The DOI matches its Crossref record; 30 of the 33 references it cites were found in a registry or an index; 1 of the 20 sources its claims cite were checked for support.
Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC
Open accessAbstract
Introduction: EGFR‐mutant NSCLC displays diverse outcomes to tyrosine kinase inhibitor (TKI) treatment. Because co‐occurring genomic alterations might describe different biological subsets of patients with this cancer, exploring co‐occurring genomic alterations that impact patients’ outcomes using a comprehensive gene panel is potentially important. Methods: This retrospective cohort study was conducted with the panel‐sequencing data acquired from January 2014 to May 2017, and clinical outcome data collected until February 2018. This study includes all eligible patients who possess panel‐sequencing data before treatment with first‐/second‐generation EGFR‐TKIs (cohort 1) or third‐generation EGFR‐TKIs following initial EGFR‐TKI failure (cohort 2). Results: Seventy‐five patients (mean [SD] age, 58.5 [11.0] years; 68.0% women) were included in cohort 1, and 82 patients (mean [SD] age, 57.3 [9.1] years; 67.1% women) were included in cohort 2. In cohort 1, alterations in TP53 were independently associated with worse progression‐free survival (PFS) (hazard ratio [HR]: 2.02; 95% confidence interval [CI]: 1.04–3.93; p = 0.038) in multivariate analysis. In cohort 2, TP53 mutation was associated with significantly worse PFS (8.9 versus 12.8 months; p = 0.029). RB1 mutation was significantly associated with worse (median PFS, 1.9 versus 11.7 months; p < 0.001). PTEN mutation was associated with significantly worse PFS (2.6 versus 10.3 months; p = 0.001). MDM2 amplification was associated with worse PFS (6.6 versus 10.4 months; p = 0.025). In cohort 2, multivariate analysis revealed that alterations in TP53 (HR: 2.23; 95% CI: 1.16–4.29; p = 0.017), RB1 (HR: 5.62; 95% CI: 1.96–16.13; p = 0.001), PTEN (HR: 5.84; 95% CI: 1.56–21.85; p = 0.009), and MDM2 (HR: 2.46; 95% CI: 1.02–5.94; p = 0.046) were independently associated with worse PFS. Conclusions: Co‐occurring genomic alterations detected by panel sequencing are associated with the clinical outcomes of EGFR‐TKI treatment in NSCLC.
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28 Own result · 14 Not checked yet · 11 Own interpretation · 7 Own method · 1 Partly supported · accuracy not yet measured
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In the paper
“However, specific co-occurring genetic alterations that affect the clinical outcomes of EGFR-TKI 3rd in addition to primary driver mutations remain largely unknown.12”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Introduction
What the sources say
- Partly supportedcites [12] Yu, 2018, Concurrent alterations in EGFR-mutant lung cancers associated with resistance to EGFR kinase inhibitors and characterization of MTOR as a mediator of resistance, Clin Cancer Res sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) says there are no established molecular features predicting duration of benefit from EGFR-TKI therapy for patients with common sensitizing EGFR mutations. That supports the general knowledge gap, but the passage does not specify third-generation EGFR-TKIs; the Results discuss outcomes for EGFR-TKIs without establishing that the findings apply to third-generation treatment specifically. (LLM, conf=0.85)
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“RB1 (HR: 5.62; 95% CI: 1.96-16.13;p ¼ 0.001)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Abstract
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In the paper
