Evidence map›Paper›PMID 31756890›Full record

ArticleNutrients2019

Hormonal Therapy Resistance and Breast Cancer: Involvement of Adipocytes and Leptin.

Laetitia Delort, Lauriane Bougaret, Juliette Cholet, Marion Vermerie, Hermine Billard, Caroline Decombat, Céline Bourgne, Marc Berger, Charles Dumontet, Florence Caldefie-Chezet

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Leptin increases chemosensitivity by inhibitingJournal of gastrointestinal oncology · 2024
    Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
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  15. Review
  16. The pleiotropic roles of adipocyte secretome in remodeling breast cancer.Journal of experimental & clinical cancer research : CR · 2022
    Review
  17. Obesity and endocrine therapy resistance in breast cancer: Mechanistic insights and perspectives.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022
    Review
  18. Article
  19. Review
  20. Review
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 5 institutions in 1 country.

Laetitia DelortINRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, Université Clermont Auvergne, F-63000 Clermont-Ferrand, France.
Lauriane BougaretINRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, Université Clermont Auvergne, F-63000 Clermont-Ferrand, France.
Juliette CholetINRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, Université Clermont Auvergne, F-63000 Clermont-Ferrand, France.
Marion VermerieINRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, Université Clermont Auvergne, F-63000 Clermont-Ferrand, France.
Hermine BillardINRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, Université Clermont Auvergne, F-63000 Clermont-Ferrand, France.
Caroline DecombatINRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, Université Clermont Auvergne, F-63000 Clermont-Ferrand, France.
Céline BourgneService d'Hématologie Biologique, CHU Estaing, F-63000 Clermont-Ferrand, France.
Marc BergerService d'Hématologie Biologique, CHU Estaing, F-63000 Clermont-Ferrand, France.
Charles DumontetUniversité Lyon 1, INSERM U1052, CNRS 5286, Cancer Research Center of Lyon, 69008 Lyon, France.
Florence Caldefie-ChezetINRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, Université Clermont Auvergne, F-63000 Clermont-Ferrand, France.
Université Clermont Auvergne · FRCentre Hospitalier Universitaire de Clermont-Ferrand · FRUnité de Nutrition Humaine · FRCentre de Recherche en Nutrition Humaine d'Auvergne · FRUniversité Claude Bernard Lyon 1 · FR

Funding

Institut National Du Cancer INCA PL-2013-66
6 · The paper itself

Abstract

Obesity, a recognized risk factor for breast cancer in postmenopausal women, is associated with higher mortality rates regardless of menopausal status, which could in part be explained by therapeutic escape. Indeed, adipose microenvironment has been described to influence the efficiency of chemo- and hormonal therapies. Residual cancer stem cells could also have a key role in this process. To understand the mechanisms involved in the reduced efficacy of hormonal therapy on breast cancer cells in the presence of adipose secretome, human adipose stem cells (hMAD cell line) differentiated into mature adipocytes were co-cultured with mammary breast cancer cells and treated with hormonal therapies (tamoxifen, fulvestrant). Proliferation and apoptosis were measured (fluorescence test, impedancemetry, cytometry) and the gene expression profile was evaluated. Cancer stem cells were isolated from mammospheres made from MCF-7. The impact of chemo- and hormonal therapies and leptin was evaluated in this population. hMAD-differentiated mature adipocytes and their secretions were able to increase mammary cancer cell proliferation and to suppress the antiproliferative effect of tamoxifen, confirming previous data and validating our model. Apoptosis and cell cycle did not seem to be involved in this process. The evaluation of gene expression profiles suggested that STAT3 could be a possible target. On the contrary, leptin did not seem to be involved. The study of isolated cancer stem cells revealed that their proliferation was stimulated in the presence of anticancer therapies (tamoxifen, fulvestrant, doxorubicine) and leptin. Our study confirmed the role of adipocytes and their secretome, but above all, the role of communication between adipose and cancer cells in interfering with the efficiency of hormonal therapy. Among the pathophysiological mechanisms involved, leptin does not seem to interfere with the estrogenic pathway but seems to promote the proliferation of cancer stem cells.

Indexed as

Drug Resistance, NeoplasmAdipocytesAntineoplastic Agents, HormonalBreast NeoplasmsCell CommunicationCell ProliferationCoculture TechniquesFemaleFulvestrantGene Expression Regulation, NeoplasticHumansLeptinMCF-7 CellsNeoplastic Stem CellsSignal TransductionSTAT3 Transcription FactorAntineoplastic Agents, HormonalFulvestrantLEP protein, humanLeptinSTAT3 protein, humanSTAT3 Transcription FactorTamoxifenadipose secretomebreast cancercancer stem cellshormonal therapy resistanceleptin

Identifiers

PMID31756890
PMCPMC6950701
OpenAlexW2990171706

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.