Evidence map›Paper›PMID 41293424›Full record

ReviewFrontiers in cell and developmental biology2025

Clinical application and drug resistance mechanism of gemcitabine.

Xuanrui Zhang, Bing Qi, Jing Chen

Abstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. 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

3 authors.

Xuanrui ZhangCollege of Life Sciences, North China University of Science and Technology, Tangshan, Hebei, China.
Bing QiCollege of Life Sciences, North China University of Science and Technology, Tangshan, Hebei, China.
Jing ChenCollege of Life Sciences, North China University of Science and Technology, Tangshan, Hebei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gemcitabine, as a nucleoside analog, exerts a broad-spectrum antitumor effect by interfering with DNA synthesis, but its clinical application is limited by drug resistance. The drug resistance mechanism involves metabolic abnormalities (such as downregulation of deoxycytidine kinase (dCK), nucleoside transporter hENT1 deficiency), enhanced DNA repair (overexpression of ribonucleotide reductase ribonucleotide reductase catalytic subunit M1 (RRM1)/ribonucleotide reductase catalytic subunit M2 (RRM2), and tumor microenvironment remodeling (such as secretion of immunosuppressive factors by CAFs). This article systematically reviews the drug resistance mechanism of gemcitabine and explores the breakthrough direction of new drug delivery systems (liposomes, albumin nanoparticles) and combination therapy strategies (targeted drugs, immune checkpoint inhibitors). In addition, cutting-edge technologies such as single-cell sequencing and artificial intelligence drug sensitivity prediction provide a new paradigm for precision treatment. In the future, it is necessary to build a "prevention-monitoring-intervention" full-chain management system through dynamic monitoring of multi-omics biomarkers (such as circulating tumor DNA tracking RRM2 amplification) and coordinated intervention of traditional Chinese and Western medicine (such as curcumin reversing drug resistance).

Indexed as

combination therapygemcitabineprecision medicineresistance mechanismtumor microenvironment

Identifiers

PMID41293424
PMCPMC12641025

What OpenQuestion holds

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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.