“The TP53 mutation was associated with a trend toward a shorter PFS as compared with wild-type TP53 (median PFS, 12.5 [95% confidence interval (CI): 11.1-13.9versus 14.7 [95% CI: 7.2-22.2]months; p ¼ 0.087).”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Genomic Predictors of Survival Outcome for First-or Second-Generation TKI Therapy
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“PTEN mutation was found in three (3.7%)patients and predictive of significantly shorter PFS (median PFS, 2.6 [95% CI: .4-5.2] versus 10.3 [95% CI: 7.4-13.2]months; p ¼ 0.001) (Fig. 3C and Supplementary Fig. 2C) and worse OS (median OS, 13.2 [95% CI: 4.9-26.5]versus 24.3 [95% CI: 21.1-27.5]months; p ¼ 0.005)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Genomic Predictors of Survival Outcome for Third-Generation TKI Therapy
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In the paper
“and the PI3K pathway (n ¼ 10; median PFS, 4.9 [95% CI: 0-11.6]versus 10.8 [95% CI: 8.2-13.4]months; p ¼ 0.008; median OS, 11.3 [95% CI: 4.9-NR] versus 24.5 [95% CI: 21.9-NR] months; p < 0.001)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Pathway Alterations in Cohort 2
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In the paper
“PTEN (HR: 5.84; 95% CI: 1.56-21.85;p ¼ 0.009)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Abstract
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In the paper
“TP53 mutation had a significantly shorter PFS and worse OS as compared with wild-type TP53 (median PFS, 8.9 [95% CI: 6.7-11.1]versus 12.8 [95% CI: 6.9-18.7]months; p ¼ 0.029; median OS, 17.8 [95% CI: 9.6-26.0]versus 26.6 [95% CI: 25.8-not reached (NR)] months; p ¼ 0.007)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Genomic Predictors of Survival Outcome for Third-Generation TKI Therapy
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In the paper
“In cohort 2, multivariate analysis revealed that alterations in TP53 (HR: 2.23; 95% CI: 1.16-4.29;p ¼ 0.017)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Abstract
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In the paper
“In cohort 2, TP53 mutation was associated with significantly worse PFS (8.9 versus 12.8 months; p ¼ 0.029).”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Abstract
plaincorrelationaln = 82 ·- Asserted: passes — The authors put it forward as true.
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In the paper
“Patients harboring at least one alteration in the TP53 pathway were detected in 58 (70%) cases and showed significantly shorter PFS and worse OS as compared with patients without TP53 pathway alteration (median PFS, 8.7 [95% CI: 6.7-10.7]versus 19.0 [95% CI: 12.6-25.4]months; p ¼ 0.005; median OS, 17.8 [95% CI: 8.8-26.9]versus NR [95% CI: 26.6-NR]; p ¼ 0.001).”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Pathway Alterations in Cohort 2
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In the paper
“Subclones harboring EGFR T790M and FANCA R1400H disappeared in post-osimertinib lung tumor tissue, but metastasized to the brain.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Longitudinal Genomic Profiling
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In the paper
“We also found that alterations of the cell cycle pathway (n ¼ 12; median PFS, 4.3 [95% CI: 0-9.9] versus 10.8 [95% CI: 7.8-13.8]months; p ¼ 0.005; median OS, 13.2 [95% CI: 1.8-24.6]versus 24.3 [95% CI: 21.3-27.3]months; p ¼ 0.015)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Pathway Alterations in Cohort 2
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“PTEN mutation was associated with significantly worse PFS (2.6 versus 10.3 months; p ¼ 0.001).”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Abstract
plaincorrelationaln = 82 ·- Asserted: passes — The authors put it forward as true.
