Evidence map›Paper›PMID 32696094›Full record

ArticleMedical oncology (Northwood, London, England)2020

Wee1 kinase inhibitor AZD1775 potentiates CD8+ T cell-dependent antitumour activity via dendritic cell activation following a single high dose of irradiation.

Bin Wang, Lin Sun, Zhiyong Yuan, Zhen Tao

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 6 pooled it
1.6field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 6 syntheses or guidelines pooled it, 25 citations in OpenAlex.

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  18. Targeting DNA Damage Response in Prostate and Breast Cancer.International journal of molecular sciences · 2020
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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

4 authors at 1 institution in 1 country.

Bin WangKey Laboratory of Cancer Prevention and Therapy, Tianjin Clinical Research Center for Cancer, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, People's Republic of China.
Lin SunDepartment of Pathology, National Clinical Research Center of Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Zhiyong YuanKey Laboratory of Cancer Prevention and Therapy, Tianjin Clinical Research Center for Cancer, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, People's Republic of China. zyuan@tmu.edu.cn.
Zhen TaoKey Laboratory of Cancer Prevention and Therapy, Tianjin Clinical Research Center for Cancer, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, People's Republic of China. ztao@tmu.edu.cn.ORCID http://orcid.org/0000-0002-4316-3315
Tianjin Medical University Cancer Institute and Hospital · CN

Funding

National Natural Science Foundation of China (CN) 81472797National Natural Science Foundation of China (CN) 81602678Natural Science Foundation of Tianjin City 17JCQNJC12300
6 · The paper itself

Abstract

As standard treatments for cancer, DNA-damaging chemotherapeutic agents and irradiation therapy improve survival in patients with various cancers. Wee1, a kinase associated with the cell cycle, causes G2/M cell cycle arrest to allow repair of injured DNA in cancer cells, and a Wee1 inhibitor has been confirmed to lead to apoptosis in cancer cells. Recently, there has been renewed interest in exploring the immune environment which plays a significant role in tumour suppression. A Wee1 inhibitor combined with radiotherapy has been tested in lung, pancreatic, and prostate cancer and melanoma in vivo or in vitro. There is still no research evaluating the immunoregulatory effects of AZD1775 plus high-dose irradiation (IR) in vivo. T cell killing and CD8+ T cell depletion assays demonstrated that the combination of AZD1775 and IR delayed tumour growth in breast cancer mouse models. Additionally, combination treatment also suppressed the expression of PD-L1, a co-inhibitor, through the STAT3-IRF1 axis. The importance and originality of this study are that it explores the internal and external mechanisms of AZD1775 combined with a single high dose of IR and provides a rationale for applying the combination therapy described above in a clinical trial.

Indexed as

AnimalsBreast NeoplasmsCD8-Positive T-LymphocytesCell Cycle ProteinsCell Line, TumorCombined Modality TherapyDendritic CellsDisease Models, AnimalEnzyme InhibitorsFemaleHumansMiceMice, Inbred BALB CProtein-Tyrosine KinasesPyrazolesPyrimidinonesadavosertibCell Cycle ProteinsEnzyme InhibitorsProtein-Tyrosine KinasesPyrazolesPyrimidinonesWEE1 protein, humanAZD1775CD8+ T cellsIRPD-L1Tumour immune microenvironmentWee1

Identifiers

PMID32696094
OpenAlexW3044207329

What OpenQuestion holds

Textmetadata
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.