Evidence map›Paper›PMID 30121967›Full record

ArticleCancer research and treatment2019

Disulfiram, a Re-positioned Aldehyde Dehydrogenase Inhibitor, Enhances Radiosensitivity of Human Glioblastoma Cells In Vitro.

Hyeon Kang Koh, Soo Yeon Seo, Jin Ho Kim, Hak Jae Kim, Eui Kyu Chie, Seung-Ki Kim, Il Han Kim

Open access · diamondAbstract read
In one paragraph

Article in Cancer research and treatment, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  5. Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024
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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

7 authors at 3 institutions in 1 country.

Hyeon Kang KohDepartment of Radiation Oncology, Konkuk University Medical Center, Seoul, Korea.
Soo Yeon SeoCancer Research Institute, Seoul National University, Seoul, Korea.
Jin Ho KimDepartment of Radiation Oncology, Seoul National University College of Medicine, Seoul, Korea.
Hak Jae KimDepartment of Radiation Oncology, Seoul National University College of Medicine, Seoul, Korea.
Eui Kyu ChieDepartment of Radiation Oncology, Seoul National University College of Medicine, Seoul, Korea.
Seung-Ki KimDivision of Pediatric Neurosurgery, Pediatric Clinical Neuroscience Center, Seoul National University Children's Hospital, Seoul, Korea.
Il Han KimDepartment of Radiation Oncology, Seoul National University College of Medicine, Seoul, Korea.
Seoul National University · KRKonkuk University Medical Center · KRSeoul National University Children's Hospital · KR

Funding

Seoul National University Hospital 03-2017-0080
6 · The paper itself

Abstract

purposeGlioblastoma, the most common brain tumor in adults, has poor prognosis. The purpose of this study was to determine the effect of disulfiram (DSF), an aldehyde dehydrogenase inhibitor, on in vitro radiosensitivity of glioblastoma cells with different methylation status of O6-methylguanine-DNA methyltransferase (MGMT) promoter and the underlying mechanism of such effect. MATERIALS AND

methodsFive human glioblastoma cells (U138MG, T98G, U251MG, U87MG, and U373MG) and one normal human astrocyte (NHA) cell were cultured and treated with DSF or 6MV X-rays (0, 2, 4, 6, and 8 Gy). For combined treatment, cells were treated with DSF before irradiation. Surviving fractions fit from cell survival based on colony forming ability. Apoptosis, DNA damage repair, and cell cycle distributionwere assayed bywestern blot for cleaved caspase-3, γH2AX staining, and flow cytometry, respectively.

resultsDSF induced radiosensitization in most of the glioblastoma cells, especially, in the cells with radioresistance as wildtype unmethylated promoter (MGMT-wt), but did not in normal NHA cell. DSF augmented or induced cleavage of caspase-3 in all cells after irradiation. DSF inhibited repair of radiation-induced DNA damage in MGMT-wt cells, but not in cells with methylated MGMT promoter. DSF abrogated radiation-induced G2/M arrest in T98G and U251MG cells.

conclusionRadiosensitivity of glioblastoma cells were preferentially enhanced by pre-irradiation DSF treatment compared to normal cell, especially radioresistant cells such as MGMT-wt cells. Induction of apoptosis or inhibition of DNA damage repair may underlie DSF-induced radiosensitization. Clinical benefit of combining DSF with radiotherapy should be investigated in the future.

Indexed as

Acetaldehyde Dehydrogenase InhibitorsBrain NeoplasmsCaspase 3Cell CycleCell Line, TumorDisulfiramDNA Modification MethylasesDNA Repair EnzymesDose-Response Relationship, DrugGene ExpressionGlioblastomaHistonesHumansRadiation-Sensitizing AgentsRadiation ToleranceTumor Suppressor ProteinsAcetaldehyde Dehydrogenase InhibitorsCaspase 3DisulfiramDNA Modification MethylasesDNA Repair EnzymesHistonesMGMT protein, humanRadiation-Sensitizing AgentsTumor Suppressor ProteinsApoptosisDisulfiramDNA damage repairGlioblastomaMGMTRadiosensitivity

Identifiers

PMID30121967
PMCPMC6473295
OpenAlexW2886836644

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.