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In the paper
“MDM2 (HR: 2.46; 95% CI: 1.02-5.94;p ¼ 0.046) were independently associated with worse PFS.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Abstract
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In the paper
“Regarding OS, male, ECOG greater than 1, TP53, RB1, and MDM2 alterations were associated with shorter OS (Supplementary Fig. 6).”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Multivariate Survival Analyses of Prognostic Factors in Cohort 2
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“and the PI3K pathway (n ¼ 10; median PFS, 4.9 [95% CI: 0-11.6]versus 10.8 [95% CI: 8.2-13.4]months; p ¼ 0.008; median OS, 11.3 [95% CI: 4.9-NR] versus 24.5 [95% CI: 21.9-NR] months; p < 0.001)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Pathway Alterations in Cohort 2
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Regarding OS, male, ECOG greater than 1, TP53, RB1, and MDM2 alterations were associated with shorter OS (Supplementary Fig. 6).”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Multivariate Survival Analyses of Prognostic Factors in Cohort 2
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“RB1 mutation was significantly associated with worse (median PFS, 1.9 versus 11.7 months; p < 0.001).”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Abstract
plaincorrelationaln = 82 ·- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Regarding OS, male, ECOG greater than 1, TP53, RB1, and MDM2 alterations were associated with shorter OS (Supplementary Fig. 6).”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Multivariate Survival Analyses of Prognostic Factors in Cohort 2
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Comparison of PFS2 with these two groups revealed that long PFS1 led to longer PFS2 (7.8 [95% CI: 5.5-13.7]versus 10.8 [95% CI: 8.0-16.3]months; p ¼ 0.036)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Multivariate Survival Analyses of Prognostic Factors in Cohort 2
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“although alteration of the Wnt pathway (n ¼ 16) was not significantly associated with survival (Supplementary Fig. 4).”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Pathway Alterations in Cohort 2
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In the paper
“and worse OS (HR: 3.63 [95% CI: 1.50-8.77;p ¼ 0.004) when adjusted for age, sex, smoking status, ECOG score, and EGFR subtype”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Genomic Predictors of Survival Outcome for First-or Second-Generation TKI Therapy
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In the paper
“RB1 was significantly associated with shorter PFS (median PFS, 1.9 [95% CI: 1.4-2.4]versus 11.7 [95% CI: 8.9-14.4]months; p < 0.001) and worse OS (median OS, 7.3 [95% CI: 5.0-9.6]versus 24.3 [95% CI: 21.1-27.5]months; p ¼ 0.001)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Genomic Predictors of Survival Outcome for Third-Generation TKI Therapy
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Patients harboring at least one alteration in the TP53 pathway were detected in 58 (70%) cases and showed significantly shorter PFS and worse OS as compared with patients without TP53 pathway alteration (median PFS, 8.7 [95% CI: 6.7-10.7]versus 19.0 [95% CI: 12.6-25.4]months; p ¼ 0.005; median OS, 17.8 [95% CI: 8.8-26.9]versus NR [95% CI: 26.6-NR]; p ¼ 0.001).”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Pathway Alterations in Cohort 2
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In the paper
“We also found that alterations of the cell cycle pathway (n ¼ 12; median PFS, 4.3 [95% CI: 0-9.9] versus 10.8 [95% CI: 7.8-13.8]months; p ¼ 0.005; median OS, 13.2 [95% CI: 1.8-24.6]versus 24.3 [95% CI: 21.3-27.3]months; p ¼ 0.015)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Pathway Alterations in Cohort 2
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In the paper
“a newly emerged subclone in metastasized brain tumor tissue harbored mutations in FAT3, EPHB1, and the chromatin modifiers CHD2, TRRAP, SMARCD1, and DNMT3A, which might be associated with brain metastasis.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Longitudinal Genomic Profiling
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In the paper
“In cohort 1, alterations in TP53 were independently associated with worse progression-free survival (PFS) (hazard ratio [HR]: 2.02; 95% confidence interval [CI]: 1.04-3.93;p ¼ 0.038) in multivariate analysis.”
- Also stated in: § Genomic Predictors of Survival Outcome for First-or Second-Generation TKI Therapy · plain
“Multivariate analyses confirmed that the TP53 mutation was predictive of shorter PFS (hazard ratio [HR]: 2.02; 95% CI: 1.04-3.93;p ¼ 0.038)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Abstract
plaincorrelationaln = 5 ·- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Genomic Predictors of Survival Outcome for First-or Second-Generation TKI Therapy · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There was no significant difference in PFS between the high-mutation-burden group and low-mutation-burden group (median PFS, 12.0 [95% CI: 9.2-17.8]versus 16.7 [95% CI: 12.6-25.5]months; p ¼ 0.119)”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Genomic Predictors of Survival Outcome for First-or Second-Generation TKI Therapy
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“MDM2 amplification was associated with worse PFS (6.6 versus 10.4 months; p ¼ 0.025).”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Abstract
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In the paper
“a newly emerged subclone in metastasized brain tumor tissue harbored mutations in FAT3, EPHB1, and the chromatin modifiers CHD2, TRRAP, SMARCD1, and DNMT3A, which might be associated with brain metastasis.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Longitudinal Genomic Profiling
hedgedcorrelationalSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“PFS2 is more affected by concurrent genetic alterations than PFS1.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“These data suggest that the observed clinical heterogeneity in patients with EGFR-mutant NSCLC is likely due in part to differences in co-occurring molecular events.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
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In the paper
“These molecular biomarkers can be used to predict outcomes in EGFR-mutant NSCLC patients for EGFR-targeted therapy.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
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In the paper
“Our analysis shows that NGS enabled identification of not only potentially actionable mutations, but also important co-occurring genomic alterations that have impact on prognosis of EGFR-TKI treatment.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Conclusions
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None of the sources cited for this claim have been checked yet.
