Evidence map›Paper›PMID 34830777›Full record

ReviewCancers2021

Understanding the Role of Autophagy in Cancer Formation and Progression Is a Real Opportunity to Treat and Cure Human Cancers.

Simone Patergnani, Sonia Missiroli, Giampaolo Morciano, Mariasole Perrone, Cristina M Mantovani, Gabriele Anania, Francesco Fiorica, Paolo Pinton, Carlotta Giorgi

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 60 citations in OpenAlex.

  1. Terpenoids as modulators of autophagy-senescence crosstalk in lung cancer.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
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  11. Exosomes, autophagy, and cancer: A complex triad.International journal of cancer · 2025
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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

9 authors at 1 institution in 1 country.

Simone PatergnaniLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-7951-9267
Sonia MissiroliLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.
Giampaolo MorcianoLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.
Mariasole PerroneLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.
Cristina M MantovaniLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-7557-9633
Gabriele AnaniaDepartment of Medical Sciences, Section of General and Thoracic Surgery, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-9255-3312
Francesco FioricaDepartment of Radiation Oncology and Nuclear Medicine, AULSS 9 Scaligera, Ospedale Mater Salutis di Legnago, 37045 Verona, Italy.ORCID 0000-0002-9404-3655
Paolo PintonLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0001-7108-6508
Carlotta GiorgiLaboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0002-2494-7405
University of Ferrara · IT

Funding

Associazione Ricerca Oncologica Sperimentale Estense (A-ROSE)European Council InflaPML 853057Italian Association for Cancer Research IG-19803Italian Association for Cancer Research IG-23670Ministero della Salute GR-2013-02356747Ministry of Education, University and Research PRIN20177E9EPYMinistry of Education, University and Research PRIN2017E5L5P3
6 · The paper itself

Abstract

The malignant transformation of a cell produces the accumulation of several cellular adaptions. These changes determine variations in biological processes that are necessary for a cancerous cell to survive during stressful conditions. Autophagy is the main nutrient recycling and metabolic adaptor mechanism in eukaryotic cells, represents a continuous source of energy and biomolecules, and is fundamental to preserve the correct cellular homeostasis during unfavorable conditions. In recent decades, several findings demonstrate a close relationship between autophagy, malignant transformation, and cancer progression. The evidence suggests that autophagy in the cancer context has a bipolar role (it may act as a tumor suppressor and as a mechanism of cell survival for established tumors) and demonstrates that the targeting of autophagy may represent novel therapeutic opportunities. Accordingly, the modulation of autophagy has important clinical benefits in patients affected by diverse cancer types. Currently, about 30 clinical trials are actively investigating the efficacy of autophagy modulators to enhance the efficacy of cytotoxic chemotherapy treatments. A deeper understanding of the molecular pathways regulating autophagy in the cancer context will provide new ways to target autophagy for improving the therapeutic benefits. Herein, we describe how autophagy participates during malignant transformation and cancer progression, and we report the ultimate efforts to translate this knowledge into specific therapeutic approaches to treat and cure human cancers.

Indexed as

autophagycancerclinical trialstherapytumor suppression

Identifiers

PMID34830777
PMCPMC8616104
OpenAlexW3213901719

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.