Evidence map›Paper›PMID 36866763›Full record

ArticleInternational journal of oncology2023

RRM1 is mediated by histone acetylation through gemcitabine resistance and contributes to invasiveness and ECM remodeling in pancreatic cancer.

Hiroaki Ono, Yoshiki Murase, Hironari Yamashita, Tomotaka Kato, Daisuke Asano, Yoshiya Ishikawa, Shuichi Watanabe, Hiroki Ueda, Keiichi Akahoshi, Kosuke Ogawa and 4 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

11 citing papers in PubMed, 33 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

14 authors at 1 institution in 1 country.

Hiroaki OnoDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Yoshiki MuraseDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Hironari YamashitaDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Tomotaka KatoDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Daisuke AsanoDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Yoshiya IshikawaDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Shuichi WatanabeDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Hiroki UedaDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Keiichi AkahoshiDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Kosuke OgawaDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Atsushi KudoDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Yoshimitsu AkiyamaDivision of Molecular Oncology, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Shinji TanakaDivision of Molecular Oncology, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Minoru TanabeDepartment of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Tokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The invasiveness of pancreatic cancer and its resistance to anticancer drugs define its malignant potential, and are considered to affect the peritumoral microenvironment. Cancer cells with resistance to gemcitabine exposed to external signals induced by anticancer drugs may enhance their malignant transformation. Ribonucleotide reductase large subunit M1 (RRM1), an enzyme in the DNA synthesis pathway, is upregulated during gemcitabine resistance, and its expression is associated with worse prognosis for pancreatic cancer. However, the biological function of RRM1 is unclear. In the present study, it was demonstrated that histone acetylation is involved in the regulatory mechanism related to the acquisition of gemcitabine resistance and subsequent RRM1 upregulation. The current

Indexed as

Antineoplastic AgentsDrug Resistance, NeoplasmExtracellular MatrixPancreatic NeoplasmsRibonucleoside Diphosphate ReductaseAcetylationGemcitabineHistonesHumansTumor MicroenvironmentAntineoplastic AgentsGemcitabineHistonesRibonucleoside Diphosphate ReductaseRRM1 protein, humanECM remodelinggemcitabine resistancehistone acetylationpancreatic cancerRRM1

Identifiers

PMID36866763
PMCPMC10019754
OpenAlexW4322771134

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.