In the paper
“Furthermore, cell-free DNA analysis might miss actionable mutations, which could be a result of small tumor volume or intratumor heterogeneity resulting in very low frequencies.27,28,31”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
What the sources say
- Not checked yetcites [27] Villaflor, 2016, Biopsy-free circulating tumor DNA assay identifies actionable mutations in lung cancer, Oncotarget source
- Not checked yetcites [28] Veldore, 2018, Validation of liquid biopsy: plasma cell-free DNA testing in clinical management of advanced non–small cell lung cancer, Lung Cancer (Auckl)
- Not checked yetcites [31] Thompson, 2016, Detection of therapeutically targetable driver and resistance mutations in lung cancer patients by next-generation sequencing of cell-free circulating tumor DNA, Clin Cancer Res source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“genomic studies using NGS of sequential and multisite biopsy samples pre-and post-treatment improved our understanding of the mutational process of complex clonal evolution and tumor heterogeneity.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Co-occurring genomic alterations detected by panel sequencing are associated with the clinical outcomes of EGFR-TKI treatment in NSCLC.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Given that the PI3K pathway is downstream of the EGFR-signaling pathway, it is likely that PTEN inactivation plays an important role in progression and/or therapeutic resistance in patients treated with EGFR-TKIs.23”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
What the sources say
- Not checked yetcites [23] Yamamoto, 2010, Loss of PTEN expression by blocking nuclear translocation of EGR1 in gefitinib-resistant lung cancer cells harboring epidermal growth factor receptor-activating mutations, Cancer Res source
hedgedconditionaln = 4- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: PTEN suppresses tumors by inhibiting PI3K pathway activation.
- Rests on an assumption: The PI3K pathway lies downstream of EGFR signaling.
In the paper
“When an EGFR-TKI blocks EGFR signaling, additional key genetic events, such as RB1 inactivation, occur and facilitate cell differentiation into a lineage that does not require EGFR signaling.20”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
What the sources say
- Not checked yetcites [20] Oser, 2015, Transformation from non–small-cell lung cancer to small-cell lung cancer: molecular drivers and cells of origin, Lancet Oncol
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“However, these noninvasive liquid biopsies cannot identify the full spectrum of mutations possibly affecting clinical outcomes due to the limited number of genes analyzed (typically 68 to 70 genes) or other concomitant resistant mechanisms.9,27,30”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
What the sources say
- Not checked yetcites [9] Blakely, 2017, Evolution and clinical impact of co-occurring genetic alterations in advanced-stage EGFR-mutant lung cancers, Nat Genet source
- Not checked yetcites [27] Villaflor, 2016, Biopsy-free circulating tumor DNA assay identifies actionable mutations in lung cancer, Oncotarget source
- Not checked yetcites [30] Minari, 2018, Primary resistance to osimertinib due to SCLC transformation: Issue of T790M determination on liquid re-biopsy, Lung Cancer source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Probably not a substantial claim. 18
- It may state two separate claims as one. 7
In the paper
“Recently, cell-free DNA analysis has shown significant clinical utility and high concordance with tissue-based genomic testing.[27][28][29]”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
What the sources say
- Not checked yetcites [27][28][29]
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“patients treated with different EGFR-TKI of different clinical efficacy are included”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Limitations
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Previous studies suggested a potential role of TP53 mutations and alterations in cell-cycle genes in poor therapeutic response.[10][11][12]”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Introduction
What the sources say
- Not checked yetcites [10][11][12]
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“however, RB1 mutation is reportedly associated with poor prognosis, which is consistent with our results.22”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
What the sources say
- Not checked yetcites [22] Burke, 2005, Prognostic implications of molecular and immunohistochemical profiles of the Rb and p53 cell cycle regulatory pathways in primary non–small cell lung carcinoma, Clin Cancer Res source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Variant detection, annotation, and filtering were performed using a previously described pipeline.14 To avoid false-positive results caused by insignificant germline variants and multiple comparisons, only variants predicted to have functional impact were selected.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Targeted Sequencing
What the sources say
- Not checked yetcites [14] Lee, 2018, Landscape of actionable genetic alterations profiled from 1,071 tumor samples in Korean cancer patients, Cancer Res Treat
