Evidence map›Paper›PMID 24577400›Full record

ReviewNature reviews. Drug discovery2014

Targeting tumour-supportive cellular machineries in anticancer drug development.

Matthias Dobbelstein, Ute Moll

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Drug discovery, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
14.1field-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

89 citing papers in PubMed, 243 citations in OpenAlex.

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  17. Silver Nanoparticles Derived byInternational journal of molecular sciences · 2021
    Article
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  19. Article
  20. mTOR regulates GPVI-mediated platelet activation.Journal of translational medicine · 2021
    Article

29 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.

Matthias DobbelsteinInstitute of Molecular Oncology, Göttingen Center of Molecular Biosciences, Ernst Caspari Haus, University Medical Center Göttingen, 37077 Göttingen, Germany.
Ute Moll1] Institute of Molecular Oncology, Göttingen Center of Molecular Biosciences, Ernst Caspari Haus, University Medical Center Göttingen, 37077 Göttingen, Germany. [2] Department of Pathology, School of Medicine, Stony Brook University, Stony Brook, New York 11794, USA.
Stony Brook University · USUniversity of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traditional anticancer chemotherapeutics targeting DNA replication and cell division have severe side effects, but they have proved to be highly successful in treating some cancers. Drugs targeting signalling oncoproteins that have gained tumour-driving functions through mutations or overexpression were subsequently developed to increase specificity and thus reduce side effects, but have limitations such as the development of resistance. Now, a new wave of small-molecule anticancer agents is emerging, targeting complex multicomponent cellular machineries - including chromatin modifiers, heat shock protein chaperones and the proteasome - which thus interfere with those support systems that are more essential for cancer cells than for normal cells. Here, we provide our perspective on the advantages and limitations of agents that target tumour-supportive cellular machineries (other than those involving DNA replication), comparing them with agents that target signalling intermediates.

Indexed as

AnimalsAntibodies, MonoclonalAntineoplastic AgentsChromatinDrug Delivery SystemsDrug DiscoveryHeat-Shock ProteinsHumansNeoplasmsNeoplastic Cells, CirculatingSignal TransductionAntibodies, MonoclonalAntineoplastic AgentsChromatinHeat-Shock Proteins

Identifiers

PMID24577400
OpenAlexW2008324827

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.