Evidence map›Paper›PMID 35171360›Full record

ArticleInternational journal of clinical oncology2022

Changes in the concentration of EGFR-mutated plasma DNA in the first hours of targeted therapy allow the prediction of tumor response in patients with EGFR-driven lung cancer.

Fedor V Moiseyenko, Ekaterina S Kuligina, Albina S Zhabina, Sergey A Belukhin, Tatiana A Laidus, Aleksandr S Martianov, Kirill A Zagorodnev, Tatyana N Sokolova, Svetlana A Chuinyshena, Maxim M Kholmatov and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in International journal of clinical oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. 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

16 authors at 3 institutions in 1 country.

Fedor V MoiseyenkoCity Cancer Center, 68A Leningradskaya street, Pesochny, Saint Petersburg, 197758, Russia.ORCID http://orcid.org/0000-0003-2544-9042
Ekaterina S Kuligina *Laboratory of Molecular Oncology, Department of Tumor Biology, N.N. Petrov Institute of Oncology, 68 Leningradskaya street, Pesochny-2, St.-Petersburg, 197758, Russia. kate.kuligina@gmail.com.ORCID http://orcid.org/0000-0002-2396-6540
Albina S ZhabinaCity Cancer Center, 68A Leningradskaya street, Pesochny, Saint Petersburg, 197758, Russia.ORCID http://orcid.org/0000-0001-9749-8519
Sergey A BelukhinCity Cancer Center, 68A Leningradskaya street, Pesochny, Saint Petersburg, 197758, Russia.ORCID http://orcid.org/0000-0002-3106-175X
Tatiana A LaidusLaboratory of Molecular Oncology, Department of Tumor Biology, N.N. Petrov Institute of Oncology, 68 Leningradskaya street, Pesochny-2, St.-Petersburg, 197758, Russia.ORCID http://orcid.org/0000-0003-4988-1796
Aleksandr S MartianovLaboratory of Molecular Oncology, Department of Tumor Biology, N.N. Petrov Institute of Oncology, 68 Leningradskaya street, Pesochny-2, St.-Petersburg, 197758, Russia.ORCID http://orcid.org/0000-0002-7690-8328
Kirill A ZagorodnevSt.-Petersburg Pediatric Medical University, 2 Litovskaya street, Saint Petersburg, 194100, Russia.
Tatyana N SokolovaLaboratory of Molecular Oncology, Department of Tumor Biology, N.N. Petrov Institute of Oncology, 68 Leningradskaya street, Pesochny-2, St.-Petersburg, 197758, Russia.ORCID http://orcid.org/0000-0002-0537-7478
Svetlana A ChuinyshenaLaboratory of Molecular Oncology, Department of Tumor Biology, N.N. Petrov Institute of Oncology, 68 Leningradskaya street, Pesochny-2, St.-Petersburg, 197758, Russia.
Maxim M KholmatovLaboratory of Molecular Oncology, Department of Tumor Biology, N.N. Petrov Institute of Oncology, 68 Leningradskaya street, Pesochny-2, St.-Petersburg, 197758, Russia.ORCID http://orcid.org/0000-0002-4201-8124
Elizaveta V ArtemievaCity Cancer Center, 68A Leningradskaya street, Pesochny, Saint Petersburg, 197758, Russia.
Ekaterina O StepanovaCity Cancer Center, 68A Leningradskaya street, Pesochny, Saint Petersburg, 197758, Russia.ORCID http://orcid.org/0000-0002-4013-181X
Tatiana N ShuginovaCity Cancer Center, 68A Leningradskaya street, Pesochny, Saint Petersburg, 197758, Russia.
Nikita M VolkovCity Cancer Center, 68A Leningradskaya street, Pesochny, Saint Petersburg, 197758, Russia.ORCID http://orcid.org/0000-0002-6232-257X
Grigoriy A YanusLaboratory of Molecular Oncology, Department of Tumor Biology, N.N. Petrov Institute of Oncology, 68 Leningradskaya street, Pesochny-2, St.-Petersburg, 197758, Russia.ORCID http://orcid.org/0000-0002-9844-4536
Evgeny N ImyanitovLaboratory of Molecular Oncology, Department of Tumor Biology, N.N. Petrov Institute of Oncology, 68 Leningradskaya street, Pesochny-2, St.-Petersburg, 197758, Russia.ORCID http://orcid.org/0000-0003-4529-7891
Institute of Oncology NN Petrov · RUCity Clinical Oncology Center · RUSaint Petersburg State Pediatric Medical University · RU

Funding

russian science foundation 18-75-10070
6 · The paper itself

Abstract

purposeThis study aimed to analyze changes in the plasma concentration of EGFR-mutated circulating tumor DNA (ctDNA) occurring immediately after the start of therapy with EGFR tyrosine kinase inhibitors (TKIs).

methodsSerial plasma samples were collected from 30 patients with EGFR-driven non-small cell lung cancer before intake of the first tablet and at 0.5, 1, 2, 3, 6, 12, 24, 36 and 48 h after the start of the therapy. The content of EGFR alleles (exon 19 deletions or L858R) in ctDNA was measured by ddPCR.

resultsctDNA was detected at base-line in 25/30 (83%) subjects. Twelve (50%) out of 24 informative patients showed > 25% reduction of the ctDNA content at 48 h time point; all these patients demonstrated disease control after 4 and 8-12 weeks of therapy. The remaining 12 individuals showed either stable content of EGFR-mutated ctDNA (n = 5) or the elevation of ctDNA concentration (n = 7). 10 of 12 patients with elevated or stable ctDNA level achieved an objective response at 4 weeks, but only 5 of 10 evaluable patients still demonstrated disease control at 8-12 weeks (p = 0.032, when compared to the group with ctDNA decrease). The decline of the amount of circulating EGFR mutant copies at 48 h also correlated with longer progression-free survival (14.7 months vs. 8.5 months, p = 0.013).

conclusionComparison of concentration of EGFR-mutated ctDNA at base-line and at 48 h after the start of therapy is predictive for the duration of TKI efficacy.

Indexed as

Carcinoma, Non-Small-Cell LungCirculating Tumor DNALung NeoplasmsErbB ReceptorsHumansMutationProtein Kinase InhibitorsCirculating Tumor DNAEGFR protein, humanErbB ReceptorsProtein Kinase InhibitorsCirculating tumor DNAEGFRNSCLCTKI therapyTumor response

Identifiers

PMID35171360
PMCPMC8853017
OpenAlexW4212785104

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.