Evidence map›Paper›PMID 28487464›Full record

ReviewThe oncologist2017

Targeting

Christina S Baik, Nathaniel J Myall, Heather A Wakelee

Open access · bronzeAbstract readReview
In one paragraph

Review in The oncologist, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 2% 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

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

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Optimizing Treatment ofJournal of the advanced practitioner in oncology · 2024
    Article
  13. Review
  14. BRAFNPJ precision oncology · 2024
    Review
  15. Review
  16. Modern therapies of nonsmall cell lung cancer.Journal of applied genetics · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. Review

5 more citing papers are in PubMed but not listed here.

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.

Christina S BaikFred Hutchinson Cancer Research Center, University of Washington, Seattle, Washington, USA cbaik2@u.washington.edu.
Nathaniel J MyallStanford University Medical Center, Palo Alto, California, USA.
Heather A WakeleeStanford University Medical Center, Palo Alto, California, USA.
Stanford Medicine · USFred Hutch Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) remains the leading cause of cancer-related deaths globally. However, the identification of oncogenic driver alterations involved in the initiation and maintenance of NSCLC, such as epidermal growth factor receptor mutations and anaplastic lymphoma kinase translocation, has led to the development of novel therapies that directly target mutant proteins and associated signaling pathways, resulting in improved clinical outcomes. As sequencing techniques have improved, the molecular heterogeneity of NSCLC has become apparent, leading to the identification of a number of potentially actionable oncogenic driver mutations. Of these, one of the most promising therapeutic targets is B-Raf proto-oncogene, serine/threonine kinase (BRAF). Mutations in BRAF, observed in 2%-4% of NSCLCs, typically lead to constitutive activation of the protein and, as a consequence, lead to activation of the mitogen-activated protein kinase signaling pathway. Direct inhibition of mutant BRAF and/or the downstream mitogen-activated protein kinase kinase (MEK) has led to prolonged survival in patients with IMPLICATIONS FOR PRACTICE: Personalized medicine has begun to provide substantial benefit to patients with oncogene-driven non-small cell lung cancer (NSCLC). However, treatment options for patients with oncogenic driver mutations lacking targeted treatment strategies remain limited. Direct inhibition of mutant B-Raf proto-oncogene, serine/threonine kinase (BRAF) and/or downstream mitogen-activated protein kinase kinase (MEK) has the potential to change the course of the disease for patients with

Indexed as

MutationAntineoplastic AgentsCarcinoma, Non-Small-Cell LungDrug Resistance, NeoplasmHumansLung NeoplasmsMolecular Targeted TherapyProto-Oncogene MasProto-Oncogene Proteins B-rafAntineoplastic AgentsBRAF protein, humanMAS1 protein, humanProto-Oncogene MasProto-Oncogene Proteins B-rafB‐Raf proto‐oncogene, serine/threonine kinaseDabrafenibNon‐small cell lung cancerTrametinibVemurafenib

Identifiers

PMID28487464
PMCPMC5507646
OpenAlexW2612306689

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.