Evidence map›Paper›PMID 38003016›Full record

ArticleGenes2023

Molecular Networks of Platinum Drugs and Their Interaction with microRNAs in Cancer.

Shihori Tanabe, Eger Boonstra, Taehun Hong, Sabina Quader, Ryuichi Ono, Horacio Cabral, Kazuhiko Aoyagi, Hiroshi Yokozaki, Edward J Perkins, Hiroki Sasaki

Open access · goldAbstract read
In one paragraph

Article in Genes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 35% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

10 authors at 6 institutions in 2 countries.

Shihori TanabeDivision of Risk Assessment, Center for Biological Safety and Research, National Institute of Health Sciences, Kawasaki 210-9501, Japan.ORCID 0000-0003-3706-0616
Eger BoonstraDepartment of Bioengineering, Graduate School of Engineering, The University of Tokyo, Tokyo 113-0033, Japan.
Taehun HongDepartment of Bioengineering, Graduate School of Engineering, The University of Tokyo, Tokyo 113-0033, Japan.
Sabina QuaderInnovation Centre of NanoMedicine (iCONM), Kawasaki Institute of Industrial Promotion, Kawasaki 210-0821, Japan.ORCID 0000-0002-9616-7408
Ryuichi OnoDivision of Cellular and Molecular Toxicology, Center for Biological Safety and Research, National Institute of Health Sciences, Kawasaki 210-9501, Japan.
Horacio CabralDepartment of Bioengineering, Graduate School of Engineering, The University of Tokyo, Tokyo 113-0033, Japan.
Kazuhiko AoyagiDepartment of Clinical Genomics, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Hiroshi YokozakiDepartment of Pathology, Kobe University of Graduate School of Medicine, Kobe 650-0017, Japan.ORCID 0000-0001-5276-3331
Edward J PerkinsUS Army Engineer Research and Development Center, Vicksburg, MS 39180, USA.
Hiroki SasakiDepartment of Translational Oncology, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
The University of Tokyo · JPNational Institute of Health Sciences · JPInnovation Center of NanoMedicine · JPKobe University · JPNational Cancer Centre Japan · JPU.S. Army Engineer Research and Development Center · US

Funding

Japan Agency for Medical Research and Development JP21mk0101216, JP22mk0101216, JP23mk0101216Japan Society for the Promotion of Science 21K12133
6 · The paper itself

Abstract

The precise mechanism of resistance to anti-cancer drugs such as platinum drugs is not fully revealed. To reveal the mechanism of drug resistance, the molecular networks of anti-cancer drugs such as cisplatin, carboplatin, oxaliplatin, and arsenic trioxide were analyzed in several types of cancers. Since diffuse-type stomach adenocarcinoma, which has epithelial-mesenchymal transition (EMT)-like characteristics, is more malignant than intestinal-type stomach adenocarcinoma, the gene expression and molecular networks in diffuse- and intestinal-type stomach adenocarcinomas were analyzed. Analysis of carboplatin revealed the causal network in diffuse large B-cell lymphoma. The upstream regulators of the molecular networks of cisplatin-treated lung adenocarcinoma included the anti-cancer drug trichostatin A (TSA), a histone deacetylase inhibitor. The upstream regulator analysis of cisplatin revealed an increase in FAS, BTG2, SESN1, and CDKN1A, and the involvement of the tumor microenvironment pathway. The molecular networks were predicted to interact with several microRNAs, which may contribute to the identification of new drug targets for drug-resistant cancer. Analysis of oxaliplatin, a platinum drug, revealed that the SPINK1 pancreatic cancer pathway is inactivated in ischemic cardiomyopathy. The study showed the importance of the molecular networks of anti-cancer drugs and tumor microenvironment in the treatment of cancer resistant to anti-cancer drugs.

Indexed as

AdenocarcinomaAntineoplastic AgentsImmediate-Early ProteinsMicroRNAsCarboplatinCisplatinHumansOxaliplatinPlatinumTrypsin Inhibitor, Kazal PancreaticTumor MicroenvironmentTumor Suppressor ProteinsAntineoplastic AgentsBTG2 protein, humanCarboplatinCisplatinImmediate-Early ProteinsMicroRNAsOxaliplatinPlatinumSPINK1 protein, humanTrypsin Inhibitor, Kazal PancreaticTumor Suppressor Proteinscisplatindrug resistancemicroRNAmolecular networkpathway analysisplatinum drugtumor microenvironment

Identifiers

PMID38003016
PMCPMC10671144
OpenAlexW4388630221

What Socratic 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 Socratic graph.