Evidence map›Paper›PMID 42747707›Full record

ArticleJournal of neuro-oncology2026

Quantitative stability of MGMT promoter methylation in recurrent glioma and implications for temozolomide rechallenge.

Henry Noren, Gabriella Pelofsky, Brianna Suffren, Laura Mittelman, Christine Yohn, Aminah Twyman, Christopher A Febres-Aldana, Arevik Abramyan, Aparna Sertil, Randy S D'Amico and 2 more

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Article in Journal of neuro-oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Henry NorenDepartment of Neurosurgery, Rutgers Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ, 08901, USA.ORCID http://orcid.org/0009-0004-9319-6846
Gabriella PelofskyDepartment of Neurosurgery, Rutgers New Jersey Medical School, Newark, NJ, USA.
Brianna SuffrenDepartment of Neurosurgery, Lenox Hill Hospital, New York, NY, USA.
Laura MittelmanDepartment of Neurosurgery, Lenox Hill Hospital, New York, NY, USA.
Christine YohnDepartment of Neurosurgery, Rutgers Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ, 08901, USA.
Aminah TwymanDepartment of Neurosurgery, Rutgers Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ, 08901, USA.
Christopher A Febres-AldanaLaboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Arevik AbramyanDepartment of Neurosurgery, Rutgers Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ, 08901, USA.
Aparna SertilCaris Life Sciences, Phoenix, AZ, USA.
Randy S D'AmicoDepartment of Neurosurgery, Lenox Hill Hospital, New York, NY, USA.
Jonathan H ShermanDepartment of Neurosurgery, Rutgers Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ, 08901, USA.
Morana VojnicRutgers Cancer Institute, New Brunswick, NJ, USA. mv858@cinj.rutgers.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeO^6^-methylguanine-DNA methyltransferase (MGMT) promoter methylation is a key predictive biomarker for temozolomide (TMZ) response in glioma. MGMT status is routinely assessed at diagnosis; however, its utility at recurrence remains incompletely characterized. We aimed to quantify MGMT methylation stability and assess the clinical relevance of reported status changes in recurrent glioma.

methodsWe analyzed paired tumor samples from 426 patients with recurrent glioma in a large commercial molecular database containing quantitative methylation percentage and binary methylation status at two sample time points. A separate multi-institutional clinical cohort (n = 27) with detailed treatment annotation was analyzed to explore associations between MGMT status at recurrence and treatment decision-making. Statistical analyses assessed quantitative methylation dynamics and time between samples as a surrogate for disease course.

resultsMGMT status remained unchanged in 84% of tumors across recurrence. 16% demonstrated a status change, commonly among tumors with low baseline methylation near classification thresholds. Longitudinal quantitative methylation changes were modest overall. Tumors that remained, gained, or lost hypermethylation demonstrated longer intervals between samples compared to consistently unmethylated tumors (p < 0.01). In the clinical cohort, TMZ rechallenge was more frequently pursued in patients retaining hypermethylation at recurrence.

conclusionMGMT promoter methylation is quantitatively stable in the majority of recurrent gliomas. Status changes predominantly occur in tumors with borderline methylation, highlighting the limitations of binary classification. These findings support routine reassessment of MGMT at recurrence and underscore the value of quantitative reporting to better inform therapeutic decision-making, particularly regarding TMZ rechallenge.

Indexed as

Antineoplastic Agents, AlkylatingBrain NeoplasmsDNA MethylationDNA Modification MethylasesDNA Repair EnzymesGliomaNeoplasm Recurrence, LocalPromoter Regions, GeneticTemozolomideTumor Suppressor ProteinsAdultAgedBiomarkers, TumorDacarbazineFemaleHumansAntineoplastic Agents, AlkylatingBiomarkers, TumorDacarbazineDNA Modification MethylasesDNA Repair EnzymesMGMT protein, humanTemozolomideTumor Suppressor ProteinsEpigeneticsMGMT promoter methylationMolecular dynamicsRecurrent GliomaTemozolomide

Identifiers

PMID42747707
PMCPMC13582029

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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.