Evidence map›Paper›PMID 29921764›Full record

ReviewMolecules (Basel, Switzerland)2018

Targeting Transcription Factors for Cancer Treatment.

Mélanie Lambert, Samy Jambon, Sabine Depauw, Marie-Hélène David-Cordonnier

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed
16.0field-weighted citation impact, top 1% 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

206 citing papers in PubMed, 361 citations in OpenAlex.

  1. Trial
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  15. Enhancer regulation in cancer: from epigenetics to mArchives of pharmacal research · 2025
    Review
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  20. Review

146 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Mélanie LambertINSERM UMR-S1172-JPARC (Jean-Pierre Aubert Research Center), Lille University and Hospital Center (CHU-Lille), Institut pour la Recherche sur le Cancer de Lille (IRCL), Place de Verdun, F-59045 Lille, France. melanie.lambert@inserm.fr.ORCID 0000-0002-7472-4146
Samy JambonINSERM UMR-S1172-JPARC (Jean-Pierre Aubert Research Center), Lille University and Hospital Center (CHU-Lille), Institut pour la Recherche sur le Cancer de Lille (IRCL), Place de Verdun, F-59045 Lille, France. samy.jambon@inserm.fr.ORCID 0000-0001-7236-3239
Sabine DepauwINSERM UMR-S1172-JPARC (Jean-Pierre Aubert Research Center), Lille University and Hospital Center (CHU-Lille), Institut pour la Recherche sur le Cancer de Lille (IRCL), Place de Verdun, F-59045 Lille, France. sabine.depauw@inserm.fr.
Marie-Hélène David-CordonnierINSERM UMR-S1172-JPARC (Jean-Pierre Aubert Research Center), Lille University and Hospital Center (CHU-Lille), Institut pour la Recherche sur le Cancer de Lille (IRCL), Place de Verdun, F-59045 Lille, France. marie-helene.david@inserm.fr.ORCID 0000-0001-9831-5577
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcription factors are involved in a large number of human diseases such as cancers for which they account for about 20% of all oncogenes identified so far. For long time, with the exception of ligand-inducible nuclear receptors, transcription factors were considered as “undruggable” targets. Advances knowledge of these transcription factors, in terms of structure, function (expression, degradation, interaction with co-factors and other proteins) and the dynamics of their mode of binding to DNA has changed this postulate and paved the way for new therapies targeted against transcription factors. Here, we discuss various ways to target transcription factors in cancer models: by modulating their expression or degradation, by blocking protein/protein interactions, by targeting the transcription factor itself to prevent its DNA binding either through a binding pocket or at the DNA-interacting site, some of these inhibitors being currently used or evaluated for cancer treatment. Such different targeting of transcription factors by small molecules is facilitated by modern chemistry developing a wide variety of original molecules designed to specifically abort transcription factor and by an increased knowledge of their pathological implication through the use of new technologies in order to make it possible to improve therapeutic control of transcription factor oncogenic functions.

Indexed as

AnimalsAntineoplastic AgentsDrug Delivery SystemsHumansNeoplasm ProteinsNeoplasmsTranscription FactorsTranscription, GeneticAntineoplastic AgentsNeoplasm ProteinsTranscription FactorsDNA bindinginhibitorsoncogenesprotein/DNA interactionprotein/protein interactiontranscription factor

Identifiers

PMID29921764
PMCPMC6100431
OpenAlexW2809413985

What Socratic 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 Socratic graph.