Evidence map›Paper›PMID 29737460›Full record

ArticleInternational journal of hematology2018

Association between OGG1 S326C CC genotype and elevated relapse risk in acute myeloid leukemia.

Nanami Gotoh, Takayuki Saitoh, Noriyuki Takahashi, Tetsuhiro Kasamatsu, Yusuke Minato, Alkebsi Lobna, Tsukasa Oda, Takumi Hoshino, Toru Sakura, Hiroaki Shimizu and 5 more

Abstract read
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In one paragraph

Article in International journal of hematology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. OGG1 augments the transcriptional activation ofProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Article
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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

15 authors at 3 institutions in 1 country.

Nanami GotohGraduate School of Health Sciences, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma, 371-8514, Japan.
Takayuki SaitohGraduate School of Health Sciences, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma, 371-8514, Japan. tsaitoh@gunma-u.ac.jp.
Noriyuki TakahashiGraduate School of Health Sciences, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma, 371-8514, Japan.
Tetsuhiro KasamatsuGraduate School of Health Sciences, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma, 371-8514, Japan.
Yusuke MinatoDepartment of Virology and Preventive Medicine, Gunma University Graduate School of Medicine, Gunma, Japan.
Alkebsi LobnaGraduate School of Health Sciences, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma, 371-8514, Japan.
Tsukasa OdaLaboratory of Molecular Genetics, Institute for Molecular and Cellular Regulation, Gunma University, Gunma, Japan.
Takumi HoshinoLeukemia Research Center, Saiseikai Maebashi Hospital, Gunma, Japan.
Toru SakuraLeukemia Research Center, Saiseikai Maebashi Hospital, Gunma, Japan.
Hiroaki ShimizuOncology Center, Gunma University Hospital, Gunma, Japan.
Makiko TakizawaDepartment of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Gunma, Japan.
Hiroshi HandaDepartment of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Gunma, Japan.
Akihiko YokohamaDivision of Blood Transfusion Service, Gunma University Hospital, Gunma, Japan.
Norifumi TsukamotoOncology Center, Gunma University Hospital, Gunma, Japan.
Hirokazu MurakamiGraduate School of Health Sciences, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma, 371-8514, Japan.
Gunma University · JPGunma University Hospital · JPGunma Saiseikai Maebashi Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have shown that tumors of relapsed acute myeloid leukemia (AML) present additional genetic mutations compared to the primary tumors. The base excision repair (BER) pathway corrects oxidatively damaged mutagenic bases and plays an important role in maintaining genetic stability. The purpose of the present study was to investigate the relationship between BER functional polymorphisms and AML relapse. We focused on five major polymorphisms: OGG1 S326C, MUTYH Q324H, APE1 D148E, XRCC1 R194W, and XRCC1 R399Q. Ninety-four adults with AML who achieved first complete remission were recruited. Genotyping was performed with the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The OGG1 S326C CC genotype (associated with lower OGG1 activity) was observed more frequently in patients with AML relapse [28.9 vs. 8.9%, odds ratio (OR) = 4.10, 95% confidence interval (CI) = 1.35-12.70, P = 0.01]. Patients with the CC genotype exhibited shorter relapse-free survival (RFS). Moreover, the TCGA database suggested that low OGG1 expression in AML cells is associated with a higher frequency of mutations. The present findings suggest that the OGG1 S326C polymorphism increased the probability of AML relapse and may be useful as a prognostic factor for AML relapse risk.

Indexed as

Genetic Association StudiesGenotypeMutationPolymorphism, GeneticAdolescentAdultAgedAged, 80 and overDisease-Free SurvivalDNA DamageDNA GlycosylasesDNA RepairFemaleGene ExpressionHumansLeukemia, Myeloid, AcuteDNA Glycosylasesoxoguanine glycosylase 1, humanReactive Oxygen SpeciesAcute myeloid leukemiaBase excision repairDNA damageOGG1Polymorphisms

Identifiers

PMID29737460
OpenAlexW2802854135

What OpenQuestion holds

Textmetadata
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.