Evidence map›Paper›PMID 39259678›Full record

ArticleCancer science2024

Identification of TPI1 As a potential therapeutic target in pancreatic cancer with dependency of TP53 mutation using multi-omics analysis.

Tomoaki Toyoda, Nami Miura, Shingo Kato, Takeshi Masuda, Ryuji Ohashi, Akira Matsushita, Fumio Matsuda, Sumio Ohtsuki, Akira Katakura, Kazufumi Honda

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2024. 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
–field-weighted citation impact
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.

  1. Article
  2. TPI and GAPDH Interact with Rad9, Linking Glycolytic Enzymes to Cancer.International journal of molecular sciences · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. 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.

Tomoaki ToyodaDepartment of Bioregulation, Graduate School of Medicine, Nippon Medical School, Bunkyo-ku, Tokyo, Japan.
Nami MiuraDepartment of Bioregulation, Institute for Advanced Medical Sciences, Nippon Medical School, Bunkyo-ku, Tokyo, Japan.
Shingo KatoDepartment of Gastroenterology and Hepatology, Yokohama City University School of Medicine, Yokohama, Kanazawa-ku, Japan.ORCID https://orcid.org/0000-0003-4785-5543
Takeshi MasudaDepartment of Pharmaceutical Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Ryuji OhashiDepartment of Integrated Diagnostic Pathology, Graduate School of Medicine, Nippon Medical School, Bunkyo-ku, Tokyo, Japan.
Akira MatsushitaDepartment of Gastroenterological Surgery, Nippon Medical School, Bunkyo-ku, Tokyo, Japan.
Fumio MatsudaDepartment of Bioinformatic Engineering, Graduate School of Information Science and Technology, Osaka University, Osaka, Japan.
Sumio OhtsukiDepartment of Pharmaceutical Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Akira KatakuraDepartment of Oral Pathobiological Science and Surgery, Tokyo Dental College, Tokyo, Japan.
Kazufumi HondaDepartment of Bioregulation, Graduate School of Medicine, Nippon Medical School, Bunkyo-ku, Tokyo, Japan.ORCID https://orcid.org/0000-0003-1321-5345

Funding

Japan Agency for Medical Research and Development P-CREATE / 21cm0106403h0006Japan Agency for Medical Research and Development P-PROMOTE / 22ama221401h0001
6 · The paper itself

Abstract

Mutations of KRAS, CDKN2A, TP53, and SMAD4 are the four major driver genes for pancreatic ductal adenocarcinoma (PDAC), of which mutations of KRAS and TP53 are the most frequently recognized. However, molecular-targeted therapies for mutations of KRAS and TP53 have not yet been developed. To identify novel molecular targets, we newly established organoids with the Kras mutation (Kras

Indexed as

Carcinoma, Pancreatic DuctalMutationPancreatic NeoplasmsTumor Suppressor Protein p53AnimalsCell Line, TumorCell ProliferationGlycolysisHumansMetabolomicsMiceMolecular Targeted TherapyMultiomicsOrganoidsProteomicsProto-Oncogene Proteins p21(ras)KRAS protein, humanProto-Oncogene Proteins p21(ras)TP53 protein, humanTriose-Phosphate IsomeraseTumor Suppressor Protein p53multi‐omicsorganoidp53pancreatic cancertriosephosphate isomerase 1 (TPI1)

Identifiers

PMID39259678
PMCPMC11531968

What OpenQuestion holds

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Registered trials

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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.