Evidence map›Paper›PMID 35273456›Full record

ArticleCurrent genomics2021

Deep Hidden Physics Modeling of Cell Signaling Networks.

Martin Seeger, James Longden, Edda Klipp, Rune Linding

Abstract read
In one paragraph

Article in Current genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

4 authors.

Martin SeegerHumboldt-Universitätzu Berlin, Theoretical Biophysics, Invalidenstr. 42, 10115 Berlin, Germany.
James LongdenRewire Tx, Humboldt-Universitätzu Berlin, Invalidenstr. 42, 10115 Berlin, Germany.
Edda KlippHumboldt-Universitätzu Berlin, Theoretical Biophysics, Invalidenstr. 42, 10115 Berlin, Germany.
Rune LindingHumboldt-Universitätzu Berlin, Theoretical Biophysics, Invalidenstr. 42, 10115 Berlin, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

According to the WHO, cancer is the second most common cause of death worldwide. The social and economic damage caused by cancer is high and rising. In Europe, the annual direct medical expenses alone amount to more than €129 billion. This results in an urgent need for new and sustainable therapeutics, which has currently not been met by the pharmaceutical industry; only 3.4% of cancer drugs entering Phase I clinical trials get to market. Phosphorylation sites are parts of the core machinery of kinase signaling networks, which are known to be dysfunctional in all types of cancer. Indeed, kinases are the second most common drug target yet. However, these inhibitors block all functions of a protein, and they commonly lead to the development of resistance and increased toxicity. To facilitate global and mechanistic modeling of cancer and clinically relevant cell signaling networks, the community will have to develop sophisticated data-driven deep-learning and mechanistic computational models that generate

Identifiers

PMID35273456
PMCPMC8822227

What OpenQuestion holds

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LicenceCC BY-NC
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.