Evidence map›Paper›PMID 36053154›Full record

ArticleCancer science2022

Inhibition of insulin-like growth factor-1 receptor enhances eribulin-induced DNA damage in colorectal cancer.

Tomoyasu Yoshihiro, Hiroshi Ariyama, Kyoko Yamaguchi, Takashi Imajima, Satoru Yamaga, Kenji Tsuchihashi, Taichi Isobe, Hitoshi Kusaba, Koichi Akashi, Eishi Baba

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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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

10 authors at 2 institutions in 1 country.

Tomoyasu YoshihiroDepartment of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
Hiroshi AriyamaDepartment of Hematology, Oncology and Cardiovascular Medicine, Kyushu University Hospital, Fukuoka, Japan.ORCID https://orcid.org/0000-0002-8374-5045
Kyoko YamaguchiDepartment of Hematology, Oncology and Cardiovascular Medicine, Kyushu University Hospital, Fukuoka, Japan.
Takashi ImajimaDepartment of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
Satoru YamagaDepartment of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
Kenji TsuchihashiDepartment of Hematology, Oncology and Cardiovascular Medicine, Kyushu University Hospital, Fukuoka, Japan.
Taichi IsobeDepartment of Oncology and Social Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.ORCID https://orcid.org/0000-0001-5686-1940
Hitoshi KusabaDepartment of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
Koichi AkashiDepartment of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
Eishi BabaDepartment of Oncology and Social Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.ORCID https://orcid.org/0000-0001-9428-6772
Kyushu University · JPKyushu University Hospital · JP

Funding

Shinnihon Foundation of Advanced Medical Treatment Research
6 · The paper itself

Abstract

Microtubule targeting agents (MTAs) such as taxanes are broadly used for the treatment of patients with cancer. Although MTAs are not effective for treatment of colorectal cancer (CRC), preclinical studies suggest that a subset of patients with CRC, especially those with cancers harboring the BRAF mutation, could benefit from such agents. However, two MTAs, eribulin (Eri) and vinorelbine, have shown limited clinical efficacy. Here, we report that insulin-like growth factor 1 receptor (IGF-1R) signaling is involved in Eri resistance. Using CRC cell lines, we showed that Eri induces activation and subsequent translocation of IGF-1R to the nucleus. When the activation and/or nuclear translocation of IGF-1R was inhibited, Eri induced DNA damage and enhanced G

Indexed as

Colorectal NeoplasmsReceptor, IGF Type 1AnimalsCell Line, TumorDNA DamageFuransHumansImidazolesInsulin-Like Growth Factor IKetonesPolyether PolyketidesProtein Kinase InhibitorsPyrazines3-(8-amino-1-(2-phenylquinolin-7-yl)imidazo(1,5-a)pyrazin-3-yl)-1-methylcyclobutanoleribulinFuransImidazolesInsulin-Like Growth Factor IKetonesPolyether PolyketidesProtein Kinase InhibitorsPyrazinesReceptor, IGF Type 1colorectal cancereribulinIGF-1RmicrotubuleROS

Identifiers

PMID36053154
PMCPMC9746063
OpenAlexW4294281151

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.