Evidence map›Paper›PMID 30864018›Full record

ReviewClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2019

Strategies to overcome acquired resistance to EGFR TKI in the treatment of non-small cell lung cancer.

J Gao, H-R Li, C Jin, J-H Jiang, J-Y Ding

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
13.4field-weighted citation impact, top 1% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

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  14. Exploring treatment options in cancer: Tumor treatment strategies.Signal transduction and targeted therapy · 2024
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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

5 authors at 1 institution in 1 country.

J GaoDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai, 200032, People's Republic of China.
H-R LiDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai, 200032, People's Republic of China.ORCID http://orcid.org/0000-0001-6926-8193
C JinDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai, 200032, People's Republic of China.
J-H JiangDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai, 200032, People's Republic of China.
J-Y DingDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai, 200032, People's Republic of China. dingjianyongmd@163.com.
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI) represents a paradigm shift in the treatment of non-small cell lung cancer (NSCLC) patients and has been the first-line therapy in clinical practice. While erlotinib, gefitinib and afatinib have achieved superior efficacy in terms of progression-free survival and overall survival compared with conventional chemotherapy in NSCLC patients, most people inevitably develop acquired resistance to them, which presents another challenge in the treatment of NSCLC. The mechanisms of acquired resistance can be classified as three types: target gene mutation, bypass signaling pathway activation and histological transformation. And the most common mechanism is T790M which accounts for approximately 50% of all subtypes. Many strategies have been explored to overcome the acquired resistance to EGFR TKI. Continuation of EGFR TKI beyond progressive disease is confined to patients in asymptomatic stage when the EGFR addiction is still preserved in some subclones. While the combination of EGFR TKI and chemotherapy or other targeted agents has improved the survival benefit in EGFR TKI resistant patients, there are controversies within them. The next-generation EGFR TKI and immunotherapy represent two novel directions for overcoming acquired resistance and have achieved promising efficacy. Liquid biopsy provides surveillance of the EGFR mutation by disclosing the entire genetic landscape but tissue biopsy is still indispensable because of the considerable rate of false-negative plasma.

Indexed as

Drug Resistance, NeoplasmAcrylamidesAfatinibAniline CompoundsAntineoplastic AgentsAxl Receptor Tyrosine KinaseCarcinoma, Non-Small-Cell LungCell Transformation, NeoplasticClass I Phosphatidylinositol 3-KinasesDisease ProgressionDrug Therapy, CombinationErbB ReceptorsErlotinib HydrochlorideGefitinibHumansImmunotherapyAcrylamidesAfatinibAniline CompoundsAntineoplastic AgentsAXL protein, humanAxl Receptor Tyrosine KinaseBRAF protein, humanClass I Phosphatidylinositol 3-KinasesdacomitinibEGFR protein, humanErbB ReceptorsErlotinib HydrochlorideGefitinibIGF1R protein, humanIndolesMET protein, humanosimertinibPIK3CA protein, humanProtein Kinase InhibitorsProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-metPyrimidinesQuinazolinonesReceptor, IGF Type 1Receptor Protein-Tyrosine KinasesAcquired resistanceEpidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI)MechanismNon-small cell lung cancer (NSCLC)Strategy

Identifiers

PMID30864018
OpenAlexW2922022182

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.