Evidence map›Paper›PMID 37174088›Full record

ReviewCancers2023

Autophagic-Related Proteins in Brain Gliomas: Role, Mechanisms, and Targeting Agents.

Cristina Pizzimenti, Vincenzo Fiorentino, Mariausilia Franchina, Maurizio Martini, Giuseppe Giuffrè, Maria Lentini, Nicola Silvestris, Martina Di Pietro, Guido Fadda, Giovanni Tuccari and 1 more

Open access · goldAbstract 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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Rab27: Molecular switch of tumor exosome secretion (Review).International journal of molecular medicine · 2026
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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

11 authors at 1 institution in 1 country.

Cristina PizzimentiTranslational Molecular Medicine and Surgery, Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, 98125 Messina, Italy.ORCID 0000-0002-4387-7174
Vincenzo FiorentinoDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Pathology Section, University of Messina, 98125 Messina, Italy.ORCID 0000-0002-1132-1761
Mariausilia FranchinaDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Pathology Section, University of Messina, 98125 Messina, Italy.
Maurizio MartiniDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Pathology Section, University of Messina, 98125 Messina, Italy.ORCID 0000-0002-6260-6310
Giuseppe GiuffrèDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Pathology Section, University of Messina, 98125 Messina, Italy.
Maria LentiniDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Pathology Section, University of Messina, 98125 Messina, Italy.
Nicola SilvestrisDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Oncology Section, University of Messina, 98125 Messina, Italy.
Martina Di PietroDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Oncology Section, University of Messina, 98125 Messina, Italy.
Guido FaddaDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Pathology Section, University of Messina, 98125 Messina, Italy.
Giovanni TuccariDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Pathology Section, University of Messina, 98125 Messina, Italy.ORCID 0000-0002-1561-4246
Antonio IeniDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Pathology Section, University of Messina, 98125 Messina, Italy.ORCID 0000-0003-2878-3572
University of Messina · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present review focuses on the phenomenon of autophagy, a catabolic cellular process, which allows for the recycling of damaged organelles, macromolecules, and misfolded proteins. The different steps able to activate autophagy start with the formation of the autophagosome, mainly controlled by the action of several autophagy-related proteins. It is remarkable that autophagy may exert a double role as a tumour promoter and a tumour suppressor. Herein, we analyse the molecular mechanisms as well as the regulatory pathways of autophagy, mainly addressing their involvement in human astrocytic neoplasms. Moreover, the relationships between autophagy, the tumour immune microenvironment, and glioma stem cells are discussed. Finally, an excursus concerning autophagy-targeting agents is included in the present review in order to obtain additional information for the better treatment and management of therapy-resistant patients.

Indexed as

autophagyautophagy-related proteinsglioblastomasgliomasprognosistreatment

Identifiers

PMID37174088
PMCPMC10177137
OpenAlexW4372293160

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.