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“we used a single center of accrual”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Limitations
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, comprehensive analysis of genomic alterations in tumor tissues via high-throughput panel sequencing can be advantageous to understand the genetic mechanisms associated with tumor progression and therapeutic resistance.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
In the paper
“A previous report showed that high expression of PTEN increases survival in patients with and EGFR-activating mutation.24”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
What the sources say
- Not checked yetcites [24] Endoh, 2006, PTEN and PIK3CA expression is associated with prolonged survival after gefitinib treatment in EGFR-mutated lung cancer patients, J Thorac Oncol
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“In advanced cases of NSCLC with the presence of EGFR mutations, treatment with EGFR-tyrosine kinase inhibitors (TKIs; e.g., gefitinib, erlotinib, and afatinib) has resulted in higher survival rates as compared with standard chemotherapy.[1][2][3]”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Introduction
What the sources say
- Not checked yetcites [1][2][3]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“RB1 is an important regulator of cell cycle progression, and its loss is involved in the small-cell transformation of NSCLC.21”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
What the sources say
- Not checked yetcites [21] Niederst, 2015, RB loss in resistant EGFR mutant lung adenocarcinomas that transform to small-cell lung cancer, Nat Commun source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This observation supports the concept that it is not just major driver mutations that affect therapeutic response and clinical outcomes and highlights the importance of conducting comprehensive genome sequencing in patients harboring an EGFR mutation.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Co-occurring genetic alterations might play a role in resistance mechanisms and could potentially explain the marked diversity of individual patient outcomes.8,9”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Introduction
What the sources say
- Not checked yetcites [8] Hong, 2018, Concomitant genetic alterations with response to treatment and epidermal growth factor receptor tyrosine kinase inhibitors in patients with EGFR-mutant advanced non–small cell lung cancer, JAMA Oncol source
- Not checked yetcites [9] Blakely, 2017, Evolution and clinical impact of co-occurring genetic alterations in advanced-stage EGFR-mutant lung cancers, Nat Genet source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Furthermore, approximately 20% to 30% of patients do not exhibit objective responses to EGFR-TKIs.[1][2][3]”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Introduction
What the sources say
- Not checked yetcites [1][2][3]
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“EGFRmutated tumors have significant inter-and intratumor heterogeneity along with various co-occurring mutations that determine the clinical efficacy of TKIs in EGFRmutated NSCLC patients.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“the generalizability of our study findings must be considered.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Limitations
plain- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our study represents a comprehensive analysis of cooccurring genomic alterations to assess their predictive efficacy of the clinical benefits of EGFR-TKI treatment in NSCLC.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Discussion
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Data collection was approved by the Samsung Medical Center Institutional Review Board/ Privacy Board (approval number: 2012-0795), and all patients provided written informed consent for the genetic analysis.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Patients and Sample Collection
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All tumor specimens were reviewed by pathologists to determine the percentage of viable tumor and its adequacy for sequencing.”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Targeted Sequencing
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“NGS data on patients who received upfront third-generation TKI were excluded from this study”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Limitations
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“the use of a retrospective database limited our ability to investigate other sources of potential bias”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Limitations
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Recently, third-generation EGFR-TKIs (EGFR-TKI 3rd ), such as osimertinib, rociletinib, and olmutinib, have displayed remarkable efficacy against T790M-related resistance mutation-positive NSCLC.[4][5][6]”
§ Concurrent Genetic Alterations Predict the Progression to Target Therapy in EGFR-Mutated Advanced NSCLC > Introduction
What the sources say
- Not checked yetcites [4][5][6]
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
The paper relies on this without support.
