Evidence map›Paper›PMID 29795269›Full record

ArticleCell death & disease2018

Loss of PUMA protects the ovarian reserve during DNA-damaging chemotherapy and preserves fertility.

Quynh-Nhu Nguyen, Nadeen Zerafa, Seng H Liew, F Hamish Morgan, Andreas Strasser, Clare L Scott, Jock K Findlay, Martha Hickey, Karla J Hutt

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
14.0field-weighted citation impact, top 1% 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

74 citing papers in PubMed, 122 citations in OpenAlex.

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  12. Susceptibility of Brca1Cancer science · 2025
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14 more citing papers are in PubMed but not listed here.

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 at 5 institutions in 2 countries.

Quynh-Nhu NguyenDepartment of Obstetrics and Gynaecology, The University of Melbourne, Parkville, VIC, Australia.
Nadeen ZerafaDevelopment and Stem Cells Program, Monash Biomedicine Discovery Institute, and Department of Anatomy and Developmental Biology, Monash University, Clayton, VIC, Australia.
Seng H LiewDevelopment and Stem Cells Program, Monash Biomedicine Discovery Institute, and Department of Anatomy and Developmental Biology, Monash University, Clayton, VIC, Australia.
F Hamish MorganDevelopment and Stem Cells Program, Monash Biomedicine Discovery Institute, and Department of Anatomy and Developmental Biology, Monash University, Clayton, VIC, Australia.
Andreas StrasserThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.
Clare L ScottThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.ORCID 0000-0002-3689-5956
Jock K FindlayCentre for Reproductive Health, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Martha HickeyDepartment of Obstetrics and Gynaecology, The University of Melbourne, Parkville, VIC, Australia.
Karla J HuttDevelopment and Stem Cells Program, Monash Biomedicine Discovery Institute, and Department of Anatomy and Developmental Biology, Monash University, Clayton, VIC, Australia. Karla.Hutt@monash.edu.
Monash University · AUThe University of Melbourne · AUDiscovery Institute · USHudson Institute of Medical Research · AURoyal Women's Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Female gametes are stored in the ovary in structures called primordial follicles, the supply of which is non-renewable. It is well established that DNA-damaging cancer treatments can deplete the ovarian reserve of primordial follicles, causing premature ovarian failure and infertility. The precise mechanisms underlying this chemotherapy-driven follicle loss are unclear, and this has limited the development of targeted ovarian-protective agents. To address this fundamental knowledge gap, we used gene deletion mouse models to examine the role of the DNA damage-induced pro-apoptotic protein, PUMA, and its transcriptional activator TAp63, in primordial follicle depletion caused by treatment with cyclophosphamide or cisplatin. Cyclophosphamide caused almost complete destruction of the primordial follicle pool in adult wild-type (WT) mice, and a significant destructive effect was also observed for cisplatin. In striking contrast, Puma

Indexed as

DNA DamageFertilityAnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsCisplatinCyclophosphamideFemaleFollicular AtresiaMice, Inbred C57BLOocytesOvarian FollicleOvarian ReservePhosphoproteinsTrans-ActivatorsAntineoplastic AgentsApoptosis Regulatory ProteinsCisplatinCyclophosphamidePhosphoproteinsPUMA protein, mouseTrans-ActivatorsTrp63 protein, mouseTumor Suppressor Proteins

Identifiers

PMID29795269
PMCPMC5966424
OpenAlexW2804421364

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.