ArticleScientific reports2015
Systemic modeling myeloma-osteoclast interactions under normoxic/hypoxic condition using a novel computational approach.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 32 citations in OpenAlex.
- Deer antler renewal gives insights into mammalian epimorphic regeneration.Cell regeneration (London, England) · 2023Review
- Editorial: Advanced computational systems biology approaches for accelerating comprehensive research of the human brain.Frontiers in genetics · 2023Article
- Redox integration of signaling and metabolism in a head and neck cancer model of radiation resistance using COSMFrontiers in oncology · 2022Article
- Phage_UniR_LGBM: Phage Virion Proteins Classification with UniRep Features and LightGBM Model.Computational and mathematical methods in medicine · 2022Article
- Identification of signaling pathways associated with achaete-scute homolog 1 in glioblastomas through ChIP-seq data bioinformatics.Frontiers in genetics · 2022Article
- Bioinformatics analysis to screen for genes related to myocardial infarction.Frontiers in genetics · 2022Article
- Hypertension-Related Drug Activity Identification Based on Novel Ensemble Method.Frontiers in genetics · 2021Article
- A linear programming computational framework integrates phosphor-proteomics and prior knowledge to predict drug efficacy.BMC systems biology · 2017Article
- WSMD: weakly-supervised motif discovery in transcription factor ChIP-seq data.Scientific reports · 2017Article
- Mathematical and Computational Modeling in Complex Biological Systems.BioMed research international · 2017Review
- A biosystems approach to identify the molecular signaling mechanisms of TMEM30A during tumor migration.PloS one · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Interaction of myeloma cells with osteoclasts (OC) can enhance tumor cell expansion through activation of complex signaling transduction networks. Both cells reside in the bone marrow, a hypoxic niche. How OC-myeloma interaction in a hypoxic environment affects myeloma cell growth and their response to drug treatment is poorly understood. In this study, we i) cultured myeloma cells in the presence/absence of OCs under normoxia and hypoxia conditions and did protein profiling analysis using reverse phase protein array; ii) computationally developed an Integer Linear Programming approach to infer OC-mediated myeloma cell-specific signaling pathways under normoxic and hypoxic conditions. Our modeling analysis indicated that in the presence OCs, (1) cell growth-associated signaling pathways, PI3K/AKT and MEK/ERK, were activated and apoptotic regulatory proteins, BAX and BIM, down-regulated under normoxic condition; (2) β1 Integrin/FAK signaling pathway was activated in myeloma cells under hypoxic condition. Simulation of drug treatment effects by perturbing the inferred cell-specific pathways showed that targeting myeloma cells with the combination of PI3K and integrin inhibitors potentially (1) inhibited cell proliferation by reducing the expression/activation of NF-κB, S6, c-Myc, and c-Jun under normoxic condition; (2) blocked myeloma cell migration and invasion by reducing the expression of FAK and PKC under hypoxic condition.
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.