PTEN suppresses tumors by inhibiting PI3K pathway activation.
“PTEN acts as a tumor suppressor by inhibiting PI3K pathway activation.”
The paper relies on this without support.
The PI3K pathway lies downstream of EGFR signaling.
“Given that the PI3K pathway is downstream of the EGFR-signaling pathway”
The paper relies on this without support.
High-throughput sequencing analysis can systematically detect clinically meaningful genetic alterations and identify patients likely to respond to targeted agents.
“Statistical analysis of high-throughput sequencing data enables systematic detection of clinically meaningful genetic alterations, making it possible to identify patients potentially sensitive to targeted agents.”
The paper relies on this without support.
NGS results from pre-treatment tumor samples represent the genomic state relevant to subsequent EGFR-TKI response.
“Cohort 1 included patients with NGS results obtained before treatment with first-/second-generation EGFR-TKIs”
The paper relies on this without support.
PFS is a valid measure of clinical benefit from EGFR-TKI treatment.
“Progression-free survival (PFS) and overall survival (OS) were measured from the first day of treatment with EGFR-TKI to tumor progression and death, respectively.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“In keeping with a more complex genomic landscape and a larger burden of clonal or sub-clonal co-drivers, multiple clinical studies have identified TP53 co-alterations as a negative prognostic marker in EGFR-mutant LUAD and a consistent predictor of worse clinical outcomes following EGFR TKI therapy72, 73, 111–116.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [116]
Citations
Cites
ANNOVAR: functional annotation of genetic variants from high-throughput sequencing data
Wang, K., Li, M., & Hakonarson, H. H. (2010) · Nucleic Acids Research · doi:10.1093/nar/gkq603 · Cited by 14,724
Rosell, R., Carcereny, E., Gervais, R., Vergnenegre, A., Massuti, B., Felip, E., Palmero, R., Garcia-Gomez, R., Pallares, C., Sanchez, J. M., et al. (2012) · The Lancet Oncology · doi:10.1016/s1470-2045(11)70393-x · Cited by 5,489
Mitsudomi, T., Morita, S., Yatabe, Y., Negoro, S., Okamoto, I., Tsurutani, J., Seto, T., Satouchi, M., Tada, H., Hirashima, T., et al. (2010) · The Lancet Oncology · doi:10.1016/s1470-2045(09)70364-x · Cited by 4,090
Analysis of 100,000 human cancer genomes reveals the landscape of tumor mutational burden
Chalmers, Z. R., Connelly, C. F., Fabrizio, D., Gay, L., Ali, S. M., Ennis, R., Schrock, A., Campbell, B., Shlien, A., Chmielecki, J., et al. (2017) · Genome Medicine · doi:10.1186/s13073-017-0424-2 · Cited by 3,519
Self-citationOsimertinib or Platinum–Pemetrexed in EGFR T790M–Positive Lung Cancer
Mok, T. S., Wu, Y.-L., Ahn, M.-J., Garassino, M. C., Kim, H. R., Ramalingam, S. S., Shepherd, F. A., He, Y., Akamatsu, H., Theelen, W. S. M. E., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1612674 · Cited by 3,379
Self-citationYang, J. C.-H., Wu, Y.-L., Schuler, M., Sebastian, M., Popat, S., Yamamoto, N., Zhou, C., Hu, C.-P., O'Byrne, K., Feng, J., et al. (2015) · The Lancet Oncology · doi:10.1016/s1470-2045(14)71173-8 · Cited by 1,574
Integrated digital error suppression for improved detection of circulating tumor DNA
Newman, A. M., Lovejoy, A. F., Klass, D. M., Kurtz, D. M., Chabon, J. J., Scherer, F., Stehr, H., Liu, C. L., Bratman, S. V., Say, C., et al. (2016) · Nature Biotechnology · doi:10.1038/nbt.3520 · Cited by 1,100
Oser, M. G., Niederst, M. J., Sequist, L. V. D., & Engelman, J. A. (2015) · The Lancet Oncology · doi:10.1016/s1470-2045(14)71180-5 · Cited by 974
TP53 Mutations and Survival in Squamous-Cell Carcinoma of the Head and Neck
