Evidence map›Paper›PMID 32277721›Full record

ArticleGenes to cells : devoted to molecular & cellular mechanisms2020

TDP2 suppresses genomic instability induced by androgens in the epithelial cells of prostate glands.

Md Rasel Al Mahmud, Kenichiro Ishii, Cristina Bernal-Lozano, Irene Delgado-Sainz, Masakazu Toi, Shusuke Akamatsu, Manabu Fukumoto, Masatoshi Watanabe, Shunichi Takeda, Felipe Cortés-Ledesma and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes to cells : devoted to molecular & cellular mechanisms, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
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  4. TDP2 suppresses genomic instability induced by androgens in the epithelial cells of prostate glands.Genes to cells : devoted to molecular & cellular mechanisms · 2020
    Article
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 5 institutions in 2 countries.

Md Rasel Al MahmudDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kenichiro IshiiDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu, Japan.
Cristina Bernal-LozanoCentro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER), CSIC-Universidad de Sevilla Universidad Pablo de Olavide, Sevilla, Spain.
Irene Delgado-SainzCentro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER), CSIC-Universidad de Sevilla Universidad Pablo de Olavide, Sevilla, Spain.
Masakazu ToiDepartment of Breast Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Shusuke AkamatsuDepartment of Urology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Manabu FukumotoRIKEN Center for Advanced Intelligence Project, Tokyo, Japan.
Masatoshi WatanabeDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu, Japan.
Shunichi TakedaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Felipe Cortés-LedesmaCentro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER), CSIC-Universidad de Sevilla Universidad Pablo de Olavide, Sevilla, Spain.
Hiroyuki SasanumaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0000-0003-2824-4499
Kyoto University · JPCentro Andaluz de Biología Molecular y Medicina Regenerativa · ESMie University · JPRIKEN Center for Advanced Intelligence Project · JPSpanish National Cancer Research Centre · ES

Funding

Mitsubishi Foundation ID30123Takeda Medical Research Foundation
6 · The paper itself

Abstract

Androgens stimulate the proliferation of epithelial cells in the prostate by activating topoisomerase 2 (TOP2) and regulating the transcription of target genes. TOP2 resolves the entanglement of genomic DNA by transiently generating double-strand breaks (DSBs), where TOP2 homodimers covalently bind to 5' DSB ends, called TOP2-DNA cleavage complexes (TOP2ccs). When TOP2 fails to rejoin TOP2ccs generating stalled TOP2ccs, tyrosyl DNA phosphodiesterase-2 (TDP2) removes 5' TOP2 adducts from stalled TOP2ccs prior to the ligation of the DSBs by nonhomologous end joining (NHEJ), the dominant DSB repair pathway in G

Indexed as

DNA Breaks, Double-StrandedAndrogensAnimalsCell LineCell ProliferationChromosome BreakageDNA-Binding ProteinsDNA End-Joining RepairEpithelial CellsG1 Phase Cell Cycle CheckpointsGenomic InstabilityHistonesHumansMaleMiceMice, Inbred C57BLAndrogensDNA-Binding ProteinsH2AX protein, humanHistonesPhosphoric Diester HydrolasesReceptors, AndrogenRNA, Small InterferingTDP2 protein, humanTDP2 protein, mouseandrogenatypical epithelial hyperplasiaDNA double-strand breakprostatic intraepithelial neoplasiaTDP2topoisomerase 2

Identifiers

PMID32277721
PMCPMC7497232
OpenAlexW3016063763

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.