Evidence map›Paper›PMID 24117156›Full record

ReviewBritish journal of pharmacology2014

JNK signalling in cancer: in need of new, smarter therapeutic targets.

Concetta Bubici, Salvatore Papa

Open access · greenAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers.

0numbers the graph read from it
0cells of the map it votes in
181citing papers in PubMed
9.1field-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

181 citing papers in PubMed, 346 citations in OpenAlex.

  1. Review
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  7. Current issues in molecular biology · 2025
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121 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

2 authors at 2 institutions in 2 countries.

Concetta BubiciSection of Inflammation and Signal Transduction, Department of Medicine, Imperial College, London, UK; Biosciences Division, School of Health Sciences and Social Care, Brunel University, London, UK.
Salvatore Papa
Foundation for Liver Research · GBRMIT University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The JNKs are master protein kinases that regulate many physiological processes, including inflammatory responses, morphogenesis, cell proliferation, differentiation, survival and death. It is increasingly apparent that persistent activation of JNKs is involved in cancer development and progression. Therefore, JNKs represent attractive targets for therapeutic intervention with small molecule kinase inhibitors. However, evidence supportive of a tumour suppressor role for the JNK proteins has also been documented. Recent studies showed that the two major JNK proteins, JNK1 and JNK2, have distinct or even opposing functions in different types of cancer. As such, close consideration of which JNK proteins are beneficial targets and, more importantly, what effect small molecule inhibitors of JNKs have on physiological processes, are essential. A number of ATP-competitive and ATP-non-competitive JNK inhibitors have been developed, but have several limitations such as a lack of specificity and cellular toxicity. In this review, we summarize the accumulating evidence supporting a role for the JNK proteins in the pathogenesis of different solid and haematological malignancies, and discuss many challenges and scientific opportunities in the targeting of JNKs in cancer.

Indexed as

Drug DesignMolecular Targeted TherapyAnimalsAntineoplastic AgentsHumansJNK Mitogen-Activated Protein KinasesMolecular Sequence DataNeoplasmsProtein Kinase InhibitorsSignal TransductionAntineoplastic AgentsJNK Mitogen-Activated Protein KinasesProtein Kinase Inhibitorsapoptosiscancer targetshepatocellular carcinomaJNK1JNK2multiple myelomaPARP14survival

Identifiers

PMID24117156
PMCPMC3874694
OpenAlexW1598771153

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.