Evidence map›Paper›PMID 24981256›Full record

ReviewNature reviews. Clinical oncology2014

Acquired resistance to TKIs in solid tumours: learning from lung cancer.

D Ross Camidge, William Pao, Lecia V Sequist

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03133546 (A Randomised Phase II Trial of Osimertinib and Bevacizumab Versus Osimertinib Alone as Second-line Treatment in Stage IIIb-IVb NSCLC With Confirmed EGFRm and T790M), which is not on this map. Cited by 466 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
466citing papers in PubMed, 3 pooled it
59.9field-weighted citation impact, top 1% 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.

NCT03133546 phase2completednot on this mapstarted 2017, after this paper: background citation

A Randomised Phase II Trial of Osimertinib and Bevacizumab Versus Osimertinib Alone as Second-line Treatment in Stage IIIb-IVb NSCLC With Confirmed EGFRm and T790M

TypeinterventionalSponsorETOP IBCSG Partners FoundationRan2017 to 2024Enrolled155ConditionsNon Small Cell Lung Cancer MetastaticArmsOsimertinib, Bevacizumab
3 · Its place in the literature

Who cites it

466 citing papers in PubMed, 3 syntheses or guidelines pooled it, 842 citations in OpenAlex.

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  15. Tyrosine phosphoproteome profiling identifies cell-intrinsic signals limiting the efficacy of tyrosine kinase inhibitor therapies.Proceedings of the National Academy of Sciences of the United States of America · 2026
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406 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

D Ross CamidgeUniversity of Colorado Comprehensive Cancer Center, Mailstop F704, Anschutz Cancer Pavilion Room 5327, Anschutz Medical Campus, Aurora, CO 80045, USA.
William PaoVanderbilt-Ingram Cancer Center, 2220 Pierce Avenue, Nashville, TN 37232, USA.
Lecia V SequistMassachusetts General Hospital Cancer Center and Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA.
Vanderbilt University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The use of advanced molecular profiling to direct the use of targeted therapy, such as tyrosine kinase inhibitors (TKIs) for patients with advanced-stage non-small-cell lung cancer (NSCLC), has revolutionized the treatment of this disease. However, acquired resistance, defined as progression after initial benefit, to targeted therapies inevitably occurs. This Review explores breakthroughs in the understanding and treatment of acquired resistance in NSCLC, focusing on EGFR mutant and ALK rearrangement-positive disease, which may be relevant across multiple different solid malignancies with oncogene-addicted subtypes. Mechanisms of acquired resistance may be pharmacological (that is, failure of delivery of the drug to its target) or biological, resulting from evolutionary selection on molecularly diverse tumours. A number of clinical approaches can maintain control of the disease in the acquired resistance setting, including the use of radiation to treat isolated areas of progression and adding or switching to cytotoxic chemotherapy. Furthermore, novel approaches that have already proven successful include the development of second-generation and third-generation inhibitors and the combination of some of these inhibitors with antibodies directed against the same target. With our increased understanding of the spectrum of acquired resistance, major changes in how we conduct clinical research in this setting are now underway.

Indexed as

Antineoplastic AgentsCarcinoma, Non-Small-Cell LungDrug Resistance, NeoplasmHumansLung NeoplasmsProtein Kinase InhibitorsProtein-Tyrosine KinasesAntineoplastic AgentsProtein Kinase InhibitorsProtein-Tyrosine Kinases

Identifiers

PMID24981256
OpenAlexW1990013637

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.