Evidence map›Paper›PMID 26483300›Full record

ReviewNature reviews. Clinical oncology2016

The influence of subclonal resistance mutations on targeted cancer therapy.

Michael W Schmitt, Lawrence A Loeb, Jesse J Salk

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Clinical oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed
9.0field-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.

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

138 citing papers in PubMed, 228 citations in OpenAlex.

  1. Phase II Study of Sunitinib in Tumors WithJCO precision oncology · 2024
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  11. Molecular origin, discovery, validation and application of neoantigens.Asian journal of pharmaceutical sciences · 2026
    Review
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  13. Review
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78 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 2 institutions in 1 country.

Michael W SchmittDepartments of Biochemistry and Pathology, University of Washington, 1959 Northeast Pacific Street, Box 357705, Seattle, WA 98195, USA.
Lawrence A LoebDepartments of Biochemistry and Pathology, University of Washington, 1959 Northeast Pacific Street, Box 357705, Seattle, WA 98195, USA.
Jesse J SalkDepartments of Biochemistry and Pathology, University of Washington, 1959 Northeast Pacific Street, Box 357705, Seattle, WA 98195, USA.
University of Washington · USUniversity of Washington Medical Center · US

Funding

TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI John Kyung Lee · 2002 to 2026
$58.1M
University of Washington Medical Scientist Training Program: MD/PhDT32GM007266 · NIGMS · UNIVERSITY OF WASHINGTON · PI HORWITZ, MARSHALL S. · 1985 to 2023
$30.4M
TRAINING IN CANCER BIOLOGY &TRANSPLANTATIONT32CA009515 · NCI · UNIVERSITY OF WASHINGTON · PI NANCY ELLEN DAVIDSON, Effie W Petersdorf · 1985 to 2026
$16.2M
RESEARCH TRAINING IN HEMATOLOGYT32HL007093 · NHLBI · UNIVERSITY OF WASHINGTON · PI Janis L Abkowitz · 1985 to 2026
$13.9M
Clonally Expanded Mutations Identify Cancer Precursors in Chronic InflammationR01CA160674 · NCI · UNIVERSITY OF WASHINGTON · PI BRENTNALL, TERESA A, LOEB, LAWRENCE A · 2012 to 2016
$2.8M
Validation and Advanced Development of Duplex SequencingR33CA181771 · NCI · UNIVERSITY OF WASHINGTON · PI LOEB, LAWRENCE A · 2014 to 2016
$1.1M
NCI NIH HHS P50 CA097186NCI NIH HHS R01 CA160674NCI NIH HHS R33 CA181771NCI NIH HHS T32 CA009515NHLBI NIH HHS T32 HL007093NIGMS NIH HHS T32 GM007266
6 · The paper itself

Abstract

Clinical oncology is being revolutionized by the increasing use of molecularly targeted therapies. This paradigm holds great promise for improving cancer treatment; however, allocating specific therapies to the patients who are most likely to derive a durable benefit continues to represent a considerable challenge. Evidence continues to emerge that cancers are characterized by extensive intratumour genetic heterogeneity, and that patients being considered for treatment with a targeted agent might, therefore, already possess resistance to the drug in a minority of cells. Indeed, multiple examples of pre-existing subclonal resistance mutations to various molecularly targeted agents have been described, which we review herein. Early detection of pre-existing or emerging drug resistance could enable more personalized use of targeted cancer therapy, as patients could be stratified to receive the therapies that are most likely to be effective. We consider how monitoring of drug resistance could be incorporated into clinical practice to optimize the use of targeted therapies in individual patients.

Indexed as

Drug Resistance, NeoplasmErbB ReceptorsFusion Proteins, bcr-ablGenes, erbB-1HumansMAP Kinase Kinase KinasesMAP Kinase Signaling SystemMolecular Targeted TherapyMutationNeoplasmsProtein-Tyrosine KinasesProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-kitARG tyrosine kinaseBCR-ABL1 fusion protein, humanBRAF protein, humanEGFR protein, humanErbB ReceptorsFusion Proteins, bcr-ablMAP Kinase Kinase KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-kit

Identifiers

PMID26483300
PMCPMC4838548
OpenAlexW1809016129

What OpenQuestion holds

Textmetadata
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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.