Evidence map›Paper›PMID 26443342›Full record

ArticleInternational journal of obesity (2005)2016

Secreted factors derived from obese visceral adipose tissue regulate the expression of breast malignant transformation genes.

A B Crujeiras, B Cabia, M C Carreira, M Amil, J Cueva, S Andrade, L M Seoane, M Pardo, A Sueiro, J Baltar and 4 more

Registry-linked trialOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in International journal of obesity (2005), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06046755 (Evaluation of Changes in the Methylome and Prognosis of Obesity-related Breast Cancer After Nutritional Intervention-induced Weight Loss During the Oncological Treatment), which is not on this map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 14% 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.

NCT06046755 naunknown statusnot on this mapstarted 2023, after this paper: background citation

Evaluation of Changes in the Methylome and Prognosis of Obesity-related Breast Cancer After Nutritional Intervention-induced Weight Loss During the Oncological Treatment

TypeinterventionalSponsorHospital Clinico Universitario de SantiagoRan2023 to 2025Enrolled220ConditionsBreast Cancer, Obesity, Weight Change, Body, Epigenetic DisorderArmsVery low calorie ketogenic diet (VLCKD), Group educational intervention program (IGOBE)
3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 35 citations in OpenAlex.

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  11. Ketotherapy as an epigenetic modifier in cancer.Reviews in endocrine & metabolic disorders · 2020
    Review
  12. Ketogenic diets as treatment of obesity and type 2 diabetes mellitus.Reviews in endocrine & metabolic disorders · 2020
    Review
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  14. Article
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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

14 authors at 3 institutions in 2 countries.

A B CrujeirasLaboratory of Molecular and Cellular Endocrinology, Instituto de Investigación Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS) and Santiago de Compostela University (USC), Santiago de Compostela, Spain.
B CabiaLaboratory of Molecular and Cellular Endocrinology, Instituto de Investigación Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS) and Santiago de Compostela University (USC), Santiago de Compostela, Spain.
M C CarreiraLaboratory of Molecular and Cellular Endocrinology, Instituto de Investigación Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS) and Santiago de Compostela University (USC), Santiago de Compostela, Spain.
M AmilLaboratory of Molecular and Cellular Endocrinology, Instituto de Investigación Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS) and Santiago de Compostela University (USC), Santiago de Compostela, Spain.
J CuevaDivision of Medical Oncology, Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS), Santiago de Compostela, Spain.
S AndradeLaboratory of Molecular and Cellular Endocrinology, Instituto de Investigación Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS) and Santiago de Compostela University (USC), Santiago de Compostela, Spain.
L M SeoaneGrupo Fisiopatologia Endocrina, Instituto de Investigacion Sanitaria de Santiago de Compostela (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS), Santiago de Compostela, Spain.
M PardoGrupo Obesidomica, Instituto de Investigacion Sanitaria de Santiago de Compostela (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS), Santiago de Compostela, Spain.ORCID http://orcid.org/0000-0002-9967-1650
A SueiroLaboratory of Molecular and Cellular Endocrinology, Instituto de Investigación Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS) and Santiago de Compostela University (USC), Santiago de Compostela, Spain.
J BaltarDivision of General Surgery, Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS), Santiago de Compostela, Spain.
T MoraisClinical and Experimental Endocrinology, Department of Anatomy, Multidisciplinary Unit for Biomedical Research (UMIB), ICBAS, University of Porto, Porto, Portugal.
M P MonteiroClinical and Experimental Endocrinology, Department of Anatomy, Multidisciplinary Unit for Biomedical Research (UMIB), ICBAS, University of Porto, Porto, Portugal.
R Lopez-LopezDivision of Medical Oncology, Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS), Santiago de Compostela, Spain.
F F CasanuevaLaboratory of Molecular and Cellular Endocrinology, Instituto de Investigación Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS) and Santiago de Compostela University (USC), Santiago de Compostela, Spain.
Complejo Hospitalario Universitario de Santiago · ESCentro de Investigación Biomédica en Red · ESUniversidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesObese adipose tissue, especially the visceral depot, exhibits altered production of several molecules that could have a role on the initiation/promotion of breast cancer development. The aim of this work was to evaluate the effect of excess adipose tissue and its secreted factors on the expression of genes involved in the early steps of tumor promotion on the mammary gland. SUBJECTS AND

methodsCarcinogenesis-related gene expression was evaluated in mammary gland tissue from female diet-induced obese (DIO) Sprague-Dawley rats and circulating leukocytes isolated from a group of breast cancer diagnosed and non-diagnosed obese women and compared with their normal weight counterparts. In addition, the human non-tumoral mammary epithelial cell line MCF10A was treated in vitro with the visceral (retroperitoneal adipose tissue (RPAT)) or subcutaneous adipose tissue (SAT) secretome and with rising concentrations of the lipid peroxidation by-product 4-hydroxynonenal (4-HNE).

resultsDIO rats were classified as susceptible to DIO (DIO-S) or partially resistant to DIO (DIO-R) according to the maximum fat mass gain of the lean group as a cut-off. As compared with lean and DIO-R, the DIO-S group showed a higher fat mass and lower lean mass. The anatomical characteristic of DIO-S was correlated with differential expression of cellular proliferation (ALDH3A1 and MYC) and antioxidant and DNA protection (GSTM2, SIRT1), and tumor suppression (TP53, PTEN, TGFB1) genes. Remarkably, this carcinogenesis-related gene expression pattern was reproduced in MCF10A treated with the RPAT secretome from DIO-S rats and with the lipid peroxidation by-product 4-HNE. Moreover, this pattern was also detected in leukocytes from obese women compared with normal weight women without evidence of breast cancer.

conclusionsLipid peroxides secreted by the obese visceral adipose tissue could be among the relevant factors that promote changes involved in the early steps of tumor development in mammary gland. These changes can be detected even before histological alterations and in circulating leukocytes.

Indexed as

AnimalsApoptosisBlotting, WesternBreast NeoplasmsCell ProliferationCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseNeoplasm ProteinsObesityOxidative StressRatsRats, Sprague-DawleySubcutaneous FatNeoplasm Proteins

Identifiers

PMID26443342
OpenAlexW2190836040

What OpenQuestion holds

Textmetadata
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Registered trials

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.