Evidence map›Paper›PMID 37231193›Full record

ArticleScientific reports2023

Whole exome and transcriptome analysis revealed the activation of ERK and Akt signaling pathway in canine histiocytic sarcoma.

Hajime Asada, Akiyoshi Tani, Hiroki Sakuma, Miyuki Hirabayashi, Yuki Matsumoto, Kei Watanabe, Masaya Tsuboi, Shino Yoshida, Kei Harada, Takao Uchikai and 10 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

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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

20 authors at 4 institutions in 2 countries.

Hajime Asada *Department of Veterinary Internal Medicine, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Akiyoshi Tani *Department of Veterinary Internal Medicine, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Hiroki Sakuma *Department of Veterinary Internal Medicine, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Miyuki HirabayashiDepartment of Veterinary Pathology, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Yuki MatsumotoAnicom Specialty Medical Institute Inc., Shinjuku-ku, Tokyo, Japan.
Kei WatanabeAnicom Specialty Medical Institute Inc., Shinjuku-ku, Tokyo, Japan.
Masaya TsuboiVeterinary Medical Center, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Shino YoshidaDepartment of Veterinary Internal Medicine, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Kei HaradaJapan Small Animal Cancer Center, Tokorozawa, Saitama, Japan.
Takao UchikaiAnicom Specialty Medical Institute Inc., Shinjuku-ku, Tokyo, Japan.
Yuko Goto-KoshinoDepartment of Veterinary Internal Medicine, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
James K ChambersDepartment of Veterinary Pathology, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Genki IshiharaAnicom Specialty Medical Institute Inc., Shinjuku-ku, Tokyo, Japan.
Tetsuya KobayashiJapan Small Animal Cancer Center, Tokorozawa, Saitama, Japan.
Mitsuhiro IrieShikoku Veterinary Medical Center, Kita-gun, Kagawa, Japan.
Kazuyuki UchidaDepartment of Veterinary Pathology, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Koichi OhnoDepartment of Veterinary Internal Medicine, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Makoto BonkobaraDepartment of Veterinary Clinical Pathology, Nippon Veterinary and Life Science University, Musashino, Tokyo, Japan.
Hajime TsujimotoDepartment of Veterinary Internal Medicine, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Hirotaka TomiyasuDepartment of Veterinary Internal Medicine, the University of Tokyo, Bunkyo-ku, Tokyo, Japan. atomi@g.ecc.u-tokyo.ac.jp.
The University of Tokyo · JPJapan Small Animal Medical Center · JPVeterinary Medical Center · JPNippon Veterinary and Life Science University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histiocytic sarcoma (HS) is an incurable aggressive tumor, and no consensus has been made on the treatment due to its rare occurrence. Since dogs spontaneously develop the disease and several cell lines are available, they have been advocated as translational animal models. In the present study, therefore, we explored gene mutations and aberrant molecular pathways in canine HS by next generation sequencing to identify molecular targets for treatment. Whole exome sequencing and RNA-sequencing revealed gene mutations related to receptor tyrosine kinase pathways and activation of ERK1/2, PI3K-AKT, and STAT3 pathways. Analysis by quantitative PCR and immunohistochemistry revealed that fibroblast growth factor receptor 1 (FGFR1) is over-expressed. Moreover, activation of ERK and Akt signaling were confirmed in all HS cell lines, and FGFR1 inhibitors showed dose-dependent growth inhibitory effects in two of the twelve canine HS cell lines. The findings obtained in the present study indicated that ERK and Akt signaling were activated in canine HS and drugs targeting FGFR1 might be effective in part of the cases. The present study provides translational evidence that leads to establishment of novel therapeutic strategies targeting ERK and Akt signaling in HS patients.

Indexed as

Histiocytic SarcomaAnimalsCell Line, TumorDogsExomeGene Expression ProfilingPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID37231193
PMCPMC10212919
OpenAlexW4378212537

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.