Evidence map›Paper›PMID 36757577›Full record

ReviewCancer metastasis reviews2023

Dormancy, stemness, and therapy resistance: interconnected players in cancer evolution.

Federica Francescangeli, Maria Laura De Angelis, Rachele Rossi, Adriano Cuccu, Alessandro Giuliani, Ruggero De Maria, Ann Zeuner

Open access · hybridFull text readReview
In one paragraph

Review in Cancer metastasis reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
14.5field-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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
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  16. The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026
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2 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

7 authors at 3 institutions in 1 country.

Federica FrancescangeliDepartment of Oncology and Molecular Medicine, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161, Rome, Italy.ORCID http://orcid.org/0000-0002-1086-5265
Maria Laura De AngelisDepartment of Oncology and Molecular Medicine, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161, Rome, Italy.ORCID http://orcid.org/0000-0003-4220-8822
Rachele RossiDepartment of Oncology and Molecular Medicine, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161, Rome, Italy.ORCID http://orcid.org/0000-0002-7570-2934
Adriano CuccuDepartment of Statistical Sciences, La Sapienza University of Rome, Piazzale Aldo Moro 5, 00185, Rome, Italy.ORCID http://orcid.org/0000-0001-7539-1868
Alessandro GiulianiEnvironment and Health Department, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161, Rome, Italy.ORCID http://orcid.org/0000-0002-4640-804X
Ruggero De MariaInstitute of General Pathology, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168, Rome, Italy.ORCID http://orcid.org/0000-0003-2255-0583
Ann ZeunerDepartment of Oncology and Molecular Medicine, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161, Rome, Italy. a.zeuner@iss.it.ORCID http://orcid.org/0000-0002-8295-3715
Istituto Superiore di Sanità · ITSapienza University of Rome · ITUniversità Cattolica del Sacro Cuore · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The biological complexity of cancer represents a tremendous clinical challenge, resulting in the frequent failure of current treatment protocols. In the rapidly evolving scenario of a growing tumor, anticancer treatments impose a drastic perturbation not only to cancer cells but also to the tumor microenvironment, killing a portion of the cells and inducing a massive stress response in the survivors. Consequently, treatments can act as a double-edged sword by inducing a temporary response while laying the ground for therapy resistance and subsequent disease progression. Cancer cell dormancy (or quiescence) is a central theme in tumor evolution, being tightly linked to the tumor's ability to survive cytotoxic challenges, metastasize, and resist immune-mediated attack. Accordingly, quiescent cancer cells (QCCs) have been detected in virtually all the stages of tumor development. In recent years, an increasing number of studies have focused on the characterization of quiescent/therapy resistant cancer cells, unveiling QCCs core transcriptional programs, metabolic plasticity, and mechanisms of immune escape. At the same time, our partial understanding of tumor quiescence reflects the difficulty to identify stable QCCs biomarkers/therapeutic targets and to control cancer dormancy in clinical settings. This review focuses on recent discoveries in the interrelated fields of dormancy, stemness, and therapy resistance, discussing experimental evidences in the frame of a nonlinear dynamics approach, and exploring the possibility that tumor quiescence may represent not only a peril but also a potential therapeutic resource.

Indexed as

Antineoplastic AgentsNeoplasmsDisease ProgressionHumansNeoplastic Stem CellsTumor MicroenvironmentAntineoplastic AgentsCancer stem cellsDormancyQuiescenceStemnessTherapy resistanceTumor relapse

Identifiers

PMID36757577
PMCPMC10014678
OpenAlexW4319656668

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read5
identifiers read1
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.