Evidence map›Paper›PMID 27669169›Full record

ArticleAmerican journal of respiratory and critical care medicine2017

Genetic Modifiers of Progression-Free Survival in Never-Smoking Lung Adenocarcinoma Patients Treated with First-Line Tyrosine Kinase Inhibitors.

I-Shou Chang, Shih Sheng Jiang, James Chih-Hsin Yang, Wu-Chou Su, Li-Hsin Chien, Chin-Fu Hsiao, Jih-Hsiang Lee, Chih-Yi Chen, Chung-Hsing Chen, Gee-Chen Chang and 18 more

Abstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  7. Implications of TDP-43 in non-neuronal systems.Cell communication and signaling : CCS · 2023
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  9. Recalibrating Risk Prediction Models by Synthesizing Data Sources: Adapting the Lung Cancer PLCO Model for Taiwan.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2022
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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

28 authors at 16 institutions in 6 countries.

I-Shou Chang1 National Institute of Cancer Research.
Shih Sheng Jiang1 National Institute of Cancer Research.
James Chih-Hsin Yang2 Department of Oncology and.
Wu-Chou Su4 Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Li-Hsin Chien5 Institute of Population Health Sciences, and.
Chin-Fu Hsiao5 Institute of Population Health Sciences, and.
Jih-Hsiang Lee2 Department of Oncology and.
Chih-Yi Chen7 Institute of Medicine and.
Chung-Hsing Chen1 National Institute of Cancer Research.
Gee-Chen Chang9 Faculty of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Zhaoming Wang11 Cancer Genomics Research Laboratory, Division of Cancer Epidemiology and Genetics, and.
Fang-Yi Lo5 Institute of Population Health Sciences, and.
Kuan-Yu Chen12 Division of Pulmonary Medicine, Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, National Taiwan University, Taipei, Taiwan.
Wen-Chang Wang5 Institute of Population Health Sciences, and.
Yuh-Min Chen15 College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Ming-Shyan Huang16 Department of Internal Medicine, Kaohsiung Medical University Hospital, School of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Ying-Huang Tsai17 Division of Pulmonary and Critical Care Medicine, Chiayi Chang Gung Memorial Hospital, Chiayi, Taiwan.
Yu-Chun Su5 Institute of Population Health Sciences, and.
Wan-Shan Hsieh5 Institute of Population Health Sciences, and.
Wen-Chi Shih5 Institute of Population Health Sciences, and.
Shwn-Huey Shieh18 Department of Health Services Administration and.
Tsung-Ying Yang10 Division of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.
Qing Lan20 Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.
Nathaniel Rothman20 Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.
Chien-Jen Chen21 Genomic Research Center, Academia Sinica, Taipei, Taiwan.
Stephen J Chanock20 Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.
Pan-Chyr Yang22 Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, National Taiwan University, Taipei, Taiwan.
Chao A Hsiung5 Institute of Population Health Sciences, and.
Institute of Population and Public Health · CAGenomics Research Center, Academia Sinica · TWNational Cancer Institute · USInstitute of Cancer Research · CANational Taiwan University Hospital · TWCancer Genetics (United States) · USCancer Research Center · USChiayi Chang Gung Memorial Hospital · TWChina Medical University · TWKaohsiung Medical University · TWNational Cheng Kung University Hospital · TWNational Health Research Institutes · TWNational Yang Ming Chiao Tung University · TWTaichung Veterans General Hospital · TWTaipei Veterans General Hospital · TWTexas Oncology · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationalePatients with non-small cell lung cancer (NSCLC) with mutated epidermal growth factor receptor (EGFR) are relatively sensitive to EGFR-tyrosine kinase inhibitor (TKI) treatment and have longer progression-free survival (PFS) when treated with EGFR-TKI compared with platinum-based chemotherapy. However, many patients with advanced NSCLC who have mutated EGFR do not respond to first-line EGFR-TKI treatment and still have shorter PFS.

objectivesThe aim of this study was to identify genetic variants associated with PFS among patients with lung adenocarcinoma who were treated with first-line EGFR-TKIs.

methodsA genome-wide association study on PFS was performed in never-smoking women diagnosed with lung adenocarcinoma and who were treated with first-line EGFR-TKIs (n = 128). Significant single-nucleotide polymorphisms (SNPs) were selected for follow-up association analysis (n = 198) and for replication assay in another independent cohort (n = 153). MEASUREMENTS AND MAIN

resultsWe identified SNPs at 4q12 associated with PFS at genome-wide significance (P < 10

conclusionsGenetic variants in 4q12 merit further investigation to assess their potential as pharmacogenomic predictors for and to understand the biology underlying its influence on PFS in patients treated with TKI therapy.

Indexed as

AdultAgedAged, 80 and overCarcinoma, Non-Small-Cell LungDisease-Free SurvivalErbB ReceptorsFemaleFollow-Up StudiesGenome-Wide Association StudyHumansLung NeoplasmsMaleMiddle AgedPolymorphism, Single NucleotideProtein Kinase InhibitorsYoung AdultErbB ReceptorsProtein Kinase Inhibitorsgenome-wide association studylung neoplasmsmolecular targeted therapynever-smokerssingle-nucleotide polymorphism

Identifiers

PMID27669169
PMCPMC5363976
OpenAlexW2526843003

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.