Evidence map›Paper›PMID 18794886›Full record

ArticleOncogene2008

The PTEN-PI3K pathway: of feedbacks and cross-talks.

A Carracedo, P P Pandolfi

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 446 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
446citing papers in PubMed, 2 pooled it
21.7field-weighted citation impact, top 1% 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

446 citing papers in PubMed, 2 syntheses or guidelines pooled it, 891 citations in OpenAlex.

  1. Pooled it
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386 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

2 authors at 1 institution in 1 country.

A CarracedoCancer Genetics Program, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Harvard Medical School, Boston, MA 02215, USA.
P P Pandolfi
Cancer Genetics (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor suppressor PTEN was originally identified as a negative regulator of the phosphoinositide 3-kinase (PI3K) signaling, a main regulator of cell growth, metabolism and survival. Yet this function of PTEN is extremely relevant for its tumor-suppressive ability, albeit the recent characterization of many PI3K-independent tumor-suppressive activities. PI3K-mediated PIP(3) production leads to the activation of the canonical AKT-mTORC1 pathway. The implications of this signaling cascade in health and disease have been underscored by the high number of regulators within the pathway whose alterations give rise to different malignancies, including familiar syndromes, metabolic dysfunctions and cancer. Moreover, PI3K is tightly buffered at multiple levels by downstream components, which have turned this signaling pathway literally upside down. PI3K and its downstream components in turn cross-talk with a number of other pathways, thereby leading to a complex network of signals that may have dramatic consequences when perturbed. Here, we review the current status of the PTEN-PI3K signaling pathway with special emphasis on the most recent data on targets and regulation of the PTEN-PI3K axis. This provides novel provocative therapeutic implications based on the targeted modulation of PI3K-cross-talking signals.

Indexed as

AnimalsFeedback, PhysiologicalHumansModels, BiologicalPhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseReceptor Cross-TalkSignal TransductionPhosphatidylinositol 3-KinasesPTEN Phosphohydrolase

Identifiers

PMID18794886
OpenAlexW2014096417

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.