Evidence map›Paper›PMID 25414119›Full record

ReviewDrugs2014

The biology and clinical development of MEK inhibitors for cancer.

Jason J Luke, Patrick A Ott, Geoffrey I Shapiro

Abstract readReview
PubMed Publisher
In one paragraph

Review in Drugs, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Human DNA Virus Exploitation of the MAPK-ERK Cascade.International journal of molecular sciences · 2019
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Emerging Systemic Therapies for Colorectal Cancer.Clinics in colon and rectal surgery · 2018
    Review
  18. Review
  19. Article
  20. 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

3 authors.

Jason J LukeMelanoma and Developmental Therapeutics Clinics, University of Chicago Cancer Center, University of Chicago, 5841 S. Maryland Ave., MC2115, Chicago, IL, 60637, USA, jluke@medicine.bsd.uchicago.edu.
Patrick A Ott
Geoffrey I Shapiro

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mitogen-activated protein kinase kinases (MAPKK) MEK1 and MEK2 are integral members of the MAPK/ERK signaling pathway and are of interest in the development of anti-cancer therapeutics. The MAPK/ERK pathway is dysregulated in more than 30 % of cancers, predominately by mutations in RAS and BRAF proteins, and MEK serves as a potential downstream target for both of these. The biology of MEK inhibition is complex, as the molecule is differentially regulated by upstream RAS or RAF. This has impacted on the past development of MEK inhibitors as treatments for cancer and may be exploited in more rational, molecularly selected drug development plans in the future. The role of MEK in cancer and the mechanism of action of MEK inhibitors is reviewed. Furthermore, MEK inhibitors that are available in standard practice, as well as those most advanced in clinical development, are discussed. Finally, next steps in the development of MEK inhibitors are considered.

Indexed as

Antineoplastic AgentsMAP Kinase Kinase 1MAP Kinase Kinase 2NeoplasmsDrug DiscoveryFeedback, PhysiologicalHumansMAP Kinase Kinase Kinase 3MAP Kinase Signaling SystemProto-Oncogene Proteins B-rafras ProteinsTherapies, InvestigationalAntineoplastic AgentsMAP Kinase Kinase 1MAP Kinase Kinase 2MAP Kinase Kinase Kinase 3Proto-Oncogene Proteins B-rafras Proteins

Identifiers

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.