Evidence map›Paper›PMID 32555285›Full record

ArticleScientific reports2020

Antitumor effect of a WEE1 inhibitor and potentiation of olaparib sensitivity by DNA damage response modulation in triple-negative breast cancer.

Dong-Hyeon Ha, Ahrum Min, Seongyeong Kim, Hyemin Jang, So Hyeon Kim, Hee-Jun Kim, Han Suk Ryu, Ja-Lok Ku, Kyung-Hun Lee, Seock-Ah Im

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
4.8field-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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. International journal of oncology · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Targeting WEE1 Kinase for Breast Cancer Therapeutics: An Update.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Article
  12. Potential promising of synthetic lethality in cancer research and treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Seize the engine: Emerging cell cycle targets in breast cancer.Clinical and translational medicine · 2024
    Review
  20. 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

10 authors at 2 institutions in 3 countries.

Dong-Hyeon HaCancer Research Institute, Seoul National University, Seoul, Korea.
Ahrum MinCancer Research Institute, Seoul National University, Seoul, Korea.
Seongyeong KimCancer Research Institute, Seoul National University, Seoul, Korea.
Hyemin JangCancer Research Institute, Seoul National University, Seoul, Korea.
So Hyeon KimCancer Research Institute, Seoul National University, Seoul, Korea.
Hee-Jun KimCancer Research Institute, Seoul National University, Seoul, Korea.
Han Suk RyuDepartment of Pathology, Seoul National University College of Medicine, Seoul, Korea.
Ja-Lok KuCancer Research Institute, Seoul National University, Seoul, Korea.ORCID http://orcid.org/0000-0002-7090-537X
Kyung-Hun LeeCancer Research Institute, Seoul National University, Seoul, Korea.
Seock-Ah ImCancer Research Institute, Seoul National University, Seoul, Korea. moisa@snu.ac.kr.
Seoul National University · KRCancer Research Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Due to its regulation of CDK1/2 phosphorylation, WEE1 plays essentially roles in the regulations of G2/M checkpoint and DNA damage response (DDR). WEE1 inhibition can increase genomic instability by inducing replication stress and G2/M checkpoint inactivation, which result in increased cellular sensitivity to DNA damaging agents. We considered an increase in genomic instability induced by WEE1 inhibition might be used to augment the effects of drugs targeting DNA repair protein. Typically, PARP inhibitors are effective in germline BRCA 1/2 mutated breast and ovarian cancer, but their applicabilities in triple-negative breast cancer (TNBC) are limited. This study was conducted to investigate the anti-tumor effects of the WEE1 inhibitor, AZD1775, and the mechanism responsible for its potentiation of sensitivity to olaparib (a PARP inhibitor) via the modulation of DDR in TNBC cells. Our results suggest that AZD1775 could be used to broaden the application range of olaparib in TNBC and provide a rationale for a clinical trial of combined olaparib and AZD1775 therapy.

Indexed as

DNA DamageGene Expression Regulation, NeoplasticAnimalsApoptosisCell CycleCell Cycle ProteinsCell ProliferationDNA RepairDrug Resistance, NeoplasmDrug SynergismEnzyme InhibitorsFemaleHumansMiceMice, Inbred BALB CMice, NudeadavosertibCell Cycle ProteinsEnzyme InhibitorsolaparibPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsProtein-Tyrosine KinasesPyrazolesPyrimidinonesWEE1 protein, human

Identifiers

PMID32555285
PMCPMC7303169
OpenAlexW3035950992

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.