Evidence map›Paper›PMID 12370836›Full record

ArticleOncogene2002

Modulation of PI3K/Akt pathway by E1a mediates sensitivity to cisplatin.

Juan Guinea Viniegra, Javier Hernández Losa, Victor Javier Sánchez-Arévalo, Carlos Parada Cobo, Victor Manuel Fernández Soria, Santiago Ramón y Cajal, Ricardo Sánchez-Prieto

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 40 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Juan Guinea ViniegraUnidad de Patología Molecular, Clínica Puerta de Hierro, C/San Martín de Porres 4, 28035 Madrid, Spain.
Javier Hernández Losa
Victor Javier Sánchez-Arévalo
Carlos Parada Cobo
Victor Manuel Fernández Soria
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

In order to investigate the molecular mechanisms implicated in the induction of chemo sensitivity by adenovirus E1a gene expression, we decided to investigate which signal transduction pathways could be affected by the E1a gene in Human Normal Fibroblast (IMR90). No effect was observed in SAPK pathways (p38MAPK and JNK), but E1a was able to affect the Akt activation mediated by insulin. This result was confirmed by transient transfection experiments performed in Cos-7 cells and also observed in other transformed cell lines such as A431. Furthermore, E1a expression induces a decrease in the basal status of Akt activity. Finally we demonstrated that E1a is able to block the Akt activation mediated by cisplatin and correlates with a sensitive phenotype. In summary, our data demonstrate that specific inhibition of the PI3K/Akt pathway mediates some of the biological properties of E1a such as induction of chemosensitivity.

Indexed as

Protein Serine-Threonine KinasesSignal TransductionAdenovirus E1A ProteinsAnimalsAntineoplastic AgentsCisplatinCOS CellsDNA DamageDrug Resistance, NeoplasmGenes, rasHumansInsulinPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene ProteinsProto-Oncogene Proteins c-aktAdenovirus E1A ProteinsAKT1 protein, humanAntineoplastic AgentsCisplatinInsulinPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID12370836
OpenAlexW2025151398

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.