Evidence map›Paper›PMID 25109330›Full record

ReviewOncogene2015

Tumor heterogeneity and plasticity as elusive drivers for resistance to MAPK pathway inhibition in melanoma.

A Roesch

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
7.3field-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

63 citing papers in PubMed, 114 citations in OpenAlex.

  1. AScience signaling · 2026
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  3. Review
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  14. Review
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  16. Connecting Metabolic Rewiring With Phenotype Switching in Melanoma.Frontiers in cell and developmental biology · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. Article

3 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

1 author at 1 institution in 1 country.

A RoeschUniversity Hospital Essen, Department of Dermatology, Essen, Germany.
Essen University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the recent success of MAPK signaling-targeted drugs in melanoma, the majority of patients with metastatic melanoma still undergo disease progression after initial tumor shrinkage indicating gradually developing therapy resistance. This review will give an overview on currently suggested concepts of resistance to MAPK pathway inhibitors in melanoma with particular focus on inter- and intraindividual as well as intratumor heterogeneity. The high plasticity of melanoma cells promotes both the clonal evolution of genetic resistance, for example, because of mutations in the MAPK or PI3K/AKT/PTEN pathways, and the emergence of cell phenotypes that functionally and metabolically overcome MAPK inhibition. Like a 'moving target', melanoma cells are shifting between different metabolic, cell cycle and differentiation states reflecting a highly dynamic potential to adapt to exogenous stressors including drugs. The introduction of MAPK inhibitors into the clinics has tremendously pushed the field of melanoma research not just because of the historic therapeutic success but also by providing a new tool to study human melanoma in its natural microenvironment.

Indexed as

Drug Resistance, NeoplasmGenetic HeterogeneityAnimalsAntineoplastic AgentsHumansMAP Kinase Signaling SystemMelanomaProtein Kinase InhibitorsAntineoplastic AgentsProtein Kinase Inhibitors

Identifiers

PMID25109330
OpenAlexW2074974517

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.