Evidence map›Paper›PMID 25289090›Full record

ArticleOncology letters2014

Improved ataxia telangiectasia mutated kinase inhibitor KU60019 provides a promising treatment strategy for non-invasive breast cancer.

Ying Zhu, Changfei Mao, Jianzhong Wu, Shuchun Li, Rong Ma, Haixia Cao, Minghua Ji, Changwen Jing, Jinhai Tang

RetractedOpen access · diamondAbstract readRetracted Publication
In one paragraph

Article in Oncology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  11. Ataxia-Telangiectasia Mutated (ATM) Protein Signaling Participates in Development of Pulmonary Arterial Hypertension in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Ying ZhuDepartment of General Surgery, The Affiliated Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China ; Research Center of Clinical Oncology, The Affiliated Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.
Changfei MaoDepartment of General Surgery, The Affiliated Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China ; Research Center of Clinical Oncology, The Affiliated Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.
Jianzhong WuResearch Center of Clinical Oncology, The Affiliated Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.
Shuchun LiSchool of Pharmaceutical Science, Nanjing University of Technology, Nanjing, Jiangsu 210000, P.R. China.
Rong MaResearch Center of Clinical Oncology, The Affiliated Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.
Haixia CaoResearch Center of Clinical Oncology, The Affiliated Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.
Minghua JiDepartment of Radiotherapy, The Affiliated Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.
Changwen JingResearch Center of Clinical Oncology, The Affiliated Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.
Jinhai TangDepartment of General Surgery, The Affiliated Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.
Jiangsu Cancer Hospital · CNNanjing Medical University · CNNanjing Tech University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has previously been reported that KU60019, as a highly effective radiosensitizer, inhibits the DNA damage response and blocks radiation-induced phosphorylation of key ataxia telangiectasia mutated targets in human glioma cells. The present study investigated whether KU60019 affects cell physiological activities and strengthens the efficacy of doxorubicin-induced DNA damage. It was demonstrated that the compound suppressed the proliferation of MCF-7 cells and significantly increased chemosensitization. In addition, KU60019 (without doxorubicin) inhibited MCF-7 cell motility and invasion, potentially by acting on the phosphorylated-Akt and E-cadherin signaling pathways. Although the majority of MCF-7 cells were arrested at the G

Indexed as

ataxia telangiectasia mutatedchemosensitivitydoxorubicinKU60019p-p53 (Ser15)

Identifiers

PMID25289090
PMCPMC4186532
OpenAlexW2022323702

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.