Evidence map›Paper›PMID 35625984›Full record

ArticleCancers2022

Disentangling ERBB Signaling in Breast Cancer Subtypes-A Model-Based Analysis.

Svenja Kemmer, Mireia Berdiel-Acer, Eileen Reinz, Johanna Sonntag, Nooraldeen Tarade, Stephan Bernhardt, Mirjam Fehling-Kaschek, Max Hasmann, Ulrike Korf, Stefan Wiemann and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. 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

11 authors at 3 institutions in 1 country.

Svenja KemmerInstitute of Physics, University of Freiburg, 79104 Freiburg, Germany.ORCID 0000-0001-7708-0545
Mireia Berdiel-AcerDivision of Molecular Genome Analysis, German Cancer Research Center, 69120 Heidelberg, Germany.ORCID 0000-0002-9777-9457
Eileen ReinzDivision of Molecular Genome Analysis, German Cancer Research Center, 69120 Heidelberg, Germany.
Johanna SonntagDivision of Molecular Genome Analysis, German Cancer Research Center, 69120 Heidelberg, Germany.ORCID 0000-0002-5066-808X
Nooraldeen TaradeDivision of Molecular Genome Analysis, German Cancer Research Center, 69120 Heidelberg, Germany.ORCID 0000-0001-5301-6450
Stephan BernhardtDivision of Molecular Genome Analysis, German Cancer Research Center, 69120 Heidelberg, Germany.ORCID 0000-0002-8817-3672
Mirjam Fehling-KaschekInstitute of Physics, University of Freiburg, 79104 Freiburg, Germany.
Max HasmannRoche Diagnostics, 82377 Penzberg, Germany.
Ulrike KorfDivision of Molecular Genome Analysis, German Cancer Research Center, 69120 Heidelberg, Germany.
Stefan WiemannDivision of Molecular Genome Analysis, German Cancer Research Center, 69120 Heidelberg, Germany.ORCID 0000-0003-4683-3174
Jens TimmerInstitute of Physics, University of Freiburg, 79104 Freiburg, Germany.ORCID 0000-0003-4517-1383
German Cancer Research Center · DEUniversity of Freiburg · DERoche Pharma AG (Germany) · DE

Funding

Deutsche Forschungsgemeinschaft 390939984Else Kröner-Fresenius-Stiftung HEReFederal Ministry of Education and Research 031A429Federal Ministry of Education and Research 031L0048
6 · The paper itself

Abstract

Targeted therapies have shown striking success in the treatment of cancer over the last years. However, their specific effects on an individual tumor appear to be varying and difficult to predict. Using an integrative modeling approach that combines mechanistic and regression modeling, we gained insights into the response mechanisms of breast cancer cells due to different ligand-drug combinations. The multi-pathway model, capturing ERBB receptor signaling as well as downstream MAPK and PI3K pathways was calibrated on time-resolved data of the luminal breast cancer cell lines MCF7 and T47D across an array of four ligands and five drugs. The same model was then successfully applied to triple negative and HER2-positive breast cancer cell lines, requiring adjustments mostly for the respective receptor compositions within these cell lines. The additional relevance of cell-line-specific mutations in the MAPK and PI3K pathway components was identified via L

Indexed as

breast cancerERBB signalingmathematical modelingsignal transductionsystems biologytargeted therapy

Identifiers

PMID35625984
PMCPMC9139462
OpenAlexW4280552812

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.