Evidence map›Paper›PMID 39062685›Full record

ReviewGenes2024

The Potential Links between lncRNAs and Drug Tolerance in Lung Adenocarcinoma.

William J H Davis, Catherine J Drummond, Sarah Diermeier, Glen Reid

Abstract readReview
In one paragraph

Review in Genes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
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

4 authors.

William J H DavisDepartment of Pathology, Dunedin School of Medicine, University of Otago, P.O. Box 56, Dunedin 9054, New Zealand.ORCID 0009-0003-0870-5419
Catherine J DrummondDepartment of Pathology, Dunedin School of Medicine, University of Otago, P.O. Box 56, Dunedin 9054, New Zealand.
Sarah DiermeierDepartment of Biochemistry, University of Otago, P.O. Box 56, Dunedin 9054, New Zealand.ORCID 0000-0002-6120-2744
Glen ReidDepartment of Pathology, Dunedin School of Medicine, University of Otago, P.O. Box 56, Dunedin 9054, New Zealand.ORCID 0000-0001-6465-5223

Funding

Cancer Research Trust CRTNZ 2176Otago Medical Research Fund AP37609Royal Society Te Apārangi UOO1903
6 · The paper itself

Abstract

Lung cancer patients treated with targeted therapies frequently respond well but invariably relapse due to the development of drug resistance. Drug resistance is in part mediated by a subset of cancer cells termed "drug-tolerant persisters" (DTPs), which enter a dormant, slow-cycling state that enables them to survive drug exposure. DTPs also exhibit stem cell-like characteristics, broad epigenetic reprogramming, altered metabolism, and a mutagenic phenotype mediated by adaptive mutability. While several studies have characterised the transcriptional changes that lead to the altered phenotypes exhibited in DTPs, these studies have focused predominantly on protein coding changes. As long non-coding RNAs (lncRNAs) are also implicated in the phenotypes altered in DTPs, it is likely that they play a role in the biology of drug tolerance. In this review, we outline how lncRNAs may contribute to the key characteristics of DTPs, their potential roles in tolerance to targeted therapies, and the emergence of genetic resistance in lung adenocarcinoma.

Indexed as

Adenocarcinoma of LungDrug Resistance, NeoplasmLung NeoplasmsRNA, Long NoncodingAntineoplastic AgentsDrug ToleranceGene Expression Regulation, NeoplasticHumansAntineoplastic AgentsRNA, Long Noncodingacquired drug resistancedrug tolerancelncRNAlung adenocarcinomatargeted therapy

Identifiers

PMID39062685
PMCPMC11276205

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.