Evidence map›Paper›PMID 25763354›Full record

ReviewFrontiers in oncology2015

PTEN: Multiple Functions in Human Malignant Tumors.

Michele Milella, Italia Falcone, Fabiana Conciatori, Ursula Cesta Incani, Anais Del Curatolo, Nicola Inzerilli, Carmen M A Nuzzo, Vanja Vaccaro, Sabrina Vari, Francesco Cognetti and 1 more

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 254 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
254citing papers in PubMed, 1 pooled it
16.1field-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

254 citing papers in PubMed, 1 synthesis or guideline pooled it, 458 citations in OpenAlex.

  1. Pooled it
  2. Exploratory biomarker analysis from a phase III study of the PI3K inhibitor, copanlisib, in combination with rituximab in patients with indolent non-Hodgkin lymphoma, a retrospective study.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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194 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

11 authors at 1 institution in 1 country.

Michele MilellaDivision of Medical Oncology A, Regina Elena National Cancer Institute , Rome , Italy.
Italia FalconeDivision of Medical Oncology A, Regina Elena National Cancer Institute , Rome , Italy.
Fabiana ConciatoriDivision of Medical Oncology A, Regina Elena National Cancer Institute , Rome , Italy.
Ursula Cesta IncaniDivision of Medical Oncology A, Regina Elena National Cancer Institute , Rome , Italy.
Anais Del CuratoloDivision of Medical Oncology A, Regina Elena National Cancer Institute , Rome , Italy.
Nicola InzerilliDivision of Medical Oncology A, Regina Elena National Cancer Institute , Rome , Italy.
Carmen M A NuzzoDivision of Medical Oncology A, Regina Elena National Cancer Institute , Rome , Italy.
Vanja VaccaroDivision of Medical Oncology A, Regina Elena National Cancer Institute , Rome , Italy.
Sabrina VariDivision of Medical Oncology A, Regina Elena National Cancer Institute , Rome , Italy.
Francesco CognettiDivision of Medical Oncology A, Regina Elena National Cancer Institute , Rome , Italy.
Ludovica CiuffredaDivision of Medical Oncology A, Regina Elena National Cancer Institute , Rome , Italy.
National Cancer Institute · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PTEN is the most important negative regulator of the PI3K signaling pathway. In addition to its canonical, PI3K inhibition-dependent functions, PTEN can also function as a tumor suppressor in a PI3K-independent manner. Indeed, the PTEN network regulates a broad spectrum of biological functions, modulating the flow of information from membrane-bound growth factor receptors to nuclear transcription factors, occurring in concert with other tumor suppressors and oncogenic signaling pathways. PTEN acts through its lipid and protein phosphatase activity and other non-enzymatic mechanisms. Studies conducted over the past 10 years have expanded our understanding of the biological role of PTEN, showing that in addition to its ability to regulate proliferation and cell survival, it also plays an intriguing role in regulating genomic stability, cell migration, stem cell self-renewal, and tumor microenvironment. Changes in PTEN protein levels, location, and enzymatic activity through various molecular mechanisms can generate a continuum of functional PTEN levels in inherited syndromes, sporadic cancers, and other diseases. PTEN activity can indeed, be modulated by mutations, epigenetic silencing, transcriptional repression, aberrant protein localization, and post-translational modifications. This review will discuss our current understanding of the biological role of PTEN, how PTEN expression and activity are regulated, and the consequences of PTEN dysregulation in human malignant tumors.

Indexed as

cancerPHTSPI3KPTENsubcellular localization

Identifiers

PMID25763354
PMCPMC4329810
OpenAlexW2118263932

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.