Evidence map›Paper›PMID 27494880›Full record

ArticleOncotarget2016

Predicting the cell death responsiveness and sensitization of glioma cells to TRAIL and temozolomide.

Birgit C Weyhenmeyer, Janis Noonan, Maximilian L Würstle, Frank A Lincoln, Grainne Johnston, Markus Rehm, Brona M Murphy

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 23 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

7 authors at 2 institutions in 2 countries.

Birgit C WeyhenmeyerDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland.
Janis NoonanDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland.
Maximilian L WürstleDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland.
Frank A LincolnDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland.
Grainne JohnstonDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland.
Markus RehmDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland.
Brona M MurphyDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland.
Royal College of Surgeons in Ireland · IEUniversity of Stuttgart · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genotoxic chemotherapy with temozolomide (TMZ) is a mainstay of treatment for glioblastoma (GBM); however, at best, TMZ provides only modest survival benefit to a subset of patients. Recent insight into the heterogeneous nature of GBM suggests a more personalized approach to treatment may be necessary to overcome cancer drug resistance and improve patient care. These include novel therapies that can be used both alone and with TMZ to selectively reactivate apoptosis within malignant cells. For this approach to work, reliable molecular signatures that can accurately predict treatment responsiveness need to be identified first. Here, we describe the first proof-of-principle study that merges quantitative protein-based analysis of apoptosis signaling networks with data- and knowledge-driven mathematical systems modeling to predict treatment responsiveness of GBM cell lines to various apoptosis-inducing stimuli. These include monotherapies with TMZ and TRAIL, which activate the intrinsic and extrinsic apoptosis pathways, respectively, as well as combination therapies of TMZ+TRAIL. We also successfully employed this approach to predict whether individual GBM cell lines could be sensitized to TMZ or TRAIL via the selective targeting of Bcl-2/Bcl-xL proteins with ABT-737. Our findings suggest that systems biology-based approaches could assist in personalizing treatment decisions in GBM to optimize cell death induction.

Indexed as

Antineoplastic Agents, AlkylatingApoptosisBiphenyl CompoundsBrain NeoplasmsCell Line, TumorCell SurvivalDacarbazineDrug Resistance, NeoplasmGlioblastomaGliomaHumansModels, TheoreticalNitrophenolsPiperazinesSignal TransductionSulfonamidesABT-737Antineoplastic Agents, AlkylatingBiphenyl CompoundsDacarbazineNitrophenolsPiperazinesSulfonamidesTemozolomideTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanapoptosisglioblastomasystems biologytemozolomideTRAIL

Identifiers

PMID27494880
PMCPMC5308652
OpenAlexW2492973189

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.