ArticlePloS one2015
A computational strategy to select optimized protein targets for drug development toward the control of cancer diseases.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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.
Who cites it
16 citing papers in PubMed.
- Chemical Profiling, In Silico and In Vitro Studies to Identify Potential CDK2 and mTOR Inhibitor From Selaginella inaequalifolia (Hook. & Grev.) Spring Ethanolic Extracts.Chemistry & biodiversity · 2026Article
- Niosome-loaded silibinin and methotrexate for synergistic breast cancer combination chemotherapy: in silico and in vitro study.Cancer cell international · 2025Article
- The value of protein allostery in rational anticancer drug design: an update.Expert opinion on drug discovery · 2024Review
- Structural Characterization of Heat Shock Protein 90β and Molecular Interactions with Geldanamycin and Ritonavir: A Computational Study.International journal of molecular sciences · 2024Article
- Article
- A Strategy Utilizing Protein-Protein Interaction Hubs for the Treatment of Cancer Diseases.International journal of molecular sciences · 2023Review
- A Data Science Approach for the Identification of Molecular Signatures of Aggressive Cancers.Cancers · 2022Article
- Data-Driven Modeling of Breast Cancer Tumors Using Boolean Networks.Frontiers in big data · 2021Article
- Galaxy and MEAN Stack to Create a User-Friendly Workflow for the Rational Optimization of Cancer Chemotherapy.Frontiers in genetics · 2021Article
- Using the Gibbs Function as a Measure of Human Brain Development Trends from Fetal Stage to Advanced Age.International journal of molecular sciences · 2020Article
- Modeling Basins of Attraction for Breast Cancer Using Hopfield Networks.Frontiers in genetics · 2020Article
- Personalized therapy design for systemic lupus erythematosus based on the analysis of protein-protein interaction networks.PloS one · 2020Article
- Signaling Complexity Measured by Shannon Entropy and Its Application in Personalized Medicine.Frontiers in genetics · 2019Article
- Article
- A strategy to identify housekeeping genes suitable for analysis in breast cancer diseases.BMC genomics · 2016Article
- Toward precision medicine of breast cancer.Theoretical biology & medical modelling · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this report, we describe a strategy for the optimized selection of protein targets suitable for drug development against neoplastic diseases taking the particular case of breast cancer as an example. We combined human interactome and transcriptome data from malignant and control cell lines because highly connected proteins that are up-regulated in malignant cell lines are expected to be suitable protein targets for chemotherapy with a lower rate of undesirable side effects. We normalized transcriptome data and applied a statistic treatment to objectively extract the sub-networks of down- and up-regulated genes whose proteins effectively interact. We chose the most connected ones that act as protein hubs, most being in the signaling network. We show that the protein targets effectively identified by the combination of protein connectivity and differential expression are known as suitable targets for the successful chemotherapy of breast cancer. Interestingly, we found additional proteins, not generally targeted by drug treatments, which might justify the extension of existing formulation by addition of inhibitors designed against these proteins with the consequence of improving therapeutic outcomes. The molecular alterations observed in breast cancer cell lines represent either driver events and/or driver pathways that are necessary for breast cancer development or progression. However, it is clear that signaling mechanisms of the luminal A, B and triple negative subtypes are different. Furthermore, the up- and down-regulated networks predicted subtype-specific drug targets and possible compensation circuits between up- and down-regulated genes. We believe these results may have significant clinical implications in the personalized treatment of cancer patients allowing an objective approach to the recycling of the arsenal of available drugs to the specific case of each breast cancer given their distinct qualitative and quantitative molecular traits.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.