Evidence map›Paper›PMID 40560330›Full record

ArticleJournal of neuro-oncology2025

Molecular and clinical determinants of response to checkpoint inhibitor immunotherapy in glioblastoma.

Pushan Dasgupta, Heather Lin, Gayatri Kumar, Zaid Soomro, Max M Ayala, Edwin R Parra, Shiao-Pei Weathers, Frederick F Lang, Krishna P Bhat, John de Groot and 1 more

Abstract read
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In one paragraph

Article in Journal of neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

11 authors.

Pushan DasguptaDepartment of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Pushan.dasgupta@bcm.edu.
Heather LinDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Gayatri KumarDepartment of Research, Mayo Clinic Phoenix, Phoenix, AZ, USA.
Zaid SoomroDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Max M AyalaDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Edwin R ParraDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Shiao-Pei WeathersDepartment of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Frederick F LangDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Krishna P BhatDepartment of Research, Mayo Clinic Phoenix, Phoenix, AZ, USA.
John de GrootDepartment of Neurological Surgery, University of California-San Francisco, San Francisco, CA, USA. john.degroot@ucsf.edu.
Nazanin K MajdDepartment of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. nkmajd@mdanderson.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeWhile checkpoint inhibitor therapy (CPI) has transformed treatment in multiple solid tumors, its efficacy in glioblastoma (GBM) remains limited. Understanding the molecular and clinical factors that influence glioblastoma's response to CPI is essential to improving outcomes.

methodsWe identified patients with recurrent GBM, who had been treated with CPI and determined the association between their molecular, clinical, and demographic characteristics and survival outcomes.

resultsWe identified 35 patients with recurrent GBM treated with CPI. PIK3CA mutation was associated with a statistically significant shorter OS duration, calculated from CPI initiation (p-value = 0.014). Tumor tissue without the mutation had less PD-1 expression in CD3+/CD8 + T cells. RB1 and TERT promoter mutations were associated with shorter PFS durations (p-value = 0.009, 0.053, respectively). Length of CPI therapy of more than 6 months was associated with increased PFS and OS (p-value = 0.069, 0.088, respectively), while steroid use at baseline was associated with a shorter OS (p-value = 0.0016). Multifocal disease was associated with shorter PFS and OS durations (p-value = 0.0011, 0.0015, respectively) among all patients.

conclusionsIn glioblastoma, PIK3CA, RB1, TERT promoter mutations, steroid use prior to start of CPI, and multifocal disease may be associated with a poor response to CPI while increased length of CPI may be associated with improved response. Our results may provide the rationale for clinical trials combining PI3K inhibitors with CPI in glioblastoma. The small sample size and retrospective nature of the study carries selection bias and/or confounding effects and larger studies need to be done to validate these results.

Indexed as

Brain NeoplasmsGlioblastomaImmune Checkpoint InhibitorsImmunotherapyNeoplasm Recurrence, LocalAdultAgedBiomarkers, TumorClass I Phosphatidylinositol 3-KinasesFemaleFollow-Up StudiesHumansMaleMiddle AgedMutationPrognosisBiomarkers, TumorClass I Phosphatidylinositol 3-KinasesImmune Checkpoint InhibitorsPIK3CA protein, humanRB1 protein, humanRetinoblastoma Binding ProteinsTelomeraseTERT protein, humanUbiquitin-Protein LigasesCheckpoint inhibitorGlioblastomaHigh-grade gliomaImmunotherapyPIK3CA

Identifiers

PMID40560330

What OpenQuestion holds

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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.