Evidence map›Paper›PMID 36732798›Full record

ArticleMolecular brain2023

Elucidation of the mechanisms underlying tumor aggravation by the activation of stress-related neurons in the paraventricular nucleus of the hypothalamus.

Sara Yoshida, Yusuke Hamada, Michiko Narita, Daisuke Sato, Kenichi Tanaka, Tomohisa Mori, Hiroyuki Tezuka, Yukari Suda, Hideki Tamura, Kazunori Aoki and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular brain, 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 17% 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, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. 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

12 authors at 4 institutions in 2 countries.

Sara YoshidaDepartment of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-Ku, Tokyo, 142-8501, Japan.
Yusuke HamadaDepartment of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-Ku, Tokyo, 142-8501, Japan.
Michiko NaritaDivision of Cancer Pathophysiology, National Cancer Center Research Institute (NCCRI), 5-1-1 Tsukiji, Chuo-Ku, Tokyo, 104-0045, Japan.
Daisuke SatoDepartment of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-Ku, Tokyo, 142-8501, Japan.
Kenichi TanakaDepartment of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-Ku, Tokyo, 142-8501, Japan.
Tomohisa MoriDepartment of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-Ku, Tokyo, 142-8501, Japan.
Hiroyuki TezukaDepartment of Cellular Function Analysis, Research Promotion Headquarters, Fujita Health University, 1-98 Dengakugakubo, Kutsukake-Cho, Toyoake, Aichi, 470-1192, Japan.
Yukari SudaDepartment of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-Ku, Tokyo, 142-8501, Japan.
Hideki TamuraInstitute for Advanced Life Sciences, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-Ku, Tokyo, 142-8501, Japan.
Kazunori AokiDepartment of Immune Medicine, National Cancer Center Research Institute (NCCRI), 5-1-1 Tsukiji, Chuo-Ku, Tokyo, 104-0045, Japan.
Naoko KuzumakiDepartment of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-Ku, Tokyo, 142-8501, Japan. n-kuzumaki@hoshi.ac.jp.
Minoru NaritaDepartment of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-Ku, Tokyo, 142-8501, Japan. narita@hoshi.ac.jp.
Hoshi University · JPNational Cancer Centre Japan · JPNational Cancer Research Institute · GBFujita Health University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A growing body of evidence suggests that excess stress could aggravate tumor progression. The paraventricular nucleus (PVN) of the hypothalamus plays an important role in the adaptation to stress because the hypothalamic-pituitary-adrenal (HPA) axis can be activated by inducing the release of corticotropin-releasing hormone (CRH) from the PVN. In this study, we used pharmacogenetic techniques to investigate whether concomitant activation of CRH

Indexed as

CD8-Positive T-LymphocytesParaventricular Hypothalamic NucleusCorticosteroneCorticotropin-Releasing HormoneHypothalamusNeuronsRNA, MessengerCorticosteroneCorticotropin-Releasing HormoneRNA, MessengerCancerCorticotropin-releasing hormoneGlucocorticoidsTsc22d3Tumor-associated macrophageTumor-infiltrating lymphocytes

Identifiers

PMID36732798
PMCPMC9896675
OpenAlexW4318982588

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.