Evidence map›Paper›PMID 25533673›Full record

ReviewNature reviews. Cancer2015

PI3K in cancer: divergent roles of isoforms, modes of activation and therapeutic targeting.

Lauren M Thorpe, Haluk Yuzugullu, Jean J Zhao

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 731 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
731citing papers in PubMed, 3 pooled it
36.7field-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

731 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,325 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Review
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  11. Review
  12. Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  13. Review
  14. Article
  15. Article
  16. COSMIC-Linked Ras Mutations at the Interface Between H-Ras and PI3KγbioRxiv : the preprint server for biology · 2026
    Article
  17. Article
  18. Article
  19. Dual inhibition of GTP-bound (ON) and GDP-bound (OFF) KRASbioRxiv : the preprint server for biology · 2026
    Article
  20. Article

671 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 2 institutions in 1 country.

Lauren M Thorpe1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. [2] Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA. [3] Program in Virology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Haluk Yuzugullu1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. [2] Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Jean J Zhao1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. [2] Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Dana-Farber Cancer Institute · USHarvard University · US

Funding

Targeting the Vasular SystemP50CA165962 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI WENDY Beth LONDON · 2013 to 2026
$33.5M
Tissue and Pathology CoreP50CA168504 · NCI · DANA-FARBER CANCER INST · PI Nabihah Tayob · 2013 to 2026
$30.1M
Targeting the p110beta Isoform of PI3 Kinase in Pten Null TumorsR01CA172461 · NCI · DANA-FARBER CANCER INST · PI ZHAO, JEAN · 2013 to 2016
$1.6M
NCI NIH HHS CA172461-01NCI NIH HHS P50 CA165962NCI NIH HHS P50 CA165962-01A1NCI NIH HHS P50 CA168504NCI NIH HHS P50 CA168504-01A1NCI NIH HHS R01 CA172461
6 · The paper itself

Abstract

Phosphatidylinositol 3-kinases (PI3Ks) are crucial coordinators of intracellular signalling in response to extracellular stimuli. Hyperactivation of PI3K signalling cascades is one of the most common events in human cancers. In this Review, we discuss recent advances in our knowledge of the roles of specific PI3K isoforms in normal and oncogenic signalling, the different ways in which PI3K can be upregulated, and the current state and future potential of targeting this pathway in the clinic.

Indexed as

AnimalsAntineoplastic AgentsDrug Resistance, NeoplasmHumansIsoenzymesMolecular Targeted TherapyNeoplasmsPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPhosphoinositide-3 Kinase InhibitorsSignal TransductionAntineoplastic AgentsIsoenzymesPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPhosphoinositide-3 Kinase Inhibitors

Identifiers

PMID25533673
PMCPMC4384662
OpenAlexW1992477322

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.