Evidence map›Paper›PMID 27308431›Full record

ReviewMolecular & cellular oncology

PI3K at the crossroads of tumor angiogenesis signaling pathways.

Adriana Soler, Ana Angulo-Urarte, Mariona Graupera

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular & cellular oncology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  11. Multiparametric MR-PET Imaging Predicts Pharmacokinetics and Clinical Response to GDC-0084 in Patients with Recurrent High-Grade Glioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
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  15. PI3K: A Crucial Piece in the RAS Signaling Puzzle.Cold Spring Harbor perspectives in medicine · 2018
    Review
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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

3 authors at 1 institution in 1 country.

Adriana SolerVascular Signalling Lab; Angiogenesis Unit, Institut d'Investigació Biomèdica de Bellvitge (IDIBELL) ; Barcelona, Spain.
Ana Angulo-UrarteVascular Signalling Lab; Angiogenesis Unit, Institut d'Investigació Biomèdica de Bellvitge (IDIBELL) ; Barcelona, Spain.
Mariona GrauperaVascular Signalling Lab; Angiogenesis Unit, Institut d'Investigació Biomèdica de Bellvitge (IDIBELL) ; Barcelona, Spain.
Institut d'Investigació Biomédica de Bellvitge · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumors need blood vessels for their growth, thus providing the rationale for antiangiogenic therapy in cancer treatment. However, intrinsic and acquired resistance and low response rates have turned out to be major limitations of antiangiogenic therapy. This emphasizes the need to further understand how the vasculature in cancer can be targeted. Although endothelial cells (ECs) rely on multiple growth factors and cytokines to grow, antiangiogenic therapies have mainly centered on targeting vascular endothelial growth factor (VEGF). Phosphoinositide 3-kinases (PI3Ks) form a family of 8 isoenzymes with non-redundant functions in normal biology and cancer. The subgroup of class I PI3Ks are situated at the crossroad of a plethora of proangiogenic signals and control cell growth, survival, motility, and metabolism. These isoenzymes have pleiotropic roles in the tumor microenvironment, including cell-autonomous functions in ECs, underscoring the complexity of targeting this pathway in cancer. Here, we describe how the PI3K axis influences angiogenesis in different cell compartments and summarize the diversity of vascular responses to PI3K inhibition. Targeting PI3K signaling by isoform-selective inhibitors, together with readjusting the current doses below the maximum tolerated dose, may improve clinical responses to class I PI3K anticancer agents.

Indexed as

angiogenesisPI3Ktumor-extrinsic and intrinsic rolesVEGF

Identifiers

PMID27308431
PMCPMC4905058
OpenAlexW2009990866

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.