Evidence map›Paper›PMID 31231612›Full record

ArticleFrontiers in oncology2019

Breast Cancer Subtypes Present a Differential Production of Reactive Oxygen Species (ROS) and Susceptibility to Antioxidant Treatment.

Fabiola Lilí Sarmiento-Salinas, Alam Delgado-Magallón, José Benito Montes-Alvarado, Dalia Ramírez-Ramírez, Juan Carlos Flores-Alonso, Paulina Cortés-Hernández, Julio Reyes-Leyva, Irma Herrera-Camacho, Maricruz Anaya-Ruiz, Rosana Pelayo and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
5.1field-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

94 citing papers in PubMed, 182 citations in OpenAlex.

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  17. Multi-omics profile of exceptional long-term survivors of AJCC stage III triple-negative breast cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025
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34 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

12 authors at 3 institutions in 1 country.

Fabiola Lilí Sarmiento-SalinasCentro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla, Mexico.
Alam Delgado-MagallónCentro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla, Mexico.
José Benito Montes-AlvaradoCentro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla, Mexico.
Dalia Ramírez-RamírezCentro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla, Mexico.
Juan Carlos Flores-AlonsoCentro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla, Mexico.
Paulina Cortés-HernándezCentro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla, Mexico.
Julio Reyes-LeyvaCentro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla, Mexico.
Irma Herrera-CamachoCentro de Química, Instituto de Ciencias, Benemérita Universidad Autónoma de Puebla, Puebla, Mexico.
Maricruz Anaya-RuizCentro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla, Mexico.
Rosana PelayoCentro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla, Mexico.
Lourdes Millán-Pérez-PeñaCentro de Química, Instituto de Ciencias, Benemérita Universidad Autónoma de Puebla, Puebla, Mexico.
Paola MaycotteCONACYT-Centro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla, Mexico.
Mexican Social Security Institute · MXBenemérita Universidad Autónoma de Puebla · MXConsejo Nacional de Humanidades, Ciencias y Tecnologías · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Due to their crucial role in cell metabolism and homeostasis, alterations in mitochondrial biology and function have been related to the progression of diverse diseases including cancer. One of the consequences associated to mitochondrial dysfunction is the production of reactive oxygen species (ROS). ROS are known to have a controversial role during cancer initiation and progression and although several studies have tried to manipulate intracellular ROS levels using antioxidants or pro-oxidation conditions, it is not yet clear how to target oxidation for cancer therapy. In this study, we found differences in mitochondrial morphology in breast cancer cells when compared to a non-tumorigenic cell line and differences in mitochondrial function among breast cancer subtypes when exploring gene-expression data from the TCGA tumor dataset. Interestingly, we found increased ROS levels in triple negative breast cancer (TNBC) cell lines and a dependency on ROS for survival since antioxidant treatment induced cell death in TNBC cells but not in an estrogen receptor positive (ER+) cell line. Moreover, we identified the mitochondria as the main source of ROS in TNBC cell lines. Our results indicate a potential use for ROS as a target for therapy in the TNBC subtype which currently has the worst prognosis among all breast cancers and remains as the only breast cancer subtype which lacks a targeted therapy.

Indexed as

breast cancermitochondriamitochondrial morphologymitochondrial ROSROS

Identifiers

PMID31231612
PMCPMC6568240
OpenAlexW2948081235

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.