Evidence map›Paper›PMID 27793847›Full record

ArticleCancer research2017

DNA Repair Capacity in Multiple Pathways Predicts Chemoresistance in Glioblastoma Multiforme.

Zachary D Nagel, Gaspar J Kitange, Shiv K Gupta, Brian A Joughin, Isaac A Chaim, Patrizia Mazzucato, Douglas A Lauffenburger, Jann N Sarkaria, Leona D Samson

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

76 citing papers in PubMed, 129 citations in OpenAlex.

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16 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Zachary D NagelDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts.
Gaspar J KitangeDepartment of Radiation Oncology, Mayo Clinic, Rochester, Minnesota.
Shiv K GuptaDepartment of Radiation Oncology, Mayo Clinic, Rochester, Minnesota.
Brian A JoughinDavid H. Koch Institute for Integrative Cancer Research at MIT, Cambridge, Massachusetts.
Isaac A ChaimDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts.
Patrizia MazzucatoDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts.
Douglas A LauffenburgerDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts.
Jann N SarkariaDepartment of Radiation Oncology, Mayo Clinic, Rochester, Minnesota.
Leona D SamsonDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts. lsamson@mit.edu.
Massachusetts Institute of Technology · USMayo Clinic · US

Funding

Tumor Cell Networks CenterU54CA112967 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2004 to 2015
$26.2M
Developing novel methods to measure DNA repair capacity in human populationsDP1ES022576 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 2012 to 2013
$1.6M
Mechanisms of acquired temozolomide resistance in glioblastoma multiformeR01CA176830 · NCI · MAYO CLINIC ROCHESTER · PI SARKARIA, JANN N. · 2013 to 2017
$1.6M
NCI NIH HHS R01 CA176830NCI NIH HHS U54 CA112967NIEHS NIH HHS DP1 ES022576
6 · The paper itself

Abstract

Cancer cells can resist the effects of DNA-damaging therapeutic agents via utilization of DNA repair pathways, suggesting that DNA repair capacity (DRC) measurements in cancer cells could be used to identify patients most likely to respond to treatment. However, the limitations of available technologies have so far precluded adoption of this approach in the clinic. We recently developed fluorescence-based multiplexed host cell reactivation (FM-HCR) assays to measure DRC in multiple pathways. Here we apply a mathematical model that uses DRC in multiple pathways to predict cellular resistance to killing by DNA-damaging agents. This model, developed using FM-HCR and drug sensitivity measurements in 24 human lymphoblastoid cell lines, was applied to a panel of 12 patient-derived xenograft (PDX) models of glioblastoma to predict glioblastoma response to treatment with the chemotherapeutic DNA-damaging agent temozolomide. This work showed that, in addition to changes in O

Indexed as

Models, TheoreticalAnimalsAntineoplastic AgentsArea Under CurveBrain NeoplasmsCell Line, TumorDacarbazineDNA RepairDrug Resistance, NeoplasmGlioblastomaHumansMiceROC CurveTemozolomideXenograft Model Antitumor AssaysAntineoplastic AgentsDacarbazineTemozolomide

Identifiers

PMID27793847
PMCPMC6100738
OpenAlexW2539998067

What OpenQuestion holds

Textmetadata
LicenceTDM
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.