Evidence map›Paper›PMID 12821934›Full record

ArticleOncogene2003

Role of the p38 MAPK pathway in cisplatin-based therapy.

Javier Hernández Losa, Carlos Parada Cobo, Juan Guinea Viniegra, Victor Javier Sánchez-Arevalo Lobo, Santiago Ramón y Cajal, Ricardo Sánchez-Prieto

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 163 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Revisiting Platinum-Based Anticancer Drugs to Overcome Gliomas.International journal of molecular sciences · 2021
    Review
  10. Observational
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  18. Mode of photoexcited CBioImpacts : BI · 2019
    Article
  19. Article
  20. Article

7 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

6 authors at 1 institution in 1 country.

Javier Hernández LosaUnidad de Patología Molecular, Hospital Universitario Puerta de Hierro, C/San Martin de Porres 4, 28035 Madrid, Spain.
Carlos Parada Cobo
Juan Guinea Viniegra
Victor Javier Sánchez-Arevalo Lobo
Santiago Ramón y Cajal
Ricardo Sánchez-Prieto
Hospital Universitario Puerta de Hierro Majadahonda · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p38 MAPK has been implicated in the response to cancer therapy. To determine whether the activation of p38 MAPK could be specific to cancer therapy, we investigated the activation of p38 MAPK in response to several chemotherapeutic agents, such as cisplatin, doxorubicin and taxol in several human cell lines. Activation of p38 MAPK was measured after exposure to several chemotherapeutic agents, using specific phosphoantibodies. Only cisplatin was able to activate p38 MAPK in all the cell lines tested. Furthermore, other platinum compounds such as transplatin and platinum (IV) chloride can induce activation of p38 MAPK. The kinetics of this activation is a key event in the biological role of p38 MAPK in response to cisplatin, as we conclude from the differences observed after treatment with transplatin and cisplatin. The p38 MAPK activation is independent of the origin or genetic alterations of the cell lines and seems to be mediated through both upstream activators MKK6 and MKK3. Although the isoforms alpha/beta are mainly activated, we also demonstrated that other members of the p38 MAPK family were susceptible to activation by cisplatin when they were overexpressed in 293 T. Finally, pretreatment with specific inhibitors (SB 203580 and SKF 86002) induces a resistant phenotype in response to cisplatin. Furthermore, low activation of this SAPK pathway correlates with a resistant phenotype as demonstrated in our experimental model of head and neck cancer. Therefore, we conclude that the p38 MAPK pathway is a specific target for cisplatin-based therapy with clinical implications.

Indexed as

Mitogen-Activated Protein KinasesAnimalsAntineoplastic AgentsCalcium-Calmodulin-Dependent Protein KinasesCell LineCell SurvivalCisplatinCOS CellsCross-Linking ReagentsDose-Response Relationship, DrugDose-Response Relationship, RadiationDrug Resistance, NeoplasmEnzyme ActivationEnzyme InhibitorsHeLa CellsHumans6-(4-fluorophenyl)-2,3-dihydro-5-(4-pyridinyl)imidazo(2,1-b)thiazoleAntineoplastic AgentsCalcium-Calmodulin-Dependent Protein KinasesCisplatinCross-Linking ReagentsEnzyme InhibitorsImidazolesMAP2K3 protein, humanMAP2K6 protein, humanMAP Kinase Kinase 3MAP Kinase Kinase 6Mitogen-Activated Protein Kinase 12Mitogen-Activated Protein Kinase 13Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein Kinasesplatinum chloridePlatinum CompoundsProtein IsoformsProtein-Tyrosine KinasesPyridinesSB 203580Thiazolestransplatin

Identifiers

PMID12821934
OpenAlexW2055489321

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.