Evidence map›Paper›PMID 35534984›Full record

ReviewCancer science2022

Role of EMT in the DNA damage response, double-strand break repair pathway choice and its implications in cancer treatment.

Caroline Moyret-Lalle, Mélanie K Prodhomme, Delphine Burlet, Ayaka Kashiwagi, Virginie Petrilli, Alain Puisieux, Hiroyuki Seimiya, Agnès Tissier

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-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

18 citing papers in PubMed, 20 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 4 institutions in 3 countries.

Caroline Moyret-LalleINSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Centre of Lyon, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France.
Mélanie K ProdhommeDepartment of Epigenetics & Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Delphine BurletINSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Centre of Lyon, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France.
Ayaka KashiwagiDivision of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Virginie PetrilliINSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Centre of Lyon, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France.
Alain PuisieuxInstitut Curie, Versailles Saint-Quentin-en-Yvelines University, PSL Research University, Paris, France.
Hiroyuki SeimiyaDivision of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID https://orcid.org/0000-0003-3314-9736
Agnès TissierINSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Centre of Lyon, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France.ORCID https://orcid.org/0000-0002-5676-8719
Université Claude Bernard Lyon 1 · FRJapanese Foundation For Cancer Research · JPThe University of Texas MD Anderson Cancer Center · USUniversité de Versailles Saint-Quentin-en-Yvelines · FR

Funding

Agence Nationale de la Recherche ANR-10-LABX-0061Agence Nationale de la Recherche ANR-17-CONV-0002AMED P-CREATE 21cm0106184h0001JSPS KAKENHI 20H04789JSPS KAKENHI 20K21555Ligue Contre le Cancer EL2016.LNCC/AIPLigue Contre le Cancer EL2019.LNCC/AIPNippon Foundation
6 · The paper itself

Abstract

Numerous epithelial-mesenchymal transition (EMT) characteristics have now been demonstrated to participate in tumor development. Indeed, EMT is involved in invasion, acquisition of stem cell properties, and therapy-associated resistance of cancer cells. Together, these mechanisms offer advantages in adapting to changes in the tumor microenvironment. However, recent findings have shown that EMT-associated transcription factors (EMT-TFs) may also be involved in DNA repair. A better understanding of the coordination between the DNA repair pathways and the role played by some EMT-TFs in the DNA damage response (DDR) should pave the way for new treatments targeting tumor-specific molecular vulnerabilities, which result in selective destruction of cancer cells. Here we review recent advances, providing novel insights into the role of EMT in the DDR and repair pathways, with a particular focus on the influence of EMT on cellular sensitivity to damage, as well as the implications of these relationships for improving the efficacy of cancer treatments.

Indexed as

Epithelial-Mesenchymal TransitionNeoplasmsDNA DamageDNA RepairHumansTranscription FactorsTumor MicroenvironmentTranscription FactorsDNA damage responseDNA repairepithelial-mesenchymal transitionsynthetic lethalityZEB1

Identifiers

PMID35534984
PMCPMC9277259
OpenAlexW4229452321

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.