU2F2SACSsenescence-associated chromatin scars

Identifiers

PMID37082139
PMCPMC10112333
OpenAlexW4362641068

What OpenQuestion holds

Textmetadata
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.