Trial reportBritish journal of cancer2016
Clinical impact of mutation fraction in epidermal growth factor receptor mutation positive NSCLC patients.
Trial report in British journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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.
Who cites it
10 citing papers in PubMed.
- Non-Small Cell Lung Cancer: Targetable Variants in Concurrent Tissue and Liquid Biopsy Testing in a North Indian Cohort.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Targeting the EGF receptor family in non-small cell lung cancer-increased complexity and future perspectives.Cancer biology & medicine · 2022Review
- Reflex ROS1 IHC Screening with FISH Confirmation for Advanced Non-Small Cell Lung Cancer-A Cost-Efficient Strategy in a Public Healthcare System.Current oncology (Toronto, Ont.) · 2021Article
- Cross-oncopanel study reveals high sensitivity and accuracy with overall analytical performance depending on genomic regions.Genome biology · 2021Article
- Latency and interval therapy affect the evolution in metastatic colorectal cancer.Scientific reports · 2020Article
- Epidermal Growth Factor Receptor Mutation Frequency in Squamous Cell Carcinoma and Its Diagnostic Performance in Cytological Samples: A Molecular and Immunohistochemical Study.World journal of oncology · 2019Article
- Afatinib in advanced pretreated non-small-cell lung cancer- a Canadian experience.Current oncology (Toronto, Ont.) · 2018Article
- Analyzing EGFR mutations and their association with clinicopathological characteristics and prognosis of patients with lung adenocarcinoma.Oncology letters · 2018Article
- Resistance to epidermal growth factor receptor tyrosine kinase inhibitors, T790M, and clinical trials.Current oncology (Toronto, Ont.) · 2018Review
- Third-Generation Tyrosine Kinase Inhibitors Targeting Epidermal Growth Factor Receptor Mutations in Non-Small Cell Lung Cancer.Frontiers in oncology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe examined clinical outcomes in a population-based cohort of EGFR mutant advanced NSCLC patients, exploring the potential role of factors including tumour EGFR mutation fraction and cellularity in predicting outcomes.
methodsA cohort of patients with EGFR mutant advanced NSCLC was identified (N =2 93); clinical outcomes, pathologic and treatment details were collected. Tumour response was determined from radiology and clinical notes. Association between demographic and pathologic variables EGFR TKI response, time to treatment failure (TTF) and overall survival (OS) was examined using logistic regression and proportional hazards regression. EGFR TKI response rates were summarised by percent mutation fraction to explore their association.
resultsHigher mutation fraction was associated with greater EGFR TKI response rate (odds ratio 1.58, 95% CI = 1.21-2.07, P = 0.0008), longer TTF (hazard ratio 0.80, 95% CI = 0.68-0.92, P = 0.003) and better OS (hazard ratio 0.81, 95% CI = 0.67-0.99, P = 0.04). However, even in patients with ⩽ 5% mutation fraction, response rate was 34%. Females had longer TTF (P = 0.02).
conclusionsEGFR mutation fraction in tumour samples was significantly associated with response, TTF and OS. Despite this, no lower level of mutation fraction was detected for which EGFR TKI should be withheld in those with activating EGFR mutations.
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