Evidence map›Paper›PMID 38394152›Full record

ArticlePloS one2024

Boolean modeling of breast cancer signaling pathways uncovers mechanisms of drug synergy.

Kittisak Taoma, Marasri Ruengjitchatchawalya, Monrudee Liangruksa, Teeraphan Laomettachit

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

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  7. Leveraging preclinical models of metastatic breast cancer.Biochimica et biophysica acta. Reviews on cancer · 2024
    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

4 authors at 2 institutions in 1 country.

Kittisak TaomaBioinformatics and Systems Biology Program, School of Bioresources and Technology, King Mongkut's University of Technology Thonburi, Bangkok, Thailand.ORCID 0000-0002-8743-1393
Marasri RuengjitchatchawalyaBioinformatics and Systems Biology Program, School of Bioresources and Technology, King Mongkut's University of Technology Thonburi, Bangkok, Thailand.
Monrudee LiangruksaNational Nanotechnology Center, National Science and Technology Development Agency (NSTDA), Pathum Thani, Thailand.
Teeraphan LaomettachitBioinformatics and Systems Biology Program, School of Bioresources and Technology, King Mongkut's University of Technology Thonburi, Bangkok, Thailand.ORCID 0000-0003-3194-1391
King Mongkut's University of Technology Thonburi · THNational Science and Technology Development Agency · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is one of the most common types of cancer in females. While drug combinations have shown potential in breast cancer treatments, identifying new effective drug pairs is challenging due to the vast number of possible combinations among available compounds. Efforts have been made to accelerate the process with in silico predictions. Here, we developed a Boolean model of signaling pathways in breast cancer. The model was tailored to represent five breast cancer cell lines by integrating information about cell-line specific mutations, gene expression, and drug treatments. The models reproduced cell-line specific protein activities and drug-response behaviors in agreement with experimental data. Next, we proposed a calculation of protein synergy scores (PSSs), determining the effect of drug combinations on individual proteins' activities. The PSSs of selected proteins were used to investigate the synergistic effects of 150 drug combinations across five cancer cell lines. The comparison of the highest single agent (HSA) synergy scores between experiments and model predictions from the MDA-MB-231 cell line achieved the highest Pearson's correlation coefficient of 0.58 with a great balance among the classification metrics (AUC = 0.74, sensitivity = 0.63, and specificity = 0.64). Finally, we clustered drug pairs into groups based on the selected PSSs to gain further insights into the mechanisms underlying the observed synergistic effects of drug pairs. Clustering analysis allowed us to identify distinct patterns in the protein activities that correspond to five different modes of synergy: 1) synergistic activation of FADD and BID (extrinsic apoptosis pathway), 2) synergistic inhibition of BCL2 (intrinsic apoptosis pathway), 3) synergistic inhibition of MTORC1, 4) synergistic inhibition of ESR1, and 5) synergistic inhibition of CYCLIN D. Our approach offers a mechanistic understanding of the efficacy of drug combinations and provides direction for selecting potential drug pairs worthy of further laboratory investigation.

Indexed as

Breast NeoplasmsCell Line, TumorDrug CombinationsDrug SynergismFemaleHumansMCF-7 CellsSignal TransductionDrug Combinations

Identifiers

PMID38394152
PMCPMC10889607
OpenAlexW4392125208

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.