Evidence map›Paper›PMID 33287328›Full record

ReviewMolecules (Basel, Switzerland)2020

DNA Damaged Induced Cell Death in Oocytes.

Jakob Gebel, Marcel Tuppi, Nicole Sänger, Björn Schumacher, Volker Dötsch

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  15. The Aging Ovary and the Tales Learned Since Fetal Development.Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation · 2023
    Review
  16. Article
  17. Frontiers in endocrinology · 2023
    Article
  18. Review
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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

5 authors at 3 institutions in 1 country.

Jakob GebelInstitute of Biophysical Chemistry and Center for Biomolecular Magnetic Resonance, Goethe University, 60438 Frankfurt, Germany.
Marcel TuppiInstitute of Biophysical Chemistry and Center for Biomolecular Magnetic Resonance, Goethe University, 60438 Frankfurt, Germany.ORCID 0000-0002-2963-5902
Nicole SängerDepartment for Gynecological Endocrinology and Reproductive Medicine, University Hospital of Bonn, Venusberg-Campus 1, 53217 Bonn, Germany.
Björn SchumacherInstitute for Genome Stability in Aging and Disease, Cologne Cluster of Excellence in Cellular Stress Responses in Aging-Associated Diseases (CECAD) Research Center, and Center for Molecular Medicine, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Volker DötschInstitute of Biophysical Chemistry and Center for Biomolecular Magnetic Resonance, Goethe University, 60438 Frankfurt, Germany.ORCID 0000-0001-5720-212X
Goethe University Frankfurt · DEUniversity Hospital Bonn · DEUniversity of Cologne · DE

Funding

Deutsche Forschungsgemeinschaft DO 545/18-1, SCHU 2494/3-1, SCHU 2494/7-1, SCHU 2494/10-1, SCHU 2494/11-1
6 · The paper itself

Abstract

The production of haploid gametes through meiosis is central to the principle of sexual reproduction. The genetic diversity is further enhanced by exchange of genetic material between homologous chromosomes by the crossover mechanism. This mechanism not only requires correct pairing of homologous chromosomes but also efficient repair of the induced DNA double-strand breaks. Oocytes have evolved a unique quality control system that eliminates cells if chromosomes do not correctly align or if DNA repair is not possible. Central to this monitoring system that is conserved from nematodes and fruit fly to humans is the p53 protein family, and in vertebrates in particular p63. In mammals, oocytes are stored for a long time in the prophase of meiosis I which, in humans, can last more than 50 years. During the entire time of this arrest phase, the DNA damage checkpoint remains active. The treatment of female cancer patients with DNA damaging irradiation or chemotherapeutics activates this checkpoint and results in elimination of the oocyte pool causing premature menopause and infertility. Here, we review the molecular mechanisms of this quality control system and discuss potential therapeutic intervention for the preservation of the oocyte pool during chemotherapy.

Indexed as

AnimalsCell DeathDNA Breaks, Double-StrandedDNA DamageDNA RepairHumansOocytesCEP-1developmentoocyte deathp53 familyp63p73quality controltetramerizationtranscriptional activity

Identifiers

PMID33287328
PMCPMC7730327
OpenAlexW3107378168

What OpenQuestion holds

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LicenceCC BY
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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.