Evidence map›Paper›PMID 28558031›Full record

ArticlePloS one2017

The G2 checkpoint inhibitor CBP-93872 increases the sensitivity of colorectal and pancreatic cancer cells to chemotherapy.

Tsutomu Iwata, Tairin Uchino, Ayako Koyama, Yoshikazu Johmura, Kenichi Koyama, Takuya Saito, Seiji Ishiguro, Takashi Arikawa, Shunichiro Komatsu, Masahiko Miyachi and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

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  5. Calcineurin regulates the stability and activity of estrogen receptor α.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

13 authors at 2 institutions in 1 country.

Tsutomu IwataDepartment of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.
Tairin UchinoDepartment of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.
Ayako KoyamaDepartment of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.
Yoshikazu JohmuraDepartment of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.
Kenichi KoyamaDepartment of Gastroenterological Surgery, Aichi Medical University School of Medicine, Nagakute, Japan.
Takuya SaitoDepartment of Gastroenterological Surgery, Aichi Medical University School of Medicine, Nagakute, Japan.
Seiji IshiguroDepartment of Gastroenterological Surgery, Aichi Medical University School of Medicine, Nagakute, Japan.
Takashi ArikawaDepartment of Gastroenterological Surgery, Aichi Medical University School of Medicine, Nagakute, Japan.
Shunichiro KomatsuDepartment of Gastroenterological Surgery, Aichi Medical University School of Medicine, Nagakute, Japan.
Masahiko MiyachiDepartment of Gastroenterological Surgery, Aichi Medical University School of Medicine, Nagakute, Japan.
Tsuyoshi SanoDepartment of Gastroenterological Surgery, Aichi Medical University School of Medicine, Nagakute, Japan.
Makoto NakanishiDepartment of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.
Midori ShimadaDepartment of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.ORCID http://orcid.org/0000-0002-2718-8600
Aichi Medical University · JPNagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CBP-93872 suppresses maintenance of DNA double-stranded break-induced G2 checkpoint, by inhibiting the pathway between ataxia-telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR) activation. To examine the potential use of CBP-93872 for clinical applications, we analyzed the synergistic effects of platinum-containing drugs, oxaliplatin and cisplatin, pyrimidine antimetabolites, gemcitabine and 5-fluorouracil (5-FU), in combination with CBP-93872, on cell lethality in colorectal and pancreatic cancer cell lines. Treatment with CBP-93872 significantly increased cancer cell sensitivities to various chemotherapeutic agents tested through suppression of checkpoint activation. Our results thus reveal that combination treatment of CBP-93872 with known chemotherapeutic agents inhibits phosphorylation of ATR and Chk1, and induces cell death.

Indexed as

Aniline CompoundsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsApoptosisAtaxia Telangiectasia Mutated ProteinsCell Line, TumorCheckpoint Kinase 1Colorectal NeoplasmsDrug SynergismG2 PhaseHumansPancreatic NeoplasmsPhosphorylationPropanolaminesAniline CompoundsAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCBP-93872Checkpoint Kinase 1CHEK1 protein, humanPropanolamines

Identifiers

PMID28558031
PMCPMC5448762
OpenAlexW2617589568

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.