Evidence map›Paper›PMID 36869333›Full record

ArticleJournal of translational medicine2023

Short term starvation potentiates the efficacy of chemotherapy in triple negative breast cancer via metabolic reprogramming.

Ioannis S Pateras, Chloe Williams, Despoina D Gianniou, Aggelos T Margetis, Margaritis Avgeris, Pantelis Rousakis, Aigli-Ioanna Legaki, Peter Mirtschink, Wei Zhang, Konstantina Panoutsopoulou and 13 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

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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

23 authors at 10 institutions in 5 countries.

Ioannis S Pateras *2nd Department of Pathology, "Attikon" University Hospital, Medical School, National and Kapodistrian University of Athens, 124 62, Athens, Greece. ipateras@med.uoa.gr.
Chloe Williams *Department of Integrative Medical Biology, Umeå University, 901 87, Umeå, Sweden.
Despoina D Gianniou *Department of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, 157 84, Athens, Greece.
Aggelos T Margetis *2nd Department of Internal Medicine, Athens Naval and Veterans Hospital, 115 21, Athens, Greece.
Margaritis Avgeris *Laboratory of Clinical Biochemistry-Molecular Diagnostics, Second Department of Pediatrics, School of Medicine, National and Kapodistrian University of Athens, "P. & A. Kyriakou" Children's Hospital, 115 27, Athens, Greece.
Pantelis RousakisDepartment of Biology, School of Science, National and Kapodistrian University of Athens, 157 84, Athens, Greece.
Aigli-Ioanna LegakiDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, 115 27, Athens, Greece.
Peter MirtschinkInstitute for Clinical Chemistry and Laboratory Medicine, University Hospital and Faculty of Medicine, Technische Universität Dresden, 013 07, Dresden, Germany.
Wei ZhangSwedish Metabolomics Centre, Department of Plant Physiology, Umeå University, 901 87, Umeå, Sweden.
Konstantina PanoutsopoulouDepartment of Biochemistry and Molecular Biology, Faculty of Biology, National and Kapodistrian University of Athens, 157 71, Athens, Greece.
Anastasios D DelisCentre for Basic Research, Bioimaging Unit, Biomedical Research Foundation, Academy of Athens, 115 27, Athens, Greece.
Stamatis N PagakisCentre for Basic Research, Bioimaging Unit, Biomedical Research Foundation, Academy of Athens, 115 27, Athens, Greece.
Wei TangMolecular Epidemiology Section, Laboratory of Human Carcinogenesis, Center for Cancer Research (CCR), NCI, NIH, Bethesda, MD, 20892-4258, USA.
Stefan AmbsMolecular Epidemiology Section, Laboratory of Human Carcinogenesis, Center for Cancer Research (CCR), NCI, NIH, Bethesda, MD, 20892-4258, USA.
Ulrika Warpman BerglundScience for Life Laboratory, Department of Oncology-Pathology, Karolinska Institutet, 171 76, Stockholm, Sweden.
Thomas HelledayScience for Life Laboratory, Department of Oncology-Pathology, Karolinska Institutet, 171 76, Stockholm, Sweden.
Anastasia VarvarigouDepartment of Paediatrics, University of Patras Medical School, General University Hospital, 265 04, Patras, Greece.
Antonios ChatzigeorgiouDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, 115 27, Athens, Greece.
Anders NordströmSwedish Metabolomics Centre, Department of Plant Physiology, Umeå University, 901 87, Umeå, Sweden.
Ourania E TsitsilonisDepartment of Biology, School of Science, National and Kapodistrian University of Athens, 157 84, Athens, Greece.
Ioannis P TrougakosDepartment of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, 157 84, Athens, Greece.
Jonathan D Gilthorpe *Department of Integrative Medical Biology, Umeå University, 901 87, Umeå, Sweden.
Teresa Frisan *Department of Molecular Biology and Umeå Centre for Microbial Research (UCMR), Umeå University, 901 87, Umeå, Sweden. teresa.frisan@umu.se.
National and Kapodistrian University of Athens · GRUmeå University · SEAcademy of Athens · GRCenter for Cancer Research · USTU Dresden · DEAthens Naval & Veterans Hospital · GRGeneral University Hospital of Patras · GRKarolinska Institutet · SEScience for Life Laboratory · SEUmeå Plant Science Centre · SE

Funding

Novel Markers for Disease Outcome in Breast CancerZIABC010887 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI AMBS, STEFAN · 2009 to 2025
$11.5M
6 · The paper itself

Abstract

backgroundChemotherapy (CT) is central to the treatment of triple negative breast cancer (TNBC), but drug toxicity and resistance place strong restrictions on treatment regimes. Fasting sensitizes cancer cells to a range of chemotherapeutic agents and also ameliorates CT-associated adverse effects. However, the molecular mechanism(s) by which fasting, or short-term starvation (STS), improves the efficacy of CT is poorly characterized.

methodsThe differential responses of breast cancer or near normal cell lines to combined STS and CT were assessed by cellular viability and integrity assays (Hoechst and PI staining, MTT or H

resultsWe provide mechanistic insights into how preconditioning with STS enhances the susceptibility of breast cancer cells to CT. We showed that combined STS and CT enhanced cell death and increased reactive oxygen species (ROS) levels, in association with higher levels of DNA damage and decreased mRNA levels for the NRF2 targets genes NQO1 and TXNRD1 in TNBC cells compared to near normal cells. ROS enhancement was associated with compromised mitochondrial respiration and changes in the metabolic profile, which have a significant clinical prognostic and predictive value. Furthermore, we validate the safety and efficacy of combined periodic hypocaloric diet and CT in a TNBC mouse model.

conclusionsOur in vitro, in vivo and clinical findings provide a robust rationale for clinical trials on the therapeutic benefit of short-term caloric restriction as an adjuvant to CT in triple breast cancer treatment.

Indexed as

Drug-Related Side Effects and Adverse ReactionsTriple Negative Breast NeoplasmsAnimalsDiet, ReducingHumansMiceObesityReactive Oxygen SpeciesReactive Oxygen SpeciesBreast cancerCaloric restrictionFastingMetabolic reprogrammingMitochondriaOncological treatmentOxidative stressReactive oxygen speciesStarvationTriple negative breast cancer

Identifiers

PMID36869333
PMCPMC9983166
OpenAlexW4323042386

What OpenQuestion holds

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LicenceCC BY
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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.