Poeta, M. L., Manola, J. B., Goldwasser, M. A., Forastiere, A. A., Benoit, N. E., Califano, J. A., Ridge, J. A., Goodwin, J. W., Kenady, D. E., Saunders, J., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa073770 · Cited by 818
Rociletinib in EGFR-Mutated Non–Small-Cell Lung Cancer
Sequist, L. V., Soria, J.-C., Goldman, J. W., Wakelee, H. A., Gadgeel, S. M., Varga, A., Papadimitrakopoulou, V., Solomon, B. J., Oxnard, G. R., Dziadziuszko, R., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1413654 · Cited by 665
Cited by
Sorted by citations
Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy
Skoulidis, F., & Heymach, J. V. (2019) · Nature Reviews Cancer · doi:10.1038/s41568-019-0179-8 · Cited by 1,019
Therapy-Induced Evolution of Human Lung Cancer Revealed by Single-Cell RNA Sequencing
Maynard, A., McCoach, C. E., Rotow, J. K., Harris, L., Haderk, F., Kerr, D. L., Yu, E. A., Schenk, E. L., Tan, W., Zee, A., et al. (2020) · Cell · doi:10.1016/j.cell.2020.07.017 · Cited by 719
The role of MDM2 amplification and overexpression in therapeutic resistance of malignant tumors
Hou, H., Sun, D., & Zhang, X. (2019) · Cancer Cell International · doi:10.1186/s12935-019-0937-4 · Cited by 232
Santoni‐Rugiu, E., Melchior, L. C., Urbanska, E. M., Jakobsen, J. N., de Stricker, K., Grauslund, M., & Sørensen, J. B. (2019) · Cancers · doi:10.3390/cancers11070923 · Cited by 202
Concurrent TP53 Mutations Facilitate Resistance Evolution in EGFR-Mutant Lung Adenocarcinoma
Vokes, N. I., Chambers, E. S., Nguyen, T. T., Coolidge, A., Lydon, C., Le, X., Sholl, L. M., Heymach, J. V., Nishino, M., Allen, E. M. V., et al. (2022) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2022.02.011 · Cited by 170
Metadata
- Authors
- Kim, Y., Lee, B., Shim, J. H., Lee, S.-H., Park, W.-Y., Choi, Y.-L., Sun, J.-M., Ahn, J. S., Ahn, M.-J., & Park, K.
- Affiliations
- Samsung Medical Center (KR)
- Corresponding author
- Lee, Se-Hoon
- ORCID
- Venue
- Journal of Thoracic Oncology
- Publisher
- Elsevier BV
- Published
- 2019-02
- Volume
- 14
- Issue
- 2
- Pages
- 193-202
- ISSN
- 1556-0864 (ISSN-L)
- OpenAlex
- W2898978171
- Semantic Scholar
- b57daf65e62ec5edcc28cca0e0804fbf0e125eab
- Cited by
- 174
- References
- 33
- Citations by year
- 2026: 12 · 2025: 24 · 2024: 18 · 2023: 29 · 2022: 24 · 2021: 22 · 2020: 32 · 2019: 13
- FWCI
- 12.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Thoracic Oncology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Trade, Industry and Energy
- National Research Foundation of Korea
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Keywords
- EGFR-mutant non-small cell lung cancer, tyrosine kinase inhibitors, anti-EGFR therapy, TP53 mutation, RB1 mutation, PTEN mutation, MDM2 amplification, progression-free survival, treatment resistance, predictive biomarkers, third-generation EGFR-TKI, comprehensive genomic profiling, molecular subtypes, prognostic factors
- MeSH terms
- Progression-Free Survival, Aged, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, DNA, Neoplasm, Female, Humans, Lung Neoplasms, Male, Middle Aged, Mutation, Retrospective Studies, Signal Transduction, Survival Rate, Tumor Suppressor Protein p53, Sequence Analysis, DNA, Ubiquitin-Protein Ligases, Protein Kinase Inhibitors, PTEN Phosphohydrolase, Proto-Oncogene Proteins c-mdm2, Retinoblastoma Binding Proteins, High-Throughput Nucleotide Sequencing, ErbB Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-06, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
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Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
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