Evidence map›Paper›PMID 20450891›Full record

ReviewBiochemical pharmacology2010

Targeting the MAPK pathway in melanoma: why some approaches succeed and other fail.

Gajanan S Inamdar, SubbaRao V Madhunapantula, Gavin P Robertson

Abstract readReview
In one paragraph

Review in Biochemical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
8.2field-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

107 citing papers in PubMed, 220 citations in OpenAlex.

  1. Trial
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  3. Review
  4. Article
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  12. Mutation-informed gene pairs to predict melanoma metastasis.Cell communication and signaling : CCS · 2026
    Article
  13. Review
  14. Review
  15. Review
  16. Targeting PP2A in cancer: an underrated option.Journal of experimental & clinical cancer research : CR · 2025
    Review
  17. Article
  18. Article
  19. Article
  20. Review

47 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 1 institution in 1 country.

Gajanan S InamdarDepartments of Pharmacology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, United States.
SubbaRao V Madhunapantula
Gavin P Robertson
Pennsylvania State University · US

Funding

Akt3 Signaling as a Therapeutic TargetR01CA127892 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI ROBERTSON, GAVIN P. · 2008 to 2012
$1.5M
Melanoma Chemoprevention by Targeting Mutant (V600E) B-RafR03CA119309 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI ROBERTSON, GAVIN P. · 2006 to 2007
$142k
NCI NIH HHS CA-127892-01ANCI NIH HHS R01 CA127892NCI NIH HHS R03 CA-119309NCI NIH HHS R03 CA119309
6 · The paper itself

Abstract

The Mitogen Activated Protein Kinase (MAPK) pathway plays a key role in melanoma development making it an important therapeutic target. In normal cells, the tightly regulated pathway relays extracellular signals from cell membrane to nucleus via a cascade of phosphorylation events. In melanomas, dysregulation of the MAPK pathway occurs frequently due to activating mutations in the B-RAF and RAS genes or other genetic or epigenetic modifications, leading to increased signaling activity promoting cell proliferation, invasion, metastasis, migration, survival and angiogenesis. However, identification of ideal pathway member to therapeutically target for maximal clinical benefit to melanoma patients remains a challenge. This review provides an overview of the obstacles faced targeting the MAPK pathway and why certain therapeutic approaches succeed while others fail. The review summarizes the roles played by the proteins, therapeutic potential and the drugs available to target each member of the pathway as well as concerns related to each. Potential for targeting multiple points and inhibiting other pathways along with MAPK inhibition for optimal efficacy are discussed along with explanations for development of drug resistance, which includes discussions related to cross-talk between pathways, RAF kinase isoform switching and phosphatase deregulation. Finally, the use of nanotechnology is reviewed as an approach to target the MAPK pathway using both genetic and pharmacological agents simultaneously targeting multiple points in the pathway or in combination with other cascades.

Indexed as

MAP Kinase Signaling SystemAntineoplastic AgentsHumansMelanomaProtein Kinase InhibitorsProto-Oncogene Proteins B-rafSkin NeoplasmsAntineoplastic AgentsBRAF protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins B-raf

Identifiers

PMID20450891
PMCPMC2897908
OpenAlexW2092286514

What OpenQuestion holds

Textmetadata
LicenceTDM
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.