Evidence map›Paper›PMID 32486505›Full record

ReviewCancers2020

Metabolic Escape Routes of Cancer Stem Cells and Therapeutic Opportunities.

Alice Turdo, Gaetana Porcelli, Caterina D'Accardo, Simone Di Franco, Francesco Verona, Stefano Forte, Dario Giuffrida, Lorenzo Memeo, Matilde Todaro, Giorgio Stassi

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  13. Targeting Phosphatases and Kinases: How to Checkmate Cancer.Frontiers in cell and developmental biology · 2021
    Review
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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

10 authors at 1 institution in 1 country.

Alice TurdoDepartment of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, 90127 Palermo, Italy.
Gaetana PorcelliDepartment of Surgical, Oncological and Stomatological Sciences (DICHIRONS), University of Palermo, 90127 Palermo, Italy.
Caterina D'AccardoDepartment of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, 90127 Palermo, Italy.
Simone Di FrancoDepartment of Surgical, Oncological and Stomatological Sciences (DICHIRONS), University of Palermo, 90127 Palermo, Italy.
Francesco VeronaDepartment of Surgical, Oncological and Stomatological Sciences (DICHIRONS), University of Palermo, 90127 Palermo, Italy.
Stefano ForteDepartment of Experimental Oncology, Mediterranean Institute of Oncology (IOM), 95029 Catania, Italy.
Dario GiuffridaDepartment of Experimental Oncology, Mediterranean Institute of Oncology (IOM), 95029 Catania, Italy.
Lorenzo MemeoDepartment of Experimental Oncology, Mediterranean Institute of Oncology (IOM), 95029 Catania, Italy.
Matilde TodaroDepartment of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, 90127 Palermo, Italy.
Giorgio StassiDepartment of Surgical, Oncological and Stomatological Sciences (DICHIRONS), University of Palermo, 90127 Palermo, Italy.
University of Palermo · IT

Funding

Associazione Italiana per la Ricerca sul Cancro 14415Associazione Italiana per la Ricerca sul Cancro 16746Associazione Italiana per la Ricerca sul Cancro 9979Ministero dell'Istruzione, dell'Università e della Ricerca PRIN (2017WNKSLR)
6 · The paper itself

Abstract

Although improvement in early diagnosis and treatment ameliorated life expectancy of cancer patients, metastatic disease still lacks effective therapeutic approaches. Resistance to anticancer therapies stems from the refractoriness of a subpopulation of cancer cells-termed cancer stem cells (CSCs)-which is endowed with tumor initiation and metastasis formation potential. CSCs are heterogeneous and diverge by phenotypic, functional and metabolic perspectives. Intrinsic as well as extrinsic stimuli dictated by the tumor microenvironment (TME)have critical roles in determining cell metabolic reprogramming from glycolytic toward an oxidative phenotype and vice versa, allowing cancer cells to thrive in adverse milieus. Crosstalk between cancer cells and the surrounding microenvironment occurs through the interchange of metabolites, miRNAs and exosomes that drive cancer cells metabolic adaptation. Herein, we identify the metabolic nodes of CSCs and discuss the latest advances in targeting metabolic demands of both CSCs and stromal cells with the scope of improving current therapies and preventing cancer progression.

Indexed as

cancer metabolismcancer stem cellsglycolysislipid metabolismmetabolic reprogrammingmetabolism-based anticancer drugsOXPHOStumor microenvironment

Identifiers

PMID32486505
PMCPMC7352619
OpenAlexW3030728390

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.