Evidence map›Paper›PMID 38148368›Full record

ReviewJournal of clinical immunology2023

Modulating the PI3K Signalling Pathway in Activated PI3K Delta Syndrome: a Clinical Perspective.

Lucinda J Berglund

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of clinical immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 18 citations in OpenAlex.

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  10. CRISPR-Cpf1 system and its applications in animal genome editing.Molecular genetics and genomics : MGG · 2024
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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

1 author at 1 institution in 1 country.

Lucinda J BerglundFaculty of Medicine, University of Sydney, Sydney, NSW, Australia. Lucinda.Berglund@sydney.edu.au.ORCID 0000-0002-6595-9947
The University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activated phosphoinositide-3-kinase (PI3K) δ syndrome (APDS) is an inborn error of immunity characterised by immune dysregulation. Since the discovery of genetic mutations resulting in PI3Kδ overactivation, treatment of APDS patients has begun to focus on modulation of the PI3K pathway in addition to supportive therapies. The mTOR inhibitor sirolimus has been used effectively for some clinical manifestations of this condition, however the arrival of specific PI3Kδ inhibitor leniolisib has shown promising early results and may provide a more targeted approach. This review summarizes key aspects of PI3K pathway biology and discusses potential options for nuanced modulation of the PI3K pathway in APDS from a clinical perspective, highlighting differences from PI3K inhibition in haematological malignancies.

Indexed as

Immunologic Deficiency SyndromesPrimary Immunodeficiency DiseasesClass I Phosphatidylinositol 3-KinasesHumansPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesClass I Phosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesActivated PI3K delta syndromeAPDSleniolisibsirolimus

Identifiers

PMID38148368
PMCPMC10751257
OpenAlexW4390245142

What OpenQuestion 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 OpenQuestion graph.