Evidence map›Paper›PMID 19629070›Full record

ReviewNature reviews. Cancer2009

Targeting PI3K signalling in cancer: opportunities, challenges and limitations.

Jeffrey A Engelman

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,249 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,249citing papers in PubMed, 2 pooled it
–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

1,249 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  7. Phase I Trial of Ipatasertib plus Atezolizumab Enhances PI3K/AKT Pathway Immune Responses in Solid Tumors and Refractory Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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1,189 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

1 author.

Jeffrey A EngelmanMassachusetts General Hospital Cancer Center, Boston, Massachusetts 02129, USA. jengelman@partners.org

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There are ample genetic and laboratory studies that suggest the PI3K-Akt pathway is vital to the growth and survival of cancer cells. Inhibitors targeting this pathway are entering the clinic at a rapid pace. In this Review, the therapeutic potential of drugs targeting PI3K-Akt signalling for the treatment of cancer is discussed. I focus on the advantages and drawbacks of different treatment strategies for targeting this pathway, the cancers that might respond best to these therapies and the challenges and limitations that confront their clinical development.

Indexed as

Antineoplastic AgentsHumansNeoplasmsPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProtein KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesAntineoplastic AgentsMTOR protein, humanPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProtein KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID19629070

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.