Evidence map›Paper›PMID 32193690›Full record

ArticleJournal of neuro-oncology2020

Epigenetic preconditioning with decitabine sensitizes glioblastoma to temozolomide via induction of MLH1.

Matthew Gallitto, Rossana Cheng He, Julio F Inocencio, Huaien Wang, Yizhou Zhang, Gintaras Deikus, Isaac Wasserman, Maya Strahl, Melissa Smith, Robert Sebra and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of neuro-oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Matthew GallittoDepartments of Neurosurgery and Oncological Sciences, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue, Box 1136, New York, NY, 10029, USA.
Rossana Cheng HeDepartments of Neurosurgery and Oncological Sciences, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue, Box 1136, New York, NY, 10029, USA.
Julio F InocencioDepartment of Neurological Surgery, Albert Einstein College of Medicine, Montefiore Medical Center, New York, NY, USA.
Huaien WangDepartments of Neurosurgery and Oncological Sciences, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue, Box 1136, New York, NY, 10029, USA.
Yizhou ZhangDepartments of Neurosurgery and Oncological Sciences, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue, Box 1136, New York, NY, 10029, USA.
Gintaras DeikusDepartment of Genetics and Genomic Sciences, Icahn School of Medicine At Mount Sinai, New York, NY, USA.
Isaac WassermanDepartments of Neurosurgery and Oncological Sciences, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue, Box 1136, New York, NY, 10029, USA.
Maya StrahlDepartment of Genetics and Genomic Sciences, Icahn School of Medicine At Mount Sinai, New York, NY, USA.
Melissa SmithDepartment of Genetics and Genomic Sciences, Icahn School of Medicine At Mount Sinai, New York, NY, USA.
Robert SebraDepartment of Genetics and Genomic Sciences, Icahn School of Medicine At Mount Sinai, New York, NY, USA.
Raymund L YongDepartments of Neurosurgery and Oncological Sciences, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue, Box 1136, New York, NY, 10029, USA. raymund.yong@mountsinai.org.ORCID http://orcid.org/0000-0002-7585-4153
Icahn School of Medicine at Mount Sinai · USAlbert Einstein College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionTo improve the standard treatment paradigm for glioblastoma (GBM), efforts have been made to explore the efficacy of epigenetic agents as chemosensitizers. Recent data suggest possible synergy between decitabine (DAC), a DNA hypomethylating agent, and temozolomide (TMZ) in GBM, but the mechanism remains unclear. The objective of this study was to determine the effects of DAC on TMZ sensitization in a consecutively derived set of primary GBM cultures, with a focus on mismatch repair (MMR) proteins.

methodsHalf maximal inhibitory concentrations (IC

resultsTMZ IC

conclusionsDAC enhances TMZ cytotoxicity in a subset of GBM cell lines, comprising lines both MGMT methylated and unmethylated tumors. This effect may be driven by levels of MLH1 via E2F1 transcription factor binding. Using unbiased long-range next-generation bisulfite-sequencing, we identified a region of the proximal MLH1 promoter with differential methylation patterns that has potential utility as a clinical biomarker for TMZ sensitization.

Indexed as

Antineoplastic AgentsBrain NeoplasmsCell Line, TumorDecitabineEpigenesis, GeneticGlioblastomaHumansInhibitory Concentration 50MutL Protein Homolog 1TemozolomideAntineoplastic AgentsDecitabineMLH1 protein, humanMutL Protein Homolog 1TemozolomideChemosensitizationDecitabineDNA methylationGlioblastomaMismatch repairTemozolomide

Identifiers

PMID32193690
PMCPMC7256087
OpenAlexW3012124816

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.