Evidence map›Paper›PMID 34449560›Full record

ArticleCurrent issues in molecular biology2021

TET2 Mutation and High miR-22 Expression as Biomarkers to Predict Clinical Outcome in Myelodysplastic Syndrome Patients Treated with Hypomethylating Therapy.

Jina Yun, Young Sok Ji, Geum Ha Jang, Sung Hee Lim, Se Hyung Kim, Chan Kyu Kim, Sang Byung Bae, Jong Ho Won, Seong Kyu Park

Abstract read
In one paragraph

Article in Current issues in molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

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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

9 authors.

Jina YunDepartment of Internal Medicine, Division of Hemato-Oncology, Soonchunhyang University Bucheon Hospital, 170 Jomaru-ro, Wonmi-gu, Bucheon-si 14584, Gyeonggi-do, Korea.ORCID 0000-0001-5897-8309
Young Sok JiDepartment of Internal Medicine, Division of Hemato-Oncology, Soonchunhyang University Bucheon Hospital, 170 Jomaru-ro, Wonmi-gu, Bucheon-si 14584, Gyeonggi-do, Korea.ORCID 0000-0002-2248-2210
Geum Ha JangDepartment of Internal Medicine, Division of Hemato-Oncology, Soonchunhyang University Bucheon Hospital, 170 Jomaru-ro, Wonmi-gu, Bucheon-si 14584, Gyeonggi-do, Korea.
Sung Hee LimDepartment of Internal Medicine, Division of Hemato-Oncology, Soonchunhyang University Bucheon Hospital, 170 Jomaru-ro, Wonmi-gu, Bucheon-si 14584, Gyeonggi-do, Korea.
Se Hyung KimDepartment of Internal Medicine, Division of Hemato-Oncology, Soonchunhyang University Bucheon Hospital, 170 Jomaru-ro, Wonmi-gu, Bucheon-si 14584, Gyeonggi-do, Korea.
Chan Kyu KimDepartment of Internal Medicine, Division of Hemato-Oncology, Soonchunhyang University Bucheon Hospital, 170 Jomaru-ro, Wonmi-gu, Bucheon-si 14584, Gyeonggi-do, Korea.ORCID 0000-0002-1517-9950
Sang Byung BaeDepartment of Internal Medicine, Division of Hemato-Oncology, Soonchunhyang University Cheonan Hospital, 31, Suncheonhyang 6-gil, Dongnam-gu, Cheonan-si 31151, Chungcheongnam-do, Korea.
Jong Ho WonDepartment of Internal Medicine, Division of Hemato-Oncology, Soonchunhyang University Seoul Hospital, 59, Daesagwan-ro, Yongsan-gu, Seoul 04401, Korea.
Seong Kyu ParkDepartment of Internal Medicine, Division of Hemato-Oncology, Soonchunhyang University Bucheon Hospital, 170 Jomaru-ro, Wonmi-gu, Bucheon-si 14584, Gyeonggi-do, Korea.

Funding

HK inno. N. CS2018_0009Soonchunhyang University 10210023
6 · The paper itself

Abstract

Tet methylcytosine dioxygenase 2 (TET2) is one of the most frequently mutated genes in myelodysplastic syndrome (MDS). TET2 is known to involve a demethylation process, and the loss of TET2 is thought to cause DNA hypermethylation. Loss of TET2 function is known to be caused by genetic mutations and miRNA, such as miR-22. We analyzed 41 MDS patients receiving hypomethylating therapy (HMT) to assess whether TET2 mutation status and miR-22 expression status were associated with their clinical characteristics and treatment outcomes. Responsiveness to HMT was not affected by both TET2 mutation (odds ratio (OR) 0.900,

Indexed as

MutationAdultAgedAged, 80 and overAntimetabolites, AntineoplasticAzacitidineBiomarkersDecitabineDioxygenasesDNA-Binding ProteinsDNA MethylationFemaleHumansMaleMicroRNAsMiddle AgedAntimetabolites, AntineoplasticAzacitidineBiomarkersDecitabineDioxygenasesDNA-Binding ProteinsMicroRNAsMIRN22 microRNA, humanProto-Oncogene ProteinsTET2 protein, humancytogenetic abnormalityhypermethylationhypomethylating therapymiR-22myelodysplastic syndrome (MDS)TET2

Identifiers

PMID34449560
PMCPMC8929064

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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.