Evidence map›Paper›PMID 26893312›Full record

ReviewTherapeutic advances in respiratory disease2016

Targeting the MEK signaling pathway in non-small cell lung cancer (NSCLC) patients with RAS aberrations.

Omar Abdel-Rahman

Abstract readReview
In one paragraph

Review in Therapeutic advances in respiratory disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
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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

1 author.

Omar Abdel-RahmanClinical Oncology Department, Faculty of Medicine, Ain Shams University, Lotfy Elsayed Street, PO Box 113331, Cairo, Egypt omar.abdelrhman@med.asu.edu.eg.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With the advancement in understanding the biology of non-small cell lung cancer (NSCLC), therapies focused on novel molecular pathways have come to the forefront of NSCLC treatment. This review focuses on the preclinical and clinical aspects underlying the targeting of RAS aberrations in NSCLC with special focus on MEK inhibitors which work by inhibiting the principal downstream mediator of RAS aberrations with a view on how to optimize outcomes with these agents. Preclinical evidence of the activity of MEK inhibitors in KRAS-mutant NSCLC has pushed forward the clinical development of these agents (namely selumetinib and trametinib) in KRAS-mutant NSCLC particularly in combination with other agents. A number of randomized studies have been launched to confirm the activity of these agents and to establish their position in the treatment armamentarium of NSCLC.

Indexed as

Molecular Targeted TherapyAnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungDrug DesignHumansLung NeoplasmsMAP Kinase Signaling SystemMutationProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)Randomized Controlled Trials as TopicAntineoplastic AgentsKRAS protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)KRASlung cancerMEKselumetinibtrametinib

Identifiers

PMID26893312
PMCPMC5933606

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.