Evidence map›Paper›PMID 32440811›Full record

ReviewInternational journal of clinical oncology2020

Progress on treatment of MET signaling pathway in non-small cell lung cancer.

Xiaoqing Yu, Sizhe Yu, Yun Fan

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of clinical oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. The FOXO family of transcription factors: key molecular players in gastric cancer.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  3. Article
  4. Novel Emerging Molecular Targets in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2021
    Review
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

3 authors at 2 institutions in 1 country.

Xiaoqing YuInstitute of Cancer and Basic Medicine (ICBM), Chinese Academy of Sciences, Hangzhou, China.
Sizhe YuDepartment of Medical Oncology, Cancer Hospital, University of Chinese Academy of Sciences, Hangzhou, China.
Yun FanInstitute of Cancer and Basic Medicine (ICBM), Chinese Academy of Sciences, Hangzhou, China. fanyun_zjcc@163.com.ORCID http://orcid.org/0000-0002-4277-2725
Chinese Academy of Sciences · CNZhejiang Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MET activation includes gene mutation, amplification, and protein overexpression. Clinical evidence suggests that MET activation is both a primary oncogenic driver in lung cancer, and a secondary driver after acquired resistance to EGFR tyrosine kinase inhibitors (TKIs). Several small molecule TKIs have already shown to be effective in the MET pathway. However, the activation form and the diagnostic criteria of MET oncogene are still controversial, especially in patients resistant to EGFR TKIs or ALK TKIs. With the development of new MET inhibitors, a quantity of emerging trials has focused on the mechanism of acquired resistance to MET TKIs and therapeutic strategies after resistance.

Indexed as

Antineoplastic AgentsCarcinoma, Non-Small-Cell LungDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansLung NeoplasmsMolecular Targeted TherapyMutationProtein Kinase InhibitorsProto-Oncogene Proteins c-metSignal TransductionAntineoplastic AgentsMET protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins c-metAmplificationDysregulationMETNon-small cell lung cancerOverexpression

Identifiers

PMID32440811
OpenAlexW3028258464

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.