Evidence map›Paper›PMID 27655435›Full record

ReviewCancer discovery2016

Targeting PI3K in Cancer: Impact on Tumor Cells, Their Protective Stroma, Angiogenesis, and Immunotherapy.

Klaus Okkenhaug, Mariona Graupera, Bart Vanhaesebroeck

Open access · greenAbstract readReview
In one paragraph

Review in Cancer discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed
13.6field-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

158 citing papers in PubMed, 257 citations in OpenAlex.

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  6. 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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98 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 1 institution in 1 country.

Klaus OkkenhaugLaboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge, United Kingdom. bart.vanh@ucl.ac.uk klaus.okkenhaug@babraham.ac.uk mgraupera@idibell.cat.
Mariona GrauperaInstitut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain. bart.vanh@ucl.ac.uk klaus.okkenhaug@babraham.ac.uk mgraupera@idibell.cat.
Bart VanhaesebroeckUCL Cancer Institute, University College London, London, United Kingdom. bart.vanh@ucl.ac.uk klaus.okkenhaug@babraham.ac.uk mgraupera@idibell.cat.
CRUK Lung Cancer Centre of Excellence · GB

Funding

Biotechnology and Biological Sciences Research Council BBS/E/B/000C0407Biotechnology and Biological Sciences Research Council BBS/E/B/000C0409Cancer Research UK 15965Cancer Research UK C23338/A15965Wellcome TrustWellcome Trust 095691/Z/11/Z
6 · The paper itself

Abstract

The PI3K pathway is hyperactivated in most cancers, yet the capacity of PI3K inhibitors to induce tumor cell death is limited. The efficacy of PI3K inhibition can also derive from interference with the cancer cells' ability to respond to stromal signals, as illustrated by the approved PI3Kδ inhibitor idelalisib in B-cell malignancies. Inhibition of the leukocyte-enriched PI3Kδ or PI3Kγ may unleash antitumor T-cell responses by inhibiting regulatory T cells and immune-suppressive myeloid cells. Moreover, tumor angiogenesis may be targeted by PI3K inhibitors to enhance cancer therapy. Future work should therefore also explore the effects of PI3K inhibitors on the tumor stroma, in addition to their cancer cell-intrinsic impact. SIGNIFICANCE: The PI3K pathway extends beyond the direct regulation of cancer cell proliferation and survival. In B-cell malignancies, targeting PI3K purges the tumor cells from their protective microenvironment. Moreover, we propose that PI3K isoform-selective inhibitors may be exploited in the context of cancer immunotherapy and by targeting angiogenesis to improve drug and immune cell delivery. Cancer Discov; 6(10); 1090-105. ©2016 AACR.

Indexed as

Angiogenesis InhibitorsCell ProliferationCell SurvivalCombined Modality TherapyHumansImmunotherapyMolecular Targeted TherapyNeoplasmsPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsPurinesQuinazolinonesSignal TransductionStromal CellsAngiogenesis InhibitorsidelalisibPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsPurinesQuinazolinones

Identifiers

PMID27655435
PMCPMC5293166
OpenAlexW2522884107

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.