Evidence map›Paper›PMID 25188314›Full record

ArticlePLoS computational biology2014

Data-derived modeling characterizes plasticity of MAPK signaling in melanoma.

Marti Bernardo-Faura, Stefan Massen, Christine S Falk, Nathan R Brady, Roland Eils

Abstract read
In one paragraph

Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Computational models of melanoma.Theoretical biology & medical modelling · 2020
    Review
  6. Article
  7. Article
  8. Dynamic Targeting in Cancer Treatment.Frontiers in physiology · 2019
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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

5 authors.

Marti Bernardo-FauraDivision of Theoretical Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany; Institute of Pharmacy and Molecular Biotechnology (IPMB), Bioquant, Heidelberg University, Heidelberg, Germany.
Stefan MassenLysosomal Systems Biology, German Cancer Research Center (DKFZ), Bioquant, Heidelberg, Germany; Institute of Transplant Immunology, IFB-Tx, Hannover Medical School, Hannover, Germany.
Christine S FalkInstitute of Transplant Immunology, IFB-Tx, Hannover Medical School, Hannover, Germany; German Center for Infectious Diseases (DZIF) TTU-IICH, Hannover, Germany.
Nathan R BradySystems Biology of Cell Death Mechanisms, German Cancer Research Center (DKFZ), Bioquant, Heidelberg, Germany; Department of Surgery, Heidelberg University Hospital, Heidelberg, Germany.
Roland EilsDivision of Theoretical Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany; Institute of Pharmacy and Molecular Biotechnology (IPMB), Bioquant, Heidelberg University, Heidelberg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The majority of melanomas have been shown to harbor somatic mutations in the RAS-RAF-MEK-MAPK and PI3K-AKT pathways, which play a major role in regulation of proliferation and survival. The prevalence of these mutations makes these kinase signal transduction pathways an attractive target for cancer therapy. However, tumors have generally shown adaptive resistance to treatment. This adaptation is achieved in melanoma through its ability to undergo neovascularization, migration and rearrangement of signaling pathways. To understand the dynamic, nonlinear behavior of signaling pathways in cancer, several computational modeling approaches have been suggested. Most of those models require that the pathway topology remains constant over the entire observation period. However, changes in topology might underlie adaptive behavior to drug treatment. To study signaling rearrangements, here we present a new approach based on Fuzzy Logic (FL) that predicts changes in network architecture over time. This adaptive modeling approach was used to investigate pathway dynamics in a newly acquired experimental dataset describing total and phosphorylated protein signaling over four days in A375 melanoma cell line exposed to different kinase inhibitors. First, a generalized strategy was established to implement a parameter-reduced FL model encoding non-linear activity of a signaling network in response to perturbation. Next, a literature-based topology was generated and parameters of the FL model were derived from the full experimental dataset. Subsequently, the temporal evolution of model performance was evaluated by leaving time-defined data points out of training. Emerging discrepancies between model predictions and experimental data at specific time points allowed the characterization of potential network rearrangement. We demonstrate that this adaptive FL modeling approach helps to enhance our mechanistic understanding of the molecular plasticity of melanoma.

Indexed as

Models, BiologicalComputational BiologyFuzzy LogicHumansMAP Kinase Signaling SystemMelanomaPhosphorylation

Identifiers

PMID25188314
PMCPMC4154640

What OpenQuestion holds

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Registered trials

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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.