Evidence map›Paper›PMID 32429639›Full record

ReviewZhongguo fei ai za zhi = Chinese journal of lung cancer2020

[Gene Fusions as Acquired Resistance Mechanisms of EGFR-TKI].

Yi Shao, Diansheng Zhong

Abstract readReview
In one paragraph

Review in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

2 authors.

Yi ShaoDepartment of Medical Oncology, Tianjin Medical University General Hospital, Tianjin 300052, China.
Diansheng ZhongDepartment of Medical Oncology, Tianjin Medical University General Hospital, Tianjin 300052, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with sensitive epidermal growth factor receptor (EGFR) mutations often respond to tyrosine kinase inhibitors (TKIs), but acquired resistance will eventually develop. The most common mechanisms of acquired resistance include secondary EGFR mutation, MET amplification, and histologic transformation. Besides, gene fusions could also mediate the process of acquired resistance. Various gene fusions including rearranged during transfection (RET), v-raf murine sarcoma viral oncogene homolog B1 (BRAF) and anaplastic lymphoma kinase (ALK) could take place after TKIs resistance, the incidence of which is around 1%. The clinical cases and experiments both in vitro and in vivo have proved the role of gene fusions in EGFR-TKI resistance. The combination of EGFR inhibitors and gene fusion inhibitors might be an effective therapeutic method. The understanding of gene fusions at EGFR-TKI resistance may contribute to the subsequent diagnosis and treatment strategy.

Indexed as

Gene FusionAnaplastic Lymphoma KinaseAnimalsAntineoplastic AgentsDrug Resistance, NeoplasmErbB ReceptorsHumansLung NeoplasmsProtein Kinase InhibitorsProto-Oncogene Proteins B-rafALK protein, humanAnaplastic Lymphoma KinaseAntineoplastic AgentsBRAF protein, humanErbB ReceptorsProtein Kinase InhibitorsProto-Oncogene Proteins B-rafAcquired resistanceEpidermal growth factor receptorGene fusionLung neoplasms

Identifiers

PMID32429639
PMCPMC7260378

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Registered trials

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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.