Evidence map›Paper›PMID 31341534›Full record

ReviewOxidative medicine and cellular longevity2019

MYC Expression and Metabolic Redox Changes in Cancer Cells: A Synergy Able to Induce Chemoresistance.

Barbara Marengo, Ombretta Garbarino, Andrea Speciale, Lorenzo Monteleone, Nicola Traverso, Cinzia Domenicotti

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Chemoresistance: The hidden barrier in cancer treatment.Cancer pathogenesis and therapy · 2026
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  15. The many lives of Myc in the pancreatic β-cell.The Journal of biological chemistry
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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

6 authors at 2 institutions in 1 country.

Barbara MarengoDepartment of Experimental Medicine, General Pathology Section, University of Genova, Italy.ORCID https://orcid.org/0000-0003-3056-6569
Ombretta GarbarinoDepartment of Experimental Medicine, General Pathology Section, University of Genova, Italy.ORCID https://orcid.org/0000-0003-0589-4739
Andrea SpecialeUOC Mutagenesis and Oncologic Prevention, Ospedale Policlinico San Martino, Genova, Italy.
Lorenzo MonteleoneDepartment of Experimental Medicine, General Pathology Section, University of Genova, Italy.
Nicola TraversoDepartment of Experimental Medicine, General Pathology Section, University of Genova, Italy.ORCID https://orcid.org/0000-0002-0306-8647
Cinzia DomenicottiDepartment of Experimental Medicine, General Pathology Section, University of Genova, Italy.ORCID https://orcid.org/0000-0002-5003-7333
University of Genoa · ITOspedale Policlinico San Martino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemoresistance is due to multiple factors including the induction of a metabolic adaptation of tumor cells. In fact, in these cells, stress conditions induced by therapies stimulate a metabolic reprogramming which involves the strengthening of various pathways such as glycolysis, glutaminolysis and the pentose phosphate pathway. This metabolic reprogramming is the result of a complex network of mechanisms that, through the activation of oncogenes (i.e., MYC, HIF1, and PI3K) or the downregulation of tumor suppressors (i.e., TP53), induces an increased expression of glucose and/or glutamine transporters and of glycolytic enzymes. Therefore, in order to overcome chemoresistance, it is necessary to develop combined therapies which are able to selectively and simultaneously act on the multiple molecular targets responsible for this adaptation. This review is focused on highlighting the role of MYC in modulating the epigenetic redox changes which are crucial in the acquisition of therapy resistance.

Indexed as

Drug Resistance, NeoplasmGenes, mycGlycolysisHumansNeoplasmsOxidation-ReductionProto-Oncogene Proteins c-mycMYC protein, humanProto-Oncogene Proteins c-myc

Identifiers

PMID31341534
PMCPMC6614970
OpenAlexW2956156353

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.