Evidence map›Paper›PMID 30650664›Full record

ReviewBiomolecules2019

Impact of p85α Alterations in Cancer.

Jeremy D S Marshall, Dielle E Whitecross, Paul Mellor, Deborah H Anderson

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. PI(3,5)PScience advances · 2026
    Article
  2. Article
  3. Article
  4. Cancer-AssociatedInternational journal of medical sciences · 2025
    Review
  5. Article
  6. The Role of PIK3R1 in Metabolic Function and Insulin Sensitivity.International journal of molecular sciences · 2023
    Review
  7. Moonlighting enzymes: when cellular context defines specificity.Cellular and molecular life sciences : CMLS · 2023
    Review
  8. The Impact of PIK3R1 Mutations and Insulin-PI3K-Glycolytic Pathway Regulation in Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  9. Article
  10. Review
  11. CaMKK2 Promotes the Progression of Ovarian Carcinoma through the PI3K/PDK1/Akt Axis.Computational and mathematical methods in medicine · 2022
    Article
  12. Review
  13. Review
  14. Review
  15. Targeting the PI3K/AKT/mTOR/NFκB Axis in Ovarian Cancer.Journal of cellular immunology · 2020
    Article
  16. PI3K isoforms in cell signalling and vesicle trafficking.Nature reviews. Molecular cell biology · 2019
    Review
  17. 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

4 authors at 1 institution in 1 country.

Jeremy D S MarshallCancer Research Group, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK S7N 5E5, Canada. jem826@mail.usask.ca.
Dielle E WhitecrossCancer Research Group, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK S7N 5E5, Canada. dielle.whitecross@usask.ca.
Paul MellorCancer Research Group, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK S7N 5E5, Canada. pam187@mail.usask.ca.
Deborah H AndersonCancer Research Group, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK S7N 5E5, Canada. deborah.anderson@saskcancer.ca.
University of Saskatchewan · CA

Funding

CIHR MOP 84277
6 · The paper itself

Abstract

The phosphatidylinositol 3-kinase (PI3K) pathway plays a central role in the regulation of cell signaling, proliferation, survival, migration and vesicle trafficking in normal cells and is frequently deregulated in many cancers. The p85α protein is the most characterized regulatory subunit of the class IA PI3Ks, best known for its regulation of the p110-PI3K catalytic subunit. In this review, we will discuss the impact of p85α mutations or alterations in expression levels on the proteins p85α is known to bind and regulate. We will focus on alterations within the N-terminal half of p85α that primarily regulate Rab5 and some members of the Rho-family of GTPases, as well as those that regulate PTEN (phosphatase and tensin homologue deleted on chromosome 10), the enzyme that directly counteracts PI3K signaling. We highlight recent data, mapping the interaction surfaces of the PTEN⁻p85α breakpoint cluster region homology (BH) domain, which sheds new light on key residues in both proteins. As a multifunctional protein that binds and regulates many different proteins, p85α mutations at different sites have different impacts in cancer and would necessarily require distinct treatment strategies to be effective.

Indexed as

Class Ia Phosphatidylinositol 3-KinaseHumansMutationNeoplasmsProtein DomainsProtein SubunitsPTEN Phosphohydrolaserab5 GTP-Binding ProteinsClass Ia Phosphatidylinositol 3-KinaseProtein SubunitsPTEN Phosphohydrolaserab5 GTP-Binding Proteinscancermutationsp85α subunitPI3K (phosphatidylinositol 3-kinase)PTEN (phosphatase and tensin homologue deleted on chromosome 10)Rab5

Identifiers

PMID30650664
PMCPMC6359268
OpenAlexW2909847838

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.