Evidence map›Paper›PMID 36765741›Full record

ReviewCancers2023

Targeting Class I-II-III PI3Ks in Cancer Therapy: Recent Advances in Tumor Biology and Preclinical Research.

Benoît Thibault, Fernanda Ramos-Delgado, Julie Guillermet-Guibert

Abstract readReview
In one paragraph

Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–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

21 citing papers in PubMed.

  1. Article
  2. Review
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  5. Article
  6. Article
  7. Review
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  10. Review
  11. Review
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  13. A narrative review of autophagy in migraine.Frontiers in neuroscience · 2025
    Review
  14. Article
  15. O-GlcNAcylation: Crosstalk between Hemostasis, Inflammation, and Cancer.International journal of molecular sciences · 2024
    Review
  16. Review
  17. Article
  18. Review
  19. Regulation of PI3K signaling in cancer metabolism and PI3K-targeting therapy.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2024
    Review
  20. The essential roles of lncRNAs/PI3K/AKT axis in gastrointestinal tumors.Frontiers in cell and developmental biology · 2024
    Review
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.

Benoît ThibaultCentre de Recherches en Cancérologie de Toulouse, Université de Toulouse, Inserm, CNRS, 31037 Toulouse, France.ORCID 0000-0003-3250-1988
Fernanda Ramos-DelgadoCentre de Recherches en Cancérologie de Toulouse, Université de Toulouse, Inserm, CNRS, 31037 Toulouse, France.ORCID 0000-0002-6859-4381
Julie Guillermet-GuibertCentre de Recherches en Cancérologie de Toulouse, Université de Toulouse, Inserm, CNRS, 31037 Toulouse, France.ORCID 0000-0003-3173-4907

Funding

Agence Nationale de la Recherche Toucan, Projet-ANR-18-CE14-0013MSCA-ITN/ETN PhD-PI3K Project ID: 675392
6 · The paper itself

Abstract

Phosphatidylinositol-3-kinase (PI3K) enzymes, producing signaling phosphoinositides at plasma and intracellular membranes, are key in intracellular signaling and vesicular trafficking pathways. PI3K is a family of eight enzymes divided into three classes with various functions in physiology and largely deregulated in cancer. Here, we will review the recent evidence obtained during the last 5 years on the roles of PI3K class I, II and III isoforms in tumor biology and on the anti-tumoral action of PI3K inhibitors in preclinical cancer models. The dependency of tumors to PI3K isoforms is dictated by both genetics and context (e.g., the microenvironment). The understanding of class II/III isoforms in cancer development and progression remains scarce. Nonetheless, the limited available data are consistent and reveal that there is an interdependency between the pathways controlled by all PI3K class members in their role to promote cancer cell proliferation, survival, growth, migration and metabolism. It is unknown whether this feature contributes to partial treatment failure with isoform-selective PI3K inhibitors. Hence, a better understanding of class II/III functions to efficiently inhibit their positive and negative interactions with class I PI3Ks is needed. This research will provide the proof-of-concept to develop combination treatment strategies targeting several PI3K isoforms simultaneously.

Indexed as

cancercell signalingcombi/hybrid moleculescombination therapeuticsPI3K

Identifiers

PMID36765741
PMCPMC9913247

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.