Evidence map›Paper›PMID 28944080›Full record

ArticleNPJ systems biology and applications2017

Predicting ligand-dependent tumors from multi-dimensional signaling features.

Helge Hass, Kristina Masson, Sibylle Wohlgemuth, Violette Paragas, John E Allen, Mark Sevecka, Emily Pace, Jens Timmer, Joerg Stelling, Gavin MacBeath and 2 more

Abstract read
In one paragraph

Article in NPJ systems biology and applications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Review
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  8. Biased activation of the receptor tyrosine kinase HER2.Cellular and molecular life sciences : CMLS · 2023
    Article
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  18. Learning stable and predictive structures in kinetic systems.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  19. Extensions of ℓBMC bioinformatics · 2019
    Article
  20. Review
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

12 authors.

Helge HassMerrimack Pharmaceuticals, Inc., Cambridge, MA 02139 USA.ORCID 0000-0003-0577-2432
Kristina MassonMerrimack Pharmaceuticals, Inc., Cambridge, MA 02139 USA.
Sibylle WohlgemuthDepartment of Biosystems Science and Engineering and SIB Swiss Institute of Bioinformatics, ETH Zuerich, Zuerich, Switzerland.
Violette ParagasMerrimack Pharmaceuticals, Inc., Cambridge, MA 02139 USA.
John E AllenMerrimack Pharmaceuticals, Inc., Cambridge, MA 02139 USA.
Mark SeveckaMerrimack Pharmaceuticals, Inc., Cambridge, MA 02139 USA.
Emily PaceMerrimack Pharmaceuticals, Inc., Cambridge, MA 02139 USA.
Jens TimmerInstitute of Physics, University of Freiburg, Freiburg, Germany.
Joerg StellingDepartment of Biosystems Science and Engineering and SIB Swiss Institute of Bioinformatics, ETH Zuerich, Zuerich, Switzerland.
Gavin MacBeathMerrimack Pharmaceuticals, Inc., Cambridge, MA 02139 USA.
Birgit SchoeberlMerrimack Pharmaceuticals, Inc., Cambridge, MA 02139 USA.
Andreas RaueMerrimack Pharmaceuticals, Inc., Cambridge, MA 02139 USA.ORCID 0000-0002-9198-2489

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeted therapies have shown significant patient benefit in about 5-10% of solid tumors that are addicted to a single oncogene. Here, we explore the idea of ligand addiction as a driver of tumor growth. High ligand levels in tumors have been shown to be associated with impaired patient survival, but targeted therapies have not yet shown great benefit in unselected patient populations. Using an approach of applying Bagged Decision Trees (BDT) to high-dimensional signaling features derived from a computational model, we can predict ligand dependent proliferation across a set of 58 cell lines. This mechanistic, multi-pathway model that features receptor heterodimerization, was trained on seven cancer cell lines and can predict signaling across two independent cell lines by adjusting only the receptor expression levels for each cell line. Interestingly, for patient samples the predicted tumor growth response correlates with high growth factor expression in the tumor microenvironment, which argues for a co-evolution of both factors in vivo.

Identifiers

PMID28944080
PMCPMC5607260

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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.