Evidence map›Paper›PMID 35582596›Full record

ReviewCancer drug resistance (Alhambra, Calif.)2019

Drug-adapted cancer cell lines as preclinical models of acquired resistance.

Martin Michaelis, Mark N Wass, Jindrich Cinatl

Abstract readReview
In one paragraph

Review in Cancer drug resistance (Alhambra, Calif.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

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  13. Unveiling the mechanisms and challenges of cancer drug resistance.Cell communication and signaling : CCS · 2024
    Review
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  18. Emerging roles of 3D-culture systems in tackling tumor drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2023
    Review
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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

3 authors.

Martin MichaelisSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.
Mark N WassSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.
Jindrich CinatlInstitut für Medizinische Virologie, Klinikum der Goethe-Universität, Frankfurt am Main, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acquired resistance formation limits the efficacy of anti-cancer therapies. Acquired and intrinsic resistance differ conceptually. Acquired resistance is the consequence of directed evolution, whereas intrinsic resistance depends on the (stochastic) presence of pre-existing resistance mechanisms. Preclinical model systems are needed to study acquired drug resistance because they enable: (1) in depth functional studies; (2) the investigation of non-standard treatments for a certain disease condition (which is necessary to identify small groups of responders); and (3) the comparison of multiple therapies in the same system. Hence, they complement data derived from clinical trials and clinical specimens, including liquid biopsies. Many groups have successfully used drug-adapted cancer cell lines to identify and elucidate clinically relevant resistance mechanisms to targeted and cytotoxic anti-cancer drugs. Hence, we argue that drug-adapted cancer cell lines represent a preclinical model system in their own right that is complementary to other preclinical model systems and clinical data.

Indexed as

acquired drug resistanceCancercancer cell linescancer modelscancer therapydrug adaptation

Identifiers

PMID35582596
PMCPMC8992517

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.