Evidence map›Paper›PMID 31505812›Full record

ReviewBiomedicines2019

Temozolomide and Other Alkylating Agents in Glioblastoma Therapy.

Hannah Strobel, Tim Baisch, Rahel Fitzel, Katharina Schilberg, Markus D Siegelin, Georg Karpel-Massler, Klaus-Michael Debatin, Mike-Andrew Westhoff

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 1 pooled it
18.5field-weighted citation impact, top 1% 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

134 citing papers in PubMed, 1 synthesis or guideline pooled it, 271 citations in OpenAlex.

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74 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

8 authors at 2 institutions in 2 countries.

Hannah StrobelDepartment of Pediatrics and Adolescent Medicine, University Medical Center Ulm, D-89075 Ulm, Germany. hannah.strobel@uni-ulm.de.
Tim BaischDepartment of Pediatrics and Adolescent Medicine, University Medical Center Ulm, D-89075 Ulm, Germany. tim.baisch@uni-ulm.de.
Rahel FitzelDepartment of Pediatrics and Adolescent Medicine, University Medical Center Ulm, D-89075 Ulm, Germany. rahel.fitzel@uni-ulm.de.
Katharina SchilbergFaculty of Medicine, Ulm University, D-89081 Ulm, Germany. katharina.schilberg@uni-ulm.de.
Markus D SiegelinDepartment of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA. ms4169@cumc.columbia.edu.
Georg Karpel-MasslerDepartment of Neurosurgery, University Medical Center Ulm, D-89081 Ulm, Germany. georg.karpel@uniklinik-ulm.de.
Klaus-Michael DebatinDepartment of Pediatrics and Adolescent Medicine, University Medical Center Ulm, D-89075 Ulm, Germany. klaus-michael.debatin@uniklinik-ulm.de.ORCID 0000-0002-8397-1886
Mike-Andrew WesthoffDepartment of Pediatrics and Adolescent Medicine, University Medical Center Ulm, D-89075 Ulm, Germany. andrew.westhoff@uniklinik-ulm.de.ORCID 0000-0003-3256-7100
Universität Ulm · DEColumbia University Irving Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The alkylating agent temozolomide (TMZ) together with maximal safe bulk resection and focal radiotherapy comprises the standard treatment for glioblastoma (GB), a particularly aggressive and lethal primary brain tumor. GB affects 3.2 in 100,000 people who have an average survival time of around 14 months after presentation. Several key aspects make GB a difficult to treat disease, primarily including the high resistance of tumor cells to cell death-inducing substances or radiation and the combination of the highly invasive nature of the malignancy, i.e., treatment must affect the whole brain, and the protection from drugs of the tumor bulk-or at least of the invading cells-by the blood brain barrier (BBB). TMZ crosses the BBB, but-unlike classic chemotherapeutics-does not induce DNA damage or misalignment of segregating chromosomes directly. It has been described as a DNA alkylating agent, which leads to base mismatches that initiate futile DNA repair cycles; eventually, DNA strand breaks, which in turn induces cell death. However, while much is assumed about the function of TMZ and its mode of action, primary data are actually scarce and often contradictory. To improve GB treatment further, we need to fully understand what TMZ does to the tumor cells and their microenvironment. This is of particular importance, as novel therapeutic approaches are almost always clinically assessed in the presence of standard treatment, i.e., in the presence of TMZ. Therefore, potential pharmacological interactions between TMZ and novel drugs might occur with unforeseeable consequences.

Indexed as

alkylating agentsbrain tumorglioblastomatemozolomide (TMZ), triazene compounds

Identifiers

PMID31505812
PMCPMC6783999
OpenAlexW2972376636

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.