Evidence map›Paper›PMID 35953681›Full record

ArticleJournal of cancer research and clinical oncology2023

Precision neuro-oncology: a pilot analysis of personalized treatment in recurrent glioma.

Lazaros Lazaridis, Teresa Schmidt, Christoph Oster, Tobias Blau, Daniela Pierscianek, Jens T Siveke, Sebastian Bauer, Hans-Ulrich Schildhaus, Ulrich Sure, Kathy Keyvani and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Genomic Profiling in Glioma Patients to Explore Clinically Relevant Markers.International journal of molecular sciences · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. A Sequential Targeting Strategy Interrupts AKT-Driven Subclone-Mediated Progression in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  10. Article
  11. Article
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

17 authors at 4 institutions in 1 country.

Lazaros LazaridisDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Division of Clinical Neurooncology, University Medicine Essen, University Duisburg-Essen, Essen, Germany.
Teresa SchmidtDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Division of Clinical Neurooncology, University Medicine Essen, University Duisburg-Essen, Essen, Germany.
Christoph OsterDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Division of Clinical Neurooncology, University Medicine Essen, University Duisburg-Essen, Essen, Germany.
Tobias BlauGerman Cancer Consortium (DKTK), Partner Site University Medicine Essen, Hufelandstr. 55, 45147, Essen, Germany.
Daniela PierscianekGerman Cancer Consortium (DKTK), Partner Site University Medicine Essen, Hufelandstr. 55, 45147, Essen, Germany.
Jens T SivekeGerman Cancer Consortium (DKTK), Partner Site University Medicine Essen, Hufelandstr. 55, 45147, Essen, Germany.
Sebastian BauerGerman Cancer Consortium (DKTK), Partner Site University Medicine Essen, Hufelandstr. 55, 45147, Essen, Germany.
Hans-Ulrich SchildhausGerman Cancer Consortium (DKTK), Partner Site University Medicine Essen, Hufelandstr. 55, 45147, Essen, Germany.
Ulrich SureGerman Cancer Consortium (DKTK), Partner Site University Medicine Essen, Hufelandstr. 55, 45147, Essen, Germany.
Kathy KeyvaniGerman Cancer Consortium (DKTK), Partner Site University Medicine Essen, Hufelandstr. 55, 45147, Essen, Germany.
Christoph KleinschnitzDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Division of Clinical Neurooncology, University Medicine Essen, University Duisburg-Essen, Essen, Germany.
Martin StuschkeGerman Cancer Consortium (DKTK), Partner Site University Medicine Essen, Hufelandstr. 55, 45147, Essen, Germany.
Ken HerrmannGerman Cancer Consortium (DKTK), Partner Site University Medicine Essen, Hufelandstr. 55, 45147, Essen, Germany.
Cornelius DeuschlGerman Cancer Consortium (DKTK), Partner Site University Medicine Essen, Hufelandstr. 55, 45147, Essen, Germany.
Björn Scheffler *DKFZ-Division Translational Neurooncology at the West German Cancer Center (WTZ), DKTK Partner Site, University Medicine Essen, University Duisburg-Essen, Essen, Germany.
Sied Kebir *Department of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Division of Clinical Neurooncology, University Medicine Essen, University Duisburg-Essen, Essen, Germany.
Martin Glas *Department of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Division of Clinical Neurooncology, University Medicine Essen, University Duisburg-Essen, Essen, Germany. Martin.Glas@uk-essen.de.
Deutschen Konsortium für Translationale Krebsforschung · DEGerman Cancer Research Center · DEUniversity of Duisburg-Essen · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeWhen brain cancer relapses, treatment options are scarce. The use of molecularly matched targeted therapies may provide a feasible and efficacious way to treat individual patients based on the molecular tumor profile. Since little information is available on this strategy in neuro-oncology, we retrospectively analyzed the clinical course of 41 patients who underwent advanced molecular testing at disease relapse.

methodsWe performed Sanger sequencing, targeted next generation sequencing, and immunohistochemistry for analysis of potential targets, including programmed death ligand 1, cyclin D1, phosphorylated mechanistic target of rapamycin, telomerase reverse transcriptase promoter mutation, cyclin-dependent kinase inhibitor 2A/B deletion, or BRAF-V600E mutation. In selected patients, whole exome sequencing was conducted.

resultsThe investigation included 41 patients, of whom 32 had isocitrate dehydrogenase (IDH) wildtype glioblastoma. Molecular analysis revealed actionable targets in 31 of 41 tested patients and 18 patients were treated accordingly (matched therapy group). Twenty-three patients received molecularly unmatched empiric treatment (unmatched therapy group). In both groups, 16 patients were diagnosed with recurrent IDH wildtype glioblastoma. The number of severe adverse events was comparable between the therapy groups. Regarding the IDH wildtype glioblastoma patients, median progression-free survival (mPFS) and median overall survival (mOS) were longer in the matched therapy group (mPFS: 3.8 versus 2.0 months, p = 0.0057; mOS: 13.0 versus 4.3 months, p = 0.0357).

conclusionThese encouraging data provide a rationale for molecularly matched targeted therapy in glioma patients. For further validation, future study designs need to additionally consider the prevalence and persistence of actionable molecular alterations in patient tissue.

Indexed as

Brain NeoplasmsGlioblastomaGliomaHumansIsocitrate DehydrogenaseMutationNeoplasm Recurrence, LocalPrecision MedicineRetrospective StudiesIsocitrate DehydrogenaseGliomaMolecularly matched targeted therapyNeuro-oncologyPrecision oncologyTargeted therapy

Identifiers

PMID35953681
PMCPMC10314879
OpenAlexW4291162324

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.