Evidence map›Paper›PMID 41214145›Full record

ArticleScientific reports2025

Quantifying cancer- and drug-induced changes in Shannon information capacity of RTK signaling.

Paweł Nałęcz-Jawecki, Lee Roth, Frederic Grabowski, Sunnie Li, Marek Kochańczyk, Lukasz J Bugaj, Tomasz Lipniacki

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Paweł Nałęcz-Jawecki *Institute of Fundamental Technological Research, Polish Academy of Sciences, Warsaw, 02-106, Poland.
Lee Roth *Department of Bioengineering, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Frederic GrabowskiInstitute of Fundamental Technological Research, Polish Academy of Sciences, Warsaw, 02-106, Poland.
Sunnie LiDepartment of Bioengineering, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Marek KochańczykInstitute of Fundamental Technological Research, Polish Academy of Sciences, Warsaw, 02-106, Poland.
Lukasz J BugajDepartment of Bioengineering, University of Pennsylvania, Philadelphia, PA, 19104, USA. bugaj@seas.upenn.edu.
Tomasz LipniackiInstitute of Fundamental Technological Research, Polish Academy of Sciences, Warsaw, 02-106, Poland. tlipnia@ippt.pan.pl.

Funding

Harnessing protein clustering to understand, identify, and manipulate cellular systemsR35GM138211 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI Lukasz Bugaj · 2020 to 2026
$3.3M
Acquisition of a Cell Sorter for Systems Biology and Cellular EngineeringS10OD026986 · OD · UNIVERSITY OF PENNSYLVANIA · PI BUGAJ, LUKASZ · 2020 to 2020
$439k
Narodowe Centrum Nauki 2019/35/B/NZ2/03898NIGMS NIH HHS R35 GM138211NIH HHS R35GM138211NIH HHS S10 OD026986
6 · The paper itself

Abstract

Cancer can result from abnormal regulation of cells by their environment, potentially because cancer cells may misperceive environmental cues. However, the magnitude to which the oncogenic state alters cellular information processing has not been quantified. Here, we apply pseudorandom pulsatile optogenetic stimulation, live-cell imaging, and information theory to compare the information capacity of receptor tyrosine kinase (RTK) signaling pathways in EML4-ALK-driven lung cancer (STE-1) and in non-transformed (BEAS-2B) cells. The average information rate through RTK/ERK signaling in STE-1 cells was less than 0.5 bit/hour, compared to 7 bit/hour in BEAS-2B cells, but increased to 3 bit/hour after oncogene inhibition. Information was transmitted by 50-70% of cells, whose channel capacity (maximum information rate) was estimated through in silico protocol optimization. In BEAS-2B cells, channel capacity of the parallel RTK/calcineurin pathway surpassed that of the RTK/ERK pathway. This study highlights information capacity as a sensitive metric for identifying disease-associated dysfunction and evaluating the effects of targeted interventions.

Indexed as

Antineoplastic AgentsLung NeoplasmsReceptor Protein-Tyrosine KinasesSignal TransductionCell Line, TumorHumansMAP Kinase Signaling SystemOncogene Proteins, FusionAntineoplastic AgentsEML4-ALK fusion protein, humanOncogene Proteins, FusionReceptor Protein-Tyrosine KinasesCancerChannel capacityEML4-ALK oncogeneMAPK pathwayOptogenetics

Identifiers

PMID41214145
PMCPMC12603049

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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.