Evidence map›Paper›PMID 31191825›Full record

ArticleOncotarget2019

Shuhei Suzuki, Masahiro Yamamoto, Keita Togashi, Tomomi Sanomachi, Asuka Sugai, Shizuka Seino, Takashi Yoshioka, Chifumi Kitanaka, Masashi Okada

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
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

9 authors at 1 institution in 1 country.

Shuhei SuzukiDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Masahiro YamamotoDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Keita TogashiDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Tomomi SanomachiDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Asuka SugaiDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Shizuka SeinoDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Takashi YoshiokaDepartment of Clinical Oncology, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Chifumi KitanakaDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Masashi OkadaDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Yamagata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

From the perspective of psycho-oncology, antipsychotics are widely used for patients with cancer. Although some antipsychotic drugs have anti-tumor effects, these antipsychotic drugs are not applicable for cancer patients because of their severe side effects. Brexpiprazole, a novel serotonin-dopamine modulator with an improved side effect profile, was developed as a drug that is structurally and pharmacologically related to aripiprazole, which was reported to have anti-cancer effects. However, it remains unknown whether brexpiprazole has anti-cancer effects. In this study, we examined whether brexpiprazole has anti-tumor effects in cancer cells and cancer stem cells (CSCs) of glioblastoma, pancreatic cancer, and lung cancer. Brexpiprazole suppressed cell growth and induced cell death in the cancer cells and the CSCs, and decreased the CSC properties of the CSCs. Brexpiprazole did not exert any cytotoxic effects on non-cancer cells at the anti-cancer effect-inducing concentration. In the cancer cells and the CSCs, brexpiprazole reduced the expression of survivin, an anti-apoptotic protein, whose reduction sensitizes tumor cells to chemotherapeutic reagents. In the preclinical model in which pancreatic CSCs were subcutaneously implanted into nude mice, brexpiprazole suppressed tumor growth, in addition to reducing the expression of Sox2, a marker for CSCs, and survivin. This suggests that brexpiprazole is a promising antipsychotic drug with anti-tumor effects and an improved safety profile.

Indexed as

brexpiprazoledrug repositioningdrug repurposingserotonin-dopamine activity modulatorsurvivin

Identifiers

PMID31191825
PMCPMC6544401
OpenAlexW2988047127

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.