Evidence map›Paper›PMID 30368012›Full record

ArticleJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer2019

Hybrid Capture-Based Genomic Profiling of Circulating Tumor DNA from Patients with Advanced Non-Small Cell Lung Cancer.

Alexa B Schrock, Allison Welsh, Jon H Chung, Dean Pavlick, Eric H Bernicker, Benjamin C Creelan, Brady Forcier, Jeffrey S Ross, Philip J Stephens, Siraj M Ali and 5 more

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In one paragraph

Article in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 3 pooled it
–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

46 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
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  5. High-dose alectinib forContemporary oncology (Poznan, Poland) · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Alexa B SchrockFoundation Medicine, Inc., Cambridge, Massachusetts. Electronic address: aschrock@foundationmedicine.com.
Allison WelshFoundation Medicine, Inc., Cambridge, Massachusetts.
Jon H ChungFoundation Medicine, Inc., Cambridge, Massachusetts.
Dean PavlickFoundation Medicine, Inc., Cambridge, Massachusetts.
Eric H BernickerHouston Methodist Oncology Partners, Houston, Texas.
Benjamin C CreelanDepartment of Thoracic Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
Brady ForcierFoundation Medicine, Inc., Cambridge, Massachusetts.
Jeffrey S RossFoundation Medicine, Inc., Cambridge, Massachusetts; Department of Pathology, State University of New York Upstate Medical University, Syracuse, New York.
Philip J StephensFoundation Medicine, Inc., Cambridge, Massachusetts.
Siraj M AliFoundation Medicine, Inc., Cambridge, Massachusetts.
Ibiayi Dagogo-JackMassachusetts General Hospital, Boston, Massachusetts.
Alice T ShawMassachusetts General Hospital, Boston, Massachusetts.
Tianhong LiDivision of Hematology and Oncology, Department of Internal Medicine, University of California Davis Comprehensive Cancer Center, Sacramento, California.
Sai-Hong Ignatius OuUniversity of California Irvine School of Medicine, Chao Family Comprehensive Cancer Center, Orange, California.
Vincent A MillerFoundation Medicine, Inc., Cambridge, Massachusetts.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGenomic profiling informs selection of matched targeted therapies as part of routine clinical care in NSCLC. Tissue biopsy is the criterion standard; however, genomic profiling of blood-derived circulating tumor DNA (ctDNA) has emerged as a minimally invasive alternative.

methodsHybrid capture-based genomic profiling of 62 genes was performed on blood-based ctDNA from 1552 patients with NSCLC.

resultsEvidence of ctDNA was detected in 80% of samples, and in 86% of these cases, at least one reportable genomic alteration (GA) was detected. Frequently altered genes were tumor protein p53 gene (TP53) (59%), EGFR (25%), and KRAS (17%). Comparative analysis with a tissue genomic database (N = 21,500) showed similar frequencies of GAs per gene, although KRAS mutation and EGFR T790M were more frequent in tissue and ctDNA, respectively (both p < 0.0001), likely reflecting the use of liquid versus tissue biopsy after relapse during targeted therapy. In temporally matched ctDNA and tissue samples from 33 patients with evidence of ctDNA in their blood, 64% of GAs detected in tissue were also detected in ctDNA, including 78% of short variants (58 of 74) and 100% of rearrangements (four of four), but only 16% of amplifications (four of 25).

conclusionsGenomic profiling of ctDNA detected clinically relevant GAs in a significant subset of NSCLC cases. Most alterations detected in matched tissue were also detected in ctDNA. These results suggest the utility of ctDNA testing in advanced NSCLC as a complementary approach to tissue testing. Blood-based ctDNA testing may be particularly useful at the time of progression during targeted therapy.

Indexed as

AdenocarcinomaAdolescentAdultAgedAged, 80 and overCarcinoma, Large CellCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellChildClass I Phosphatidylinositol 3-KinasesDNA Copy Number VariationsDNA Mutational AnalysisDNA, NeoplasmErbB ReceptorsFemaleGene RearrangementClass I Phosphatidylinositol 3-KinasesDNA, NeoplasmEGFR protein, humanErbB ReceptorsKRAS protein, humanNeurofibromin 1NF1 protein, humanPIK3CA protein, humanProto-Oncogene Proteins p21(ras)TP53 protein, humanTumor Suppressor Protein p53Circulating tumor DNAGenomic profilingLiquid biopsyNSCLC

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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.