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@ARTICLE{BernardoFaura:119649,
author = {M. Bernardo-Faura$^*$ and S. Massen$^*$ and C. S. Falk and
N. Brady$^*$ and R. Eils$^*$},
title = {{D}ata-derived modeling characterizes plasticity of {MAPK}
signaling in melanoma.},
journal = {PLoS Computational Biology},
volume = {10},
number = {9},
issn = {1553-7358},
address = {San Francisco, Calif.},
publisher = {Public Library of Science},
reportid = {DKFZ-2017-00280},
pages = {e1003795 -},
year = {2014},
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.},
cin = {B080 / B170},
ddc = {570},
cid = {I:(DE-He78)B080-20160331 / I:(DE-He78)B170-20160331},
pnm = {312 - Functional and structural genomics (POF3-312)},
pid = {G:(DE-HGF)POF3-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:25188314},
pmc = {pmc:PMC4154640},
doi = {10.1371/journal.pcbi.1003795},
url = {https://inrepo02.dkfz.de/record/119649},
}