Evidence map›Paper›PMID 32274156›Full record

ArticleJournal of thoracic disease2020

Identification of somatic copy number variations in plasma cell free DNA correlating with intrinsic resistances to EGFR targeted therapy in T790M negative non-small cell lung cancer.

Lucheng Zhu, Jiafeng Liang, Bing Xia, Yasi Xu, Ziliang Qian, Shenglin Ma, Shirong Zhang

Open access · diamondAbstract read
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Article in Journal of thoracic disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 48% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Observational
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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

7 authors at 4 institutions in 2 countries.

Lucheng ZhuCenter for Translational Medicine, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, The Affiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou 310006, China.
Jiafeng LiangCenter for Translational Medicine, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, The Affiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou 310006, China.
Bing XiaDepartment of Oncology, Hangzhou Cancer Hospital, Hangzhou 310002, China.
Yasi XuCenter for Translational Medicine, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, The Affiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou 310006, China.
Ziliang QianProphet Genomics Inc, San Jose, CA, USA.
Shenglin MaCenter for Translational Medicine, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, The Affiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou 310006, China.
Shirong ZhangCenter for Translational Medicine, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, The Affiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou 310006, China.
Nanjing Medical University · CNZhejiang University · CNHangzhou Cancer Hospital · CNID Genomics (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAbout 20-30% EGFR-mutant non-small lung cancer show intrinsic resistance to EGFR targeted therapies. Compared to T790M positive in acquired resistance patients, little is known about EGFR-TKI intrinsic resistance for T790M negative patients.

methodsThirty-one patients with advanced stage lung cancer, including 18 patients with intrinsic resistance (PFS <6 months) and 13 patients with acquired resistance (PFS >36 months) but are negative for plasma T790M were recruited in the study. Plasma cell free DNA was profiled by low coverage whole genome sequencing with median genome coverage of 1.86X by Illumina X10. Sequencing coverage across chromosomes was summarized by samtools, and normalized by segmentation analysis as provided by R package 'DNACopy'.

resultsThe most frequent chromosomal changes were found on chr7, chr1 and chr8. Among them, chr7p gains were found in 12 (66.7%) intrinsic resistance and 4 (30.7%) acquired resistance patients. The gene EGFR was found located on the focal amplification peak of chr7p. The performance of 7p gain to predict intrinsic resistance reaches AUC =0.902. Similarly, focal amplifications were also found on chromosome 5, 16 and 22, where tumor related gene PCDHA

conclusionsThe results suggest cell free DNA copy number might be a useful peripheral blood tumor biomarker for predicting intrinsic resistance of EGFR targeted therapy and prognosis.

Indexed as

Copy number variations (CNV)intrinsic resistancesnon-small cell lung cancer (NSCLC)plasma cell free DNA (cfDNA)T790M negative

Identifiers

PMID32274156
PMCPMC7138977
OpenAlexW3009593641

What OpenQuestion holds

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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.