Evidence map›Paper›PMID 27354287›Full record

ArticleScientific reports2016

Network Modeling Identifies Patient-specific Pathways in Glioblastoma.

Nurcan Tuncbag, Pamela Milani, Jenny L Pokorny, Hannah Johnson, Terence T Sio, Simona Dalin, Dennis O Iyekegbe, Forest M White, Jann N Sarkaria, Ernest Fraenkel

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Nurcan TuncbagDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, 02139, USA.
Pamela MilaniDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, 02139, USA.
Jenny L PokornyDepartment of Radiation Oncology, Mayo Clinic, Rochester, Minnesota 55905, USA.
Hannah JohnsonDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, 02139, USA.
Terence T SioDepartment of Radiation Oncology, Mayo Clinic, Rochester, Minnesota 55905, USA.
Simona DalinDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, 02139, USA.
Dennis O IyekegbeDepartment of Radiation Oncology, Mayo Clinic, Rochester, Minnesota 55905, USA.
Forest M WhiteDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, 02139, USA.
Jann N SarkariaDepartment of Radiation Oncology, Mayo Clinic, Rochester, Minnesota 55905, USA.
Ernest FraenkelDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, 02139, USA.
Massachusetts Institute of Technology · USMayo Clinic · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Tumor Cell Networks CenterU54CA112967 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2004 to 2015
$26.2M
Neuron and Glial Cellular Signatures from Normal and Diseased iPS Cells-SupplementU54NS091046 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI FINKBEINER, STEVEN M, FRAENKEL, ERNEST · 2014 to 2020
$11.7M
Embryonal Brain Tumor NetworksU01CA184898 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI FRAENKEL, ERNEST, MESIROV, JILL P. · 2014 to 2019
$3.6M
NCI NIH HHS P30 CA014051NCI NIH HHS U01 CA184898NCI NIH HHS U54 CA112967NINDS NIH HHS U54 NS091046
6 · The paper itself

Abstract

Glioblastoma is the most aggressive type of malignant human brain tumor. Molecular profiling experiments have revealed that these tumors are extremely heterogeneous. This heterogeneity is one of the principal challenges for developing targeted therapies. We hypothesize that despite the diverse molecular profiles, it might still be possible to identify common signaling changes that could be targeted in some or all tumors. Using a network modeling approach, we reconstruct the altered signaling pathways from tumor-specific phosphoproteomic data and known protein-protein interactions. We then develop a network-based strategy for identifying tumor specific proteins and pathways that were predicted by the models but not directly observed in the experiments. Among these hidden targets, we show that the ERK activator kinase1 (MEK1) displays increased phosphorylation in all tumors. By contrast, protein numb homolog (NUMB) is present only in the subset of the tumors that are the most invasive. Additionally, increased S100A4 is associated with only one of the tumors. Overall, our results demonstrate that despite the heterogeneity of the proteomic data, network models can identify common or tumor specific pathway-level changes. These results represent an important proof of principle that can improve the target selection process for tumor specific treatments.

Indexed as

Models, BiologicalSignal TransductionAnimalsGlioblastomaHumansMiceNeoplasm ProteinsNeoplasms, ExperimentalPrecision MedicineNeoplasm Proteins

Identifiers

PMID27354287
PMCPMC4926112
OpenAlexW2